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A   TREATISE   ON 

DIAGNOSTIC  METHODS 

OF   EXAMINATION 


BY 
PROF.  DR.  HERMANN  SAHLI 

DIRECTOR    OF   THE    MEDICAL    CLINIC,    UNIVERSITY    OF   BERN 

EDITED,   WITH   ADDITIONS,    BY 

FRANCIS  P.  KINNICUTT,  M.D. 

PROFESSOR    OF    CLINICAL    MEDICINE    AT    COLUMBIA    UNIVERSITY    (COLLEGE    OF   PHYSICIANS 
AND    SURGEONS),    NEW   YORK;    PHYSICIAN   TO    THE   PRESBYTERIAN    HOSPITAL 

AND 

NATH'L  BOWDITCH  POTTER,  M.D, 

VISITING   PHYSICIAN   TO   THE    CITY    HOSPITAL   AND   TO   THE    FRENCH    HOSPITAL,  NEW  YORK 


Authorized  Translation  from  the  Fourth 
Revised   and  Enlarged   German    Edition 


PHILADELPHIA  AND  LONDON 

W.    B.    SAUNDERS    COMPANY 

1906 


Set  up,  electrotyped,  printed,  and  copyrighted  September  1905. 


Copyright,  1905,  by  W.  B.  Saunders  &  Company. 


Reprinted  February  1906. 


ELECTROTYPEO  BY 


PRESS  OF 


WE8T00TT  i  THOMSON.    PHILAOA.  "•   °-   SAUNDERS  COMPANY 


EDITORS'  PREFACE. 


The  first  edition  of  Professor  Sahli's  treatise,  "  Clinical  Methods  of 
Investigation,"  was  published  in  1894,  and  was  immediately  recognized 
as  a  master- work  in  this  field.  A  second  edition  appeared  in  1899,  a 
third  in  1902,  and  a  fourth  during  the  present  year  (1905).  The  present 
translation  of  the  last  edition  was  undertaken  to  render  easily  available 
to  English-speaking  students  of  medicine  a  work  too  little  known  in 
this  country  and  England. 

The  distinguished  Swiss  Professor  has  chosen  the  title  "  Lehrbuch 
der  klinischen  Untersuchungs-Methoden  " — a  title  which  inadequately 
expresses  the  great  scope  of  the  work.  Not  only  are  all  methods  of 
examination  for  the  purpose  of  diagnosis  exhaustively  considered,  but 
the  explanation  of  clinical  phenomena  is  given  and  discussed  from 
physiological  as  well  as  pathological  points  of  view,  with  a  thoroughness 
which  has  not  been  attempted  in  any  clinical  work  which  has  yet 
appeared.     Its  great  value  will  at  once  be  recognized. 

It  has  seemed  wise  to  publish  the  translation  practically  as  the 
original  came  from  the  pen  of  its  author.  A  few  notes  have  been 
added,  especially  where  methods  are  described  which  difier  from  those 
commonly  employed  by  American  and  English  clinicians.  A  brief 
review  of  the  investigations  of  American  and  English  observers  on  the 
value  of  the  clinical  estimation  of  blood-pressure,  with  the  description 
of  some  newly  devised  or  modified  instruments  for  this  purpose,  has 
been  written  by  Dr.  Theodore  C.  Janeway. 

We  are  indebted  to  Dr.  C.  P.  Flint,  of  this  city,  for  a  considerable 
part  of  the  labor  in  translation,  also  to  Drs.  Lewis  F.  Frizzell  and  H. 
D.  Meeker  for  assistance  in  revising  the  manuscript.  For  various  notes 
and  assistance  in  special  chapters  of  the  book,  we  are  indebted  to  the 
following-named  gentlemen,  whose  respective  initials  will  be  found  at 
the  end  of  the  notes  they  have  added :  Prof.  Joseph  Collins,  Professor 
of  Nervous  and  Mental  Diseases  at  the  Post-Graduate  Medical  School ; 
Dr.  Charles  Norris,  Instructor  in  Bacteriology  and  Hygiene  at  Columbia 
University  Medical  School ;  Dr.  H.  C.  Jackson,  Assistant  Professor  of 
Physiological  Chemistry  at  the  University  and  Bellevue  Medical  School ; 
Dr.  Arnold  Knapj>,  Professor  of  Ophthalmology  at  Columbia  University 
Medical  School  ;  and  Dr.  W.  Sohier  Bryant,  Instructor  in  Diseases  of 
the  Ear  at  the  Post-Graduate  Medical  School. 


PREFACE  TO  THE  FOURTH  EDITION. 


An  idea  of  the  entire  contents  of  the  present  edition  is  best  obtained 
by  consulting  the  systematic  table  of  contents  on  page  15. 

The  bringing  out  of  new  editions  is  very  much  like  keeping  a  large 
building  in  good  condition — -no  sooner  have  a  certain  number  of  repairs 
been  completed  so  that  the  agent  congratulates  himself  on  getting  a 
little  rest,  than  he  is  obliged  to  begin  again.  After  so  many  changes 
had  been  found  necessary  in  former  editions,  it  was  my  intention  to 
bring  out  the  present  (fourth)  edition  without  much  alteration  or  addi- 
tion ;  but  this  intention  I  was  forced  to  abandon.  As  in  preceding 
editions,  I  have  again  endeavored  to  lay  equal  stress  on  all  the  various 
branches  of  internal  medicine :  for  I  hold  that  all  specialization  in 
internal  medicine,  aside  from  those  branches  which  must  necessarily 
remain  separate  on  account  of  the  special  surgical  technic  which  they 
demand,  is  unjustifiable  and  destructive  of  that  symmetry  which  should 
be  an  essential  feature  of  medical  education. 

Aside  from  numerous  minor  changes  in  subject-matter  and  arrange- 
ment, I  may  mention  the  most  important  additions  by  which  I  have 
endeavored  to  increase  the  value  of  the  book. 

The  section  on  sphygmography  contains  a  full  account  of  the  changes 
made  by  Jaquet  as  well  as  myself  in  the  older  Jaquet  sphygmograph. 
These  modifications  correct  the  excessive  vibration  of  the  instrument 
and,  I  may  venture  to  say,  render  it  in  every  way  satisfactory.  In  the 
chapter  on  sphygmomanometry  a  new  clinical  pocket-manometer  of  my 
own  is  described.  In  the  section  on  the  venous  pulse,  mention  is  made 
of  Volhard's  recent  work  and  his  method  of  determining  the  phases  of 
the  venous  pulse.  Numerous  other  changes  and  additions  in  the  chap- 
ter on  physical  diagnosis  I  shall  pass  over  without  mentioning.  Much 
has  been  added  also  to  the  paragraphs  relating  to  the  examination  of  the 
digestive  apparatus.  I  may  mention,  for  example,  Reissner's  improve- 
ment of  Liitke-Martius's  method  of  determining  the  hydrochloric  acid 
in  the  gastric  juice ;  Reissner's  method  of  determining  the  chlorids  for 
the  early  diagnosis  of  cancer  of  the  stomach  ;  an  improvement  on  the 
Hehner-Malay  method  of  determining  acidity  ;  an  improvement  of 
Mett's  digestion -test  by  Nirenstein  and  Schiff;  a  refutation  of  the 
objections  to  _my  method  of  butyrometric  examination  of  the  stomach, 
with  a  few  improvements  of  the  method  ;  certain  newer  methods  for 
determining  the  "  crude  motility  "  of  the  stomach  and  for  diagnosing 
pyloric  stenosis ;  a  description  of  a  special  platform,  which  is  both 
movable  and  capable  of  being  heated,  and  is  designed  for  examining  feces 
for  amebse,  etc. ;   and,  finally,  a  table  containing  the  rarer  forms  of 


10  PREFACE  TO   THE  FOURTH  EDITION. 

tapeworm  occurring  in  man.  Some  of  the  new  features  in  the  chapter 
on  the  examination  of  the  urine  are  :  the  method  of  separating  the 
urine ;  Seliwanow's  reaction  for  levulose  •  Bial's  method  of  testing  for 
pentoses ;  a  discussion  of  the  controversy  in  regard  to  the  nature  of  the 
mucin-like  body  in  the  urine ;  the  quantitative  determination  of  urochrome 
after  Klemperer ;  the  determination  of  urea  after  Schondorff;  Hopkin, 
Folin,  and  Shaffer's  method  of  determining  uric  acid ;  detailed  direc- 
tions for  titrating  the  urine  with  phosphates  ;  and  the  quantitative 
determination  of  indican  in  the  urine.  Kjeldahl's  method  is  discussed 
more  in  detail  than  in  the  preceding  editions.  Magnus-Levy's  investi- 
gations in  regard  to  oxybutyric  acid  in  the  urine  are  also  mentioned  at 
greater  length.  The  important  recently  published  investigations  by 
IMoritz  in  regard  to  titration  of  fluids  containing  phosphates,  particularly 
urine  and  gastric  juice,  are  described  in  an  appendix,  which  also  contains 
a  discussion  of  the  question  whether  the  recent  attempt  to  substitute  the 
conception  of  concentration  of  the  ions  of  hydrogen  for  that  of  the  titri- 
metric  acidity  is  justifiable.  Osmotic  pressure  and  the  cryoscopy  of  the 
urine  are  discussed  at  length.  In  connection  with  urinary  sediments, 
Liebermann  and  Posner's  methods  of  staining  urinary  sediments  are 
described. 

In  the  chapter  devoted  to  the  bacteriology  of  the  sputum  the  micro- 
coccus catarrhalis,  as  well  as  the  bacillus  of  plague,  anthrax,  and  glanders, 
is  described.  Wanner's  investigations  in  regard  to  the  amount  of  albu- 
min contained  in  the  sputum  are  mentioned.  The  chapter  on  the 
examination  of  the  blood  has  been  thoroughly  revised  so  as  to  harmo- 
nize with  the  results  of  the  most  recent  investigations.  Some  of  the 
things  are  new  and  mentioned  for  the  first  time,  such  as  my  hemometer  ; 
Breuer  and  Turk's  cell  for  counting  leukocytes  ;  Jenner's  method  of 
staining ;  the  volume-quotient  of  the  red  blood-cells  after  Capps  ;  a 
discussion  of  rouleau-formation  and  the  net  of  fibrin  in  recent  blood 
preparations  ;  erythremia  or  polycythemia  ;  and,  finally,  the  methods  of 
determining  the  osmotic  pressure  and  the  viscosity  of  the  blood.  In  the 
section  dealing  with  the  behavior  of  the  blood  in  infectious  diseases, 
mumps,  varicella,  and  whooping-cough  have  been  added  to  the  list.  The 
chapter  on  leukemia  has  been  revised  in  accordance  with  the  more  recent 
books  on  the  subject,  and  acute  myelemia  is  also  discussed  in  addition 
to  acute  lymphatic  leukemia.  The  relation  of  lymphatic  leukemia  and 
the  pseudoleukemias  to  the  remaining  forms  of  lymphomatosis  is  dis- 
cussed on  the  basis  of  Turk's  system  of  lymphomatosis.  A  new  table 
has  been  added  to  the  section  on  hematology.  In  connection  with 
methods  of  examination  of  the  upper  air  passages  there  wall  be  found 
a  short  account  of  bronchoscopy.  Under  the  head  ()f  examination  of 
the  esophagus  are  mentioned  Mikulicz's  experiments  in  determining  the 
pressure  in  the  esophagus  ;  Eumpel's  experiment ;  and  other  matters 
relating  to  the  diagnosis  of  diffuse  dilatations  of  the  esophagus,  a  sub- 
ject which  has  been  much  discussed  in  recent  literature.  In  the  chapter 
on  exploratory  puncture,  the  controversy  in  regard  to  the  nature  of  the 
mucin-like  body  found  in  the  fluid  obtained  by  puncture  ;  the  significance 


PREFACE  TO   THE  FOURTH  EDITION.  11 

of  the  chylous  nature  of  that  body ;  cytodiagnosis  (so  called) ;  and  the 
question  of  the  osmotic  pressure  of  the  puncture  fluid  are  discussed. 
Among  the  additions  in  the  section  devoted  to  the  examination  of  the 
nervous  system  may  be  mentioned  :  the  expansion  of  the  paragraph  on 
associated  movements ;  the  adoption  of  an  explanation  of  my  own  for 
the  intention  tremor ;  the  disturbance  of  speech  and  the  forced  laugh  in 
multiple  sclerosis ;  the  peculiar  electrical  reactions  described  by  Placzek 
in  certain  cases  of  chronic  peripheral  palsy  of  long  standing ;  the  mus- 
cular atrophy  seen  in  afi'ections  of  the  central  motor  neuron ;  a  new 
scheme  of  pupillary  reaction  superseding  Bechterew's,  which  appeared 
in  the  last  edition  and  which  has  shown  itself  to  be  inadequate ;  Schir- 
mer's  studies  in  testing  the  pupillary  reaction  ;  Fragstein  and  Kempner's 
pupil-tester  for  determining  hemiopic  pupillary  rigidity ;  v.  Bezold's 
modification  of  Rinne's  experiment,  with  reference  to  the  Zimmermann- 
Helmholtz  controversy  in  regard  to  the  significations  of  the  auditory 
ossicles  ;  Weber's  and  Schwabach's  experiments ;  a  chapter  on  cerebral 
disturbances  of  sensation,  with  special  reference  to  the  distinction 
between  cerebral  disturbances  with  an  anatomic  basis  and  hysterical 
hemianesthesia  ;  sensation  in  cattle ;  and,  finally,  a  chapter  on  vertigo. 
The  section  on  aphasia  has  been  remodeled  on  the  basis  of  a  different 
theory  in  regard  to  the  speech  tract  from  that  adopted  in  former  editions. 
It  is  suggested  that  the  expressions  "  transcortical,"  "  cortical,"  and 
"  subcortical,"  which  are  really  incorrect,  be  replaced  by  the  terms 
"  transcentral,"  "  central,"  and  "  subcentral."  There  has  also  been 
added  a  chapter  on  certain  disturbances  allied  to  aphasia,  such  as  asym- 
bolia,  apraxia,  amusia,  mental  deafness,  and  mental  blindness ;  also  a 
chapter  on  spinal  hemiplegia.  The  description  of  the  functions  of  the 
bladder  and  rectum  takes  account  also  of  the  doctrine  of  sympathetic 
centres  for  the  bladder  and  rectum  and  ejaculation  centres,  as  described 
in  the  more  recent  work  of  L.  R.  Miiller.  The  neurological  section, 
as  well  as  other  portions  of  the  book,  has  been  enriched  by  a  number 
of  new  illustrations.  Finally,  the  appendix  on  the  modern  methods  of 
analyzing  arhythmia  of  the  pulse  after  Engelmann,  Wenkebach,  and 
Hering  also  contains  a  number  of  changes  and  additions. 

In  spite  of  these  very  considerable  additions  the  size  of  the  book  has 
not  been  greatly  increased,  as  some  of  the  older  methods,  which  were 
mentioned  in  former  editions  but  have  not  stood  the  test  of  time,  have 
been  eliminated.  I  received  suggestions  from  various  quarters  to  include 
a;-ray  examination  ;  but  I  could  not  bring  myself  to  do  so,  because  I 
wish  to  confine  myself  to  those  methods  the  technic  of  which  I  am 
myself  sufficiently  familiar  with  to  give  personal  advice  based  on  my 
own  experience ;  and  while  I  do  make  use  of  a^-ray  examination  for  the 
diagnosis  of  internal  diseases,  I  do  not  attend  to  the  technic  myself,  and, 
therefore,  do  not  consider  myself  a  competent  radiologist.  Another 
reason  for  excluding  .r-ray  technic  in  a  work  like  the  present,  which  is 
intended  for  the  general  education  of  the  physician,  is  that  rr-ray  exami- 
nations can  only  be  made  by  a  limited  number  of  practitioners,  who,  in 
order  to  do  so,  must  go  through  a  special  training.     The  same  may  be 


12  PREFACE  TO   THE  FOURTH  EDITION. 

said  of  cystoscopy.  It  is  true  that  I  practise  this  method  myself,  but  I 
have  not  had  sufficient  practice  and  experience  to  justify  the  effort  to 
teach  it  to  others. 

Finally,  I  cannot  refrain  from  repeating  in  this  place  that  this  work 
is  not  a  mere  compilation.  On  the  contrary,  in  almost  every  subject 
what  I  have  written  is  based  on  my  experience ;  many  of  the  theories 
advanced  and  the  cases  reported  are  my  own,  and  if  they  have  not  been 
utilized  by  me  for  original  contributions  to  the  medical  journals,  it  is 
partly  on  account  of  lack  of  time  and  partly  a  personal  aversion  to 
hack-writing  in  medicine.  I  mention  this  matter  because  the  present 
work  practically  never  enjoys  the  honor  of  being  quoted.  I  believe  an 
explanation  of  this  is  to  be  found  in  the  tendency  which  prevails  at  the 
present  time,  and  which  does  not  tend  to  further  the  symmetrical  progress 
of  our  science,  to  make  the  journals  and  periodicals  the  sole  depositaries 
of  medical  literature,  and  because  it  is  usually  presumed  that  text-books, 
aside  from  the  systems  which  are  now  so  popular  and  have  so  many 
names  on  their  title-pages,  are  mere  compilations  and  do  not  contain 
anything  new.  It  is  assumed  that  if  an  author  had  anything  important 
and  new  to  say  he  would  have  brought  it  out  on  the  "  bourse "  of 
periodical  literature.  Personally,  I  take  a  different  view,  and  the  cor- 
rectness of  my  remarks  is  shown,  among  other  things,  by  the  fact  that 
a  well-known  author  not  so  very  long  ago  (in  the  Deutsche  medicinische 
Wochenschrift,  Volume  1903,  page  716),  in  speaking  of  certain  sources 
of  error  in  the  auscultation  of  the  lungs,  states  that  among  current  text- 
books the  present  is  the  only  one  that  devotes  a  short  chapter  to  this 
subject,  based  probably  on  an  address  by  Treupel  delivered  in  the  Yerein 
der  Freiburger  Arzte.  Thus,  without  taking  the  trouble  to  investigate, 
the  author  takes  it  for  granted  that  a  text-book  cannot  contain  any  new 
ideas  and  observations  that  have  not  been  published  elsewhere.  If  he 
had  tried  to  inform  himself  on  the  point,  he  would  have  found  that  the 
chapter  in  my  text-book  to  which  he  refers  appeared  almost  in  exactly 
the  same  form  in  the  first  edition  in  1894 — /.  e.,  four  years  earlier  than 
the  time  when  the  address  to  which  he  refers  as  being  my  source  wa^^ 
printed.  '^ 

HERMANN  SAHLI. 


CONTENTS 


PAGE 

Introduction »    .    .    .  17 

History  and  Objective  Examination  .............  17 

General  Condition  of   the  Patient 23 

Posture  in    Bed 23 

Gait  and  the  Attitude .  27 

Development  and  State  of  Nutrition 27 

Body  Weight 28 

Configuration  of  the  Thorax 30 

Size  and  Shape  of  the  Head 36 

Examination  of  the  Skin 38 

Color  of  the  Skin 38 

Moisture  of  the  Skin  ;  Sweat  Excretion 47 

Swelling  and  Edema  of  the  Cutaneous  and  Subcutaneous  Tissues  .  48 

Emphysema  of  the  Skin 52 

Cutaneous    Hemorrhages 52 

Collateral  Circulation  in  the  Skin 55 

Trophic  Affections  of  the  Skin 59 

Acute  Exanthemata ;    Cutaneous    Diseases ;    Dermatitis    Medica- 
mentosa   59 

Other    Cutaneous    Manifestations   Important  from  the  Diagnostic 

Standpoint 63 

Determination  of  the  Body  Temperature    . 63 

The  Thermometer 65 

Method  of  Taking  the  Temperature 65 

The  Normal  Body  Temperature 66 

Febrile  Temperatures 67 

Prognostic  Significance  of  High  Temperatures 67 

The  Fever  Course 68 

Subnormal  Temperatures 75 

Character  of  the  Respiration 77 

Frequency  of  Respiration  under  Physiologic  Conditions 77 

Normal  Types  of  Breathing 77 

Pathologic  Variations  in  the  Type  of  Respiration 77 

Diaphragm  Phenomenon  and  Allied  Appearances  (Litten's  Sign)  .  78 
Asymmetric  Respiration  and  Pathologic  Inspiratory  Retraction  of 

the  Chest 79 

Abnormalities  in  Frequency  and  Rhythm  of  the  Respiration  ...  80 

Dyspnea 83 

Spirometry  and   Pneumatometry 93 

Character  of  the  Voice  under  Pathologic  Conditions   ...  94 

13 


14  CONTENTS 

PAGE 

Cough 95 

Localized  Prominence  of  the  Chest  in  Coughing '98 

Palpation,  Sphygmography,  and  Sphygmometry  of  the  Arte- 
rial Pulse 98 

Palpation  of  the  Pulse 99 

Sphygmography 109 

Sphygmomanometry  (Tonometry) 134 

Visible   Phenomena  of  Motion  in  the  Vessels 144 

Capillary  Pulse .  144 

Eespiratory  Phenomena  of  Motion  iu  the  Veins 145 

Different  Varieties  of  Venous  Pulse 147 

Percussion 173 

Percussion  in  General ;  Instruments 153 

Quality  of  the  Percussion 155 

Topographic  Percussion 159 

Comparative  Percussion 197 

Auscultation 217 

Auscultation  in  General  ;  Instruments 217 

Auscultation  of  the  Perspiratory  Organs 219 

Auscultation  of  the  Heart 244 

Auscultation  of  the  Vessels 282 

Auscultation  of  the  Abdomen 286 

Palpation  of  the  Lungs  and  Pleura 287 

Determination  of   Fluctuation   and   Changes  of  Resistance  in  the 

Thorax 287 

Abnormal  Pulsations  in  the  Region  of  the  Lungs  and  Pleura  .    .  287 
Testing  the  Vocal  (Tactile)  Fremitus 288 

Inspection  and  Palpation  of  the  Heart  Region  (Precordia)  .  289 

Heart  Beat  and  Apex  Beat 289 

Other  Pulsations  in  the  Precordia  and  its  Keighborhootl    ....  299 
Palpation  of  Cardiac  Murmurs 301 

Inspection  and  Palpation  of  the  Abdomen 301 

Inspection  of  the  Abdomen     . 301 

Palpation  of  the  Abdomen 304 

Diagnosis  of  Individual  Valvular  Lesions,  of  Aortic  Aneu- 
risms, AND  OF  Pericarditis 314 

Foundations  of  the  Pathologic  Physiology  of  Valvular  Lesions  .    .  314 

Individual  Valvular  Lesions 321 

Aneurism  of  the  Aorta 345 

Pericarditis 347 

Graphic  Expressions  for  the   Physical   Signs   in  Pulmonary 

Cases 348 

Examination  of  the  Stomach  and  Stomach  Contents    ....  353 
Methods  of  Examination  without  Employing  the  Stomach  Tube  .  354 
Methods  of  Examining  the  Stomach  Avith  the  Aid  of  the  Stomach 
Tube 364 


CONTENTS  15 

PAGE 

Examination  of  the  Intestine  and  Feces 415 

Local  Examination  of  the  Rectum 415 

Ueinary  Examination 449 

Amount  of  Urine 449 

Frequency  of  Urination 451 

Specific  Gravity  of  the  Urine 451 

Transparency  of  the  Urine 452 

Color  of  the  Urine 453 

Odor  of  the  Urine 455 

Reaction  of  the  Urine 455 

Separation  of  the  Urines  of  the  Two  Kidneys 457 

Qualitative  Chemical  Examination  of  the  Urine 458 

Quantitative  Urinary  Analysis 504 

Sediments  and  Turbidity  of  the  Urine 553 

Examination  of   the  Sputum 578 

Amount  of  Sputum 579 

Consistence  of  the  Sputum 579 

Reaction  of  the  Sputum 579 

Color  and  Transparency  of  the  Sputum 579 

Air  Content  of  the  Sputum 582 

Sputum    Strata 582 

Odor  of  the  Sputum 583 

Characteristic  Gross  Appearances  of  the  Sputum 583 

Microscopic  Examination  of  the  Sputum    . 586 

Chemical  Examination  of  the  Sputum 605 

Chief  Characteristics  of  the  Most  Important  Types  of  Sputa  .    .    .  605 

Examination  of   the  Blood 609 

Method  of  Obtaining  Blood  for  Examination 610 

Quantity  of  the  Blood  ;  Diagnosis  of  Hydremic  Plethora  .    .    .    .611 

Specific  Gravity  of  the  Blood 612 

Reaction  of  the  Blood 613 

Coagulation  Time  of  the  Blood 615 

Determination  of  the  Hemoglobin  in  the  Blood 616 

The  Counting  of  Blood-corpuscles 624 

Other  Morphologic  Relations  of  the  Blood 631 

Condition  of  the  Blood  in  the  Most  Impoi'tant  Blood-diseases   .    .  659 

Chemical  Examination  of  the  Blood 671 

Widal's  Serum  Test  in  Typhoid  Fever 675 

Examination  of  the  Mouth  and  Pharynx 677 

Examination  of  the  Esophagus 687 

Laryngoscopy  and  Tracheoscopy  ;  Autoscopy  of  the  Larynx 

AND  Trachea 693 

Examination  with  the  Aid  of  a  Mirror 693 

Direct  Examination  of  the  Larynx,  Trachea,  and  Bronchi      ,    .    .  698 

Bronchoscopy 700 

Combined  Laryngoscopy 701 

Rhinoscopy 701 

Ophthalmoscopy 703 


16  CONTENTS 

PAGE 

Exploratory  Punctures  and   Harpooning ,    .707 

Exploratory  Punctures 707 

Details  of  Exploratory  Punctures  in  Different  Diseased  Conditions  .  721 
Harpooning 728 

rontgen-ray  examinations 729 

Examination  of  the  Nervous  System 738 

General  Part 738 

Psychical  Examination 738 

Examination  of  Motility 741 

General  Discussion  of  the  Methods  of  Testing  the  Sensibility  .  756 

Examination  of  the  Reflexes ,■..    .  776 

Examination  for  Trophic  Disturbances 788 

Examination  of  Disturbances  of  Secretion 796 

Edema  in  Nervous  Diseases 797 

Method  of    Testing    the    Mechanical   Irritability  of  Nerves 

and  Muscles    . 797 

Method  of  Testing  the  Electric  Irritabilitv  of  Nerves   and 

Muscles " 798 

Special  Part 821 

Examination  of  the  Different  Cranial  Nerves .  821 

The  Characteristics  of  Motor  Hemiplegia ;  Pseudobulbar  Symp- 
toms       876 

Cerebral  Disturbances  of  Sensation 878 

Vertigo    .    .  " 880 

Cerebral  Localization 884 

The  Disturbances  of  Speech 888 

Disturbances    Related     to    Aphasia;    Asymolia;     Amimia  ; 
Apraxia ;  Amusia  ;  Psychic  Deafness ;  Psychic  Blindness  .  901 

Spinal  Hemiplegia 903 

Pathologic  Gaits  and  Postures  . 908 

Special  Points  in  Reference  to  the  Examination  of  the  Spinal 
Nervous  System 910 

Appendix 948 

Routine  Plans 948 

Illustrations 955 

Supplement 955 

Analysis  of  the  Irregular  Pulse 955 

Acidimetric  Titration  of  Fluids  which  Contain  Alkaline  Earths  and 
Ammonia  Salts  in  Addition  to  Salts  of  Phosphoric  Acid  .    .    .  965 


Index  . 967 


INTRODUCTION. 
HISTORY  AND   OBJECTIVE   EXAMINATION. 

To  diagnose  correctly  any  given  case  of  sickness,  it  is  customary  to 
question  the  patient  or  his  friends  upon  his  subjective  and  objective 
symptoms  of  ilhiess  and  upon  their  manner  and  course  of  develop- 
ment. This  testimony  obtained  from  the  patient  or  friends  is  called 
the  history.  It  may  be  divided  into  two  parts  :  first,  the  history  in  the 
narrow  sense  of  the  term,  including  the  patient's  story  of  his  illness  up 
to  the  time  the  physician  sees  him ;  and,  second,  his  account  of  his 
present  symptoms,  an  account  which  must  always  be  supplemented  by 
an  objective  examination.  The  answers  to  the  questions  obtained  in 
the  history  frequently  furnish  sufficient  evidence  to  make  a  compara- 
tively accurate  diagnosis  without  examining  the  patient.  Countless  ex- 
amples might  be  mentioned  in  illustration ;  for  instance :  A  patient 
says  that  a  few  days  before,  when  in  apparently  good  health,  he  was 
suddenly  seized  with  a  severe  chill  and  a  stabbing  pain  upon  one  side 
of  his  chest,  and  that  ever  since  then  he  has  been  feverish  and  short  of 
breath,  coughing,  and  expectorating  rusty  sputum.  With  such  a  story  a 
physician  would  naturally  make  the  diagnosis  of  croupous  pneumonia. 

Before  attempting  any  objective  examination,  merely  by  skilfully 
directing  his  questions,  in  this  way  can  an  experienced  physician  obtain  a 
fair  idea  of  the  disease,  even  in  cases  where  the  evidence  is  less  conclusive 
than  in  the  above  example,  although  an  exact  diagnosis  can  be  made 
only  after  completing  the  objective  examination ;  for  many  diseases 
furnish  only  subjective  symptoms.  There  are  even  cases  in  which  the 
history  affords  the  only  clue  to  diagnosis.  A  ripe  experience  is  requisite 
in  order  properly  to  utilize  the  history  in  making  a  diagnosis.  A  com- 
plete knowledge  of  the  pictures  of  all  the  diseases  which  might  enter 
into  consideration  in  any  given  case  is  very  essential  in  selecting  the 
proper  questions,  as  well  as  a  keen  critical  power  in  interpreting  the  value 
of  the  evidence  given  in  the  history,  since  otherwise  unessential  facts 
might  be  made  conclusive  points  in  a  diagnosis.  Only  years  of  experi- 
ence can  overcome  one  very  constant  difficulty — the  varying  individuality 
of  patients.  An  hysteric  society  woman  describes  to  her  physician 
symptoms  which,  in  a  sturdy  laborer,  would  be  properly  attributed 
to  pathologic  changes  ;  but  the  adept  practitioner  understands  that  such 
complaints  are  nothing  more  than  the  expression  of  the  peculiar,  sen- 
sitive and  exaggerating  mental  condition  of  an  hysteric  person,  and 
so  does  not  lay  too  much  stress  upon  their  significance.  Vice  versd, 
a  stolid,  callous  peasant  often  complains  very  little  even  when  afflicted 
with  a  serious  disease ;  or,  again,  a  patient  normally  sensitive  may  be  so 

2  17 


1 8  INTB  OD  UCTION. 

benumbed  by  a  disease  that  he  does  not  complain  at  all.  In  the  latter 
instance  the  great  contrast  between  the  subjective  well-being  and  the 
objective  visible  disease  frequently  suggests  a  very  unfavorable  prognosis. 

Without  depreciating  the  value  of  the  statements  of  the  patients  and 
their  friends,  it  is  evident  from  what  we  have  said  that  the  methods  of 
objective  examination,  with  which  this  book  is  concerned,  contain  the 
most  essential  elements  in  diagnosis.  Although  I  have  illustrated  the 
possibility  and  the  occasional  necessity  of  making  a  diagnosis  merely  from 
the  history,  yet  I  could  as  easily  mention  innumerable  instances  where 
the  most  skilled  practitioner  could  not  form  an  approximate  conception 
of  the  disease  without  the  most  searching  physical  examination.  Even 
in  the  simplest  of  cases  no  physician  should  neglect  the  precaution  of 
examining  his  patient  carefully,  including  in  such  an  examination  all  the 
organs.  For,  on  the  one  hand,  some  organic  diseases  do  not  excite  sub- 
jective symptoms ;  and,  on  the  other  hand,  along  with  some  organic 
changes  which  annoy  the  patient  sufficiently  to  lead  him  to  consult  his 
physician,  may  go  others  of  the  greatest  importance  of  which  he  has 
no  suspicion  and  which  the  objective  examination  first  discloses. 

Objective  examination  includes  a  number  of  different  methods,  some 
depending  on  mere  observation,  but  others  requiring  especial  technical, 
chemical,  or  physical  aids.  The  beginner  must  very  early  acquire 
facility  in  all  these  methods  of  examination.  Their  mastery  will  furnish 
the  groundwork  for  acquiring  extended  experience  in  clinical  observation 
upon  the  symptomatology,  the  course,  and  the  prognosis  of  disease,  and 
for  obtaining  reliable  data  for  therapy. 

A  FEW  SUGGESTIONS  FOR  TAKING  HISTORIES. 

It  is  very  difficult  to  give  any  detailed  directions  which  will  be 
generally  effective  in  taking  a  history.  In  serious  diseases  only  an 
able  and  experienced  physician  is  capable  of  performing  this  task 
thoroughly,  and  he  will  need  to  utilize  his  entire  medical  training.  Since 
we  shall  mention  in  the  appendix  upon  special  diagnosis  most  of  the 
methods  made  use  of  in  history -taking,  in  the  following  paragraphs  we 
need  only  give  a  few  rules  to  serve  as  a  framework  for  the  beginner 
to  broaden  and  build  upon  as  his  knowledge  and  experience  grow. 

Few  persons  are  so  mentally  constituted  as  to  communicate  to  the 
physician  simply  and  directly  the  medically  important  facts  of  their  ail- 
ment. Most  patients  relate  a  mass  of  unimportant  matter  and  say  nothing 
about  the  essentials,  and  only  skilfully  planned  questions  will  prevent  the 
patient  or  his  relatives  from  irrelevancy.  But  a  patient  should  never 
feel  that  he  is  being  guided,  nor  that  his  physician  does  not  enter  with 
interest  and  sympathy  into  all  the  minute  details  of  his  trouble.  Put- 
ting a  mild  curb  upon  the  patient's  volubility  does  not  mean  that  one 
should  concern  one's  self  exclusively  with  the  typical  and  characteristic 
symptoms  of  disease  ;  because  many  things  apparently  immaterial  in  the 
eyes  of  the  beginner,  who  knows  a  disease  only  as  a  scheme,  have  really 
considerable  interest  and  a  great  importance.  Even  many  conditions 
which  have  apparently  nothing  at  all  to  do  with  the  medical  aspect  of 


HISTORY  AND   OBJECTIVE  EXAMINATION.  19 

the  case — for  example,  occupation,  family  aifairs,  etc. — are  very  helpful 
in  comprehending  the  clinical  picture,  especially  the  etiology  and,  with 
it,  the  treatment.  In  short,  the  patient  should  be  led  to  relate  neither 
too  much  nor  too  little. 

It  is  quite  as  important  that  the  physician  himself  should  be  accurate 
in  framing  his  questions.  It  is  easy  enough  to  ask  too  little,  but  dif- 
ficult to  ask  too  much  or  to  question  too  minutely,  not  only  on  account 
of  the  multiplicity  of  the  appearances  of  disease  to  be  mastered,  but 
even  more  on  account  of  the  danger  of  considering  any  important  point 
as  proved  after  a  few  hasty  questions.  In  the  writer's  opinion  this  is 
the  most  frequent  and  serious  fault  which  the  beginner  perpetrates  ; 
e.  g.,  a  feverish  patient  is  asked  if  he  has  had  a  chill,  because  such  a 
symptom  would  suggest  a  definite  disease,  pneumonia.  Without  much 
thought  most  patients  answer  this  question  in  the  affirmative ;  but  more 
careful  questioning  develops  the  fact  that  the  supposed  chill  is  in 
reality  only  the  slight  chilly  feelings  accompanying  nearly  all  feverish 
diseases.  In  the  typical  chill  of  pneumonia  the  patient's  teeth  chatter, 
and  he  shakes  as  if  immersed  in  ice  water.  This  is  quite  a  diiferent 
symptom  in  its  significance  from  the  slight  shivering  of  fever.  The 
patient's  statement  that  he  has  had  a  chill  is  not  sufficient ;  we  must 
inquire  more  particularly  as  to  the  nature  of  the  chill.  Often  enough 
patients  betray  their  mistake  by  using  the  word  chill  in  the  plural. 
Similar  errors  may  arise  from  the  statements  patients  make  in  regard 
to  many  other  symptoms  or  long-standing  diseases.  The  names  they 
give  to  their  former  illnesses  are  especially  apt  to  be  incorrect  and  often 
occasion  serious  errors,  for  many  are  diagnoses  made  by  the  laity  and 
many  others  are  incorrect ;  e.  g.,  most  cases  of  so-called  "  meningitis  " 
which  have  been  cured.  Again,  patients  with  tuberculosis  often  mis- 
name an  acute  exacerbation  of  their  disease  as  "  influenza ";  further, 
so-called  "  catarrh  of  the  stomach "  is  usually  an  early  manifestation, 
or  at  least  a  forerunner,  of  tuberculosis.  "  Rheumatism  "  is  another 
diagnosis  which  must  always  be  looked  upon  a  little  skeptically.  Fre- 
quently enough  the  clinical  picture  shows  that  the  so-called  "  rheu- 
matism "  is  a  manifestation  of  tuberculosis,  or  of  pleurisy,  etc.  Simi- 
larly, many  other  names  of  diseases,  such  as  "  nervous  fever,"  "joint 
rheumatism,"  "  dysentery,"  if  accepted  without  criticism  and  without 
minute  interrogation,  may  lead  to  errors  in  diagnosis.  The  best  way  to 
avoid  such  mistakes  is  to  disregard  names  given  by  the  patient  and  to 
make  one's  own  diagnosis  by  establishing  as  objectively  and  accurately 
as  possible  the  symptoms  of  the  preceding  disease. 

A  further  and  just  as  serious  a  fault  is  the  tendency  of  many  begin- 
ners to  start  from  a  preconceived  notion  of  the  diagnosis  and  to  extract 
from  the  patient  all  possible  facts  in  the  history  which  will  coincide 
with  this  supposed  disease.  To  recognize  this  fault  should  be  sufficient 
to  effectually  avoid  it. 

We  can  hardly  ask  too  detailed  questions  as  to  the  influences  of 
heredity,  inquiring  accurately  concerning  parents,  brothers,  sisters,  chil- 
dren, uncles,  and  aunts.     An  inquiry  as  to  whether  this  or  that  disease 


20  INTR  OD  UCTION. 

has  occurred  in  the  patient's  family  will  usually  elicit  a  negative  reply. 
To  determine  the  facts  accurately  the  disease  in  question  must  be  quite 
specifically  designated,  possibly  even  a  summary  of  the  symptoms  de- 
tailed. A  patient  may  deny  the  occurrence  of  pulmonary  disease  in 
his  family  ;  but  should  we  ask  if  either  parent  had  a  chronic  cough, 
had  expectorated  blood,  or  lost  a  good  deal  of  weight,  we  can  fre- 
quently enough  become  convinced  that  one  or  the  other  suffered  from 
tuberculosis. 

In  regard  to  neuropathic  taint  we  must  question  very  accurately  and 
particularly.  For  example,  an  epileptic  will  practically  always  deny 
the  occurrence  of  any  nervous  disease  in  his  family.  We  may,  how- 
ever, obtain  a  positive  reply  by  asking  whether  his  father,  mother, 
brother,  sister,  uncle  or  aunt  was  epileptic,  if  they  had  suffered  from 
nervous  attacks,  or  if  they  had  been  nervous  or  mentally  affected  in 
some  other  way. 

If  the  histories  are  difficult  to  obtain  or  if  patients  contradict  them- 
selves, it  is  advisable  to  repeat  questions  later  on,  thus  frequently  clear- 
ing up  some  complicated  point.  The  repetition  of  our  task  with  stupid 
and  prattling  patients,  unfortunately,  obtains  for  us  little  more  than 
renewed  contradictions.  Even  this  is  a  relative  gain,  for  at  least  we 
discover  how  little  we  can  trust  them,  and  draw  no  false  conclusions. 

In  general,  good  history-taking  requires  much  diplomacy,  tact,  and 
knowledge  of  people  and  of  medicine.  A  physician  should  never  allow 
a  patient  to  feel  that  he  is  in  a  hurry.  The  public  considers  that  the 
physician  has  time  for  everything  and  everybody.  Sit  quietly,  even  if 
you  are  sitting  upon  hot  coals ;  and  wait  for  a  favorable  moment  to 
interrupt,  in  a  diplomatic  way,  the  flow  of  talk.  An  excellent  medical 
precept  is  not  to  fatigue  a  patient  seriously  ill  with  too  thorough  ques- 
tioning, but  to  obtain  as  much  as  possible  from  the  relatives,  or  to  leave 
parts  of  the  history  until  a  later  period.  Furthermore,  it  is  always 
advisable  to  discuss  with  the  patient  alone  facts  which  he  might  wish  to 
conceal  from  others.  Finally,  the  beginner  puts  only  a  small  part  of 
the  necessary  questions,  not  realizing  how  much  must  be  asked  in  order 
to  make  a  complete  history.  Few  rules  can  be  given,  but  the  following 
table  will  probably  be  of  considerable  service  : 

Scheme  for  History-taking. 

Date ;  personal  statements  (name,  age,  position,  occupation,  resi- 
dence) ;  condition — i.  e.,  married  or  not ;  complaint ;  onset  of  the  present 
illness  ;  a  description  of  the  symptoms  in  the  order  of  their  appearance. 

Etiology. — More  exact  information  about  the  occupation  and  mode 
of  life,  injuries,  strains,  taking  cold,  errors  in  diet,  etc.  Infectious 
diseases  in  the  neighborhood.    Previous  treatment  and  course  of  disease. 

Past  History. — Any  antecedent  disease  like  the  present?  If  so, 
course  of  same.  Injuries.  Other  earlier  diseases;  infectious  diseases; 
and  of  these  especially  :  joint  rheumatism,  scarlet  fever,  measles,  whoop- 
ing-cough, typhoid  fever,  erysipelas,  malaria,  sore  throat,  gonorrhea, 
syphilis.     Previous  symptoms  of  disease  :    Edema  ;  dyspnea ;    cough  ; 


HISTORY  AND   OBJECTIVE  EXAMINATION.  21 

expectoration  ;  expectoration  of  blood  ;  palpitation  of  heart ;  difficulties 
of  urination  and  alterations  in  the  urine ;  constipation  ;  diarrhea;  icterus; 
vomiting ;  vomiting  of  blood ;  abnormalities  of  hunger  and  thirst ; 
headache  ;  marked  changes  of  weight.  In  the  female  sex  :  chlorosis ; 
pregnancies  ;  births ;  menstrual  or  gynecologic  difficulties.  All  these 
symptoms  and  conclusions  which  the  past  history  furnishes  must  be 
analyzed  in  the  same  way  as  the  symptoms  of  the  present  disease.  (See 
2.  Complaint.) 
Heredity. — 

THE  GENERAL  ROUTINE  OF  A  PATIENT'S  EXAMINATION. 

The  following  plan  the  author  considers  an  excellent  method  for  a 
routine  examination ;  the  order  of  the  questions  being  the  natural  and 
practical  one.  The  individual  observer  may  expand  the  scheme  in  ac- 
cordance with  the  contents  of  the  work  in  question. 

1.  Expression  of  countenance  and  general  deportment  of  the  patient ; 
voice;  speech;  psychical  behavior. 

2.  Complaint.  (See  Scheme  for  History-taking.)  Kind  of  sich feeling  f 
Weakness  f  Loss  of  flesh  f  Disturbances  associated  with  the  nervous 
system  f     Disturbances  in  connection  with  the  organs  of  respiration  f 

Dyspnea,  constant  or  paroxysmal  ?  The  exciting  cause  of  the  par- 
oxysms ?     Breathing  slow  or  rapid  during  attack  of  dyspnea  ? 

Cough,  with  or  without  expectoration  ?  Characteristics  of  the  ex- 
pectoration ?  Admixture  of  blood  ?  Peculiarities  of  the  latter  ? 
Subjective  sensation  respecting  the  source  of  the  expectoration  (throat, 
larynx,  nose?). 

Pain  with  breathing  ?     Its  location  ? 

Disturbances  in  Connection  with  the  Circulation. — Palpitation,  con- 
stant or  paroxysmal  ?  Apparent  exciting  cause  of  the  paroxysm  (agita- 
tion, exertion,  or  posture)  ?  Palpitation  accompanied  by  sensation  of 
pain  (left  arm,  back,  precordia)  ?  Palpitation  accompanied  by  dyspnea  ? 
Subjective  sensation  of  arrhythmia  {i.  e.,  tripping  or  skipping  of  the 
heart  beat)?     Edema?     Amount  of  urine? 

Disturbances  of  the  Digestion. — Appetite  ?  Pain  ?  Influence  of  the 
ingestion  of  food  and  drink  upon  the  pain  ?  Time  of  onset  of  pain — 
soon  after  eating — during  the  night — in  a  fasting  condition  ?  More 
exact  location  and  radiation  of  pain  (back,  right  shoulder)  ?  Nausea  ? 
Vomiting?  Amount  and  character  of  the  vomitus  (mucus,  blood, 
food)  ?  Its  taste  (sour,  bitter)  ?  Time  of  vomiting  (pointing  to  reten- 
tion or  not)  ?  Belching  (sour,  bitter,  rancid)  ?  Bowels  :  Constipation  ? 
How  often  do  the  bowels  move  ?  Movements  painful  ?  Character  of 
feces  :  Color  ?  Large  scyballse,  abnormally  small  lumps  ?  Distention 
of  abdomen  and  other  discomforts  when  constipated?  Flatulence? 
Diarrhea  :  Frequency,  consistence,  color,  amount  of  each  dejection  ? 
Pain  in  defecation  ?  Tenesmus  ?  Bloody  or  slimy  evacuations  ?  Evi- 
dences of  hemorrhoids  ? 

Disturbances  of  the  Urinary  Apparatus. — Bladder  or  kidney  pain  ? 
Radiation   of  the  pain  ?     Tenesmus  of  bladder  ?     Amount  of  urine  ? 


22  INTRODUCTION. 

Conspicuous  qualitative  changes  of  the  urine  (cloudy,  bloody,  smoky)  ? 
Passing  of  stone,  gravel  or  sand  ? 

Other  Disturbances. — Fever?  Night-sweats?  Headache?  Thirst? 
Insomnia  (and  its  apparent  cause)  ? 

3.  History  proper,  in  conformity  with  the  above  plan. 

4.  Examination  propjer,  which  should  cover  the  following  points  : 
Build,  development,  and  nutrition. 

Temperature,  frequency  of  pulse  and  of  respiration. 

Characteristics  of  Skin. — Bloating,  edema,  color  (pallor,  cyanosis, 
icterus),  eruptions,  pigmentation,  scaling,  strise,  final  confirmation  of 
other  external  diseases  (joiut-afiFections,  erysipelas,  etc.). 

Head  and  Neck. — Mucous  membranes,  especially  conjunctivae, 
tongue,  gums,  pharynx,  tonsils,  herpes  labialis,  glands,  goiter?  Cer- 
vical veins  (their  dilatation  or  pulsation). 

Respiratory  Apjpiaratus. — Dyspnea  ;  its  character,  polygopnea,  oli- 
gopnea, inspiratory  or  expiratory,  stridor,  shape  of  thorax,  type  of 
breathing,  breathing  excursions,  diaphragm  phenomenon,  drawing  in 
of  thorax,  topographic  and  comparative  percussion  and  auscultation  of 
the  lungs,  fremitus. 

Circulatory  Apparcdus.^ — Inspection  and  palpation  of  the  precordia. 
Visible  and  palpable  pulsation  over  that  area.  Location  of  apex  beat. 
Thrills.  Percussion  and  auscultation  of  the  heart.  Exact  examination 
of  the  pulse.  Rapidity,  rhythm,  fulness,  tension,  resistance  of  artery 
wall,  conformity  of  the  frequency  of  the  radial  pulse  with  that  of  the 
cardiac  pulsation.  Exact  examination  of  the  venous  pulse.  Ausculta- 
tion of  the  arteries.      Liver  pulse.      Capillary  pulse. 

Digestive  Ap)paratus. — Inspection  and  palpation  of  the  abdomen; 
its  shape  and  fulness  ;  visible  peristalsis  ;  sensitiveness  to  pressure,  pal- 
pable tumors,  resistances.  Palpation  and  percussion  of  the  stomach, 
intestines,  liver,  gall  bladder,  spleen,  and  peritoneum.  Inspection  of  the 
vomitus  and  of  the  feces. 

Urinary  Apparatus. — Manner  of  urination  ;  palpation  of  the  kid- 
neys and  bladder  ;  percussion  of  bladder.  Catheterization.  Character 
of  urine  ;  amount ;  color ;  cloudiness  ;  specific  gravity ;  testing  for 
albumin  and  sugar. 

Sp>ecial  Examinations  tvhich  may  be  Necessary  or  even  the  Most  Im- 
jjortant  of  All  in  a  Given  Case. — Examination  of  the  nervous  system  in 
accordance  with  the  plan  to  be  mentioned  later.  Rhino-,  laryngo-,  oph- 
thalmo-,  otoscopic  examination.  Testing  the  blood,  including  counting 
the  corpuscles,  estimating  the  hemoglobin,  and  the  microscopic  examina- 
tion of  the  fresh  and  stained  blood.  Microscopic  examination  of  the 
sputum,  of  the  urine,  of  the  vomitus,  and  of  the  feces.  Bacteriologic 
examinations.  Sphygmography  and  sphygmomanometry.  Examina- 
tion of  the  esophagus.  Examination  of  the  stomach  by  means  of  the 
stomach  tube  (distending  with  gas,  a  test  meal).  Distention  of  the 
colon  for  the  demonstration  of  kidney  tumors.  Examination  of  the 
rectum  ;  of  the  male  and  female  genitalia.      Needle  punctures. 

^  In  a  routine  examination  the  pulse  is  usually  examined  before  the  heart. 


GENERAL   CONDITION  OF  THE  PATIENT.  23 

It  is  the  province  of  special  pathology  or  of  special  diagnosis  to 
interpret  the  signs  of  disease  discovered  in  this  manner,  to  weigh  their 
mutual  values,  and  to  unify  them  into  a  definitely  conceived  disease  of 
etiologic,  functional,  or  anatomic  nature. 


GENERAL  CONDITION  OF  THE  PATIENT. 

POSTURE  IN  BED. 

The  general  deportment  of  a  patient  is  the  first  thing  which  attracts 
our  attention  and  influences  our  judgment  as  to  his  condition.  In 
many  cases  even  the  patient's  relatives  will  reveal  whether  the  illness 
is  serious  or  slight.  Ordinarily,  physicians  see  seriously  sick  patients 
in  bed,  while  those  with  slight  ailments  walk  about.  Yet  there  are 
countless  exceptions.  Sometimes  seriously  ill  patients  go  to  bed 
only  at  the  last  extremity  ;  and,  as  is  well  known,  patients  may  walk 
about  even  during  the  height  of  typhoid  fever  or  pneumonia.  Vice 
versd,  many  patients  take  to  their  beds  on  account  of  very  slight 
ills.  These  peculiarities  depend  upon  the  social  position  and  the  em- 
ployment of  a  patient,  and  upon  the  great  diiference  in  the  individual 
susceptibility  to  sickness.  Besides,  we  must  remember  that  even  very 
slight  ailments  which  always  run  a  favorable  course  are  sometimes  associ- 
ated with  such  distressing  symptoms  that  the  patient  is  compelled  to  take 
to  his  bed.  Despite  such  exceptions,  we  may  say  that  certain  diseases 
necessitate  rest  in  bed,  others  are  ambulatory.  Patients  with  the  acute 
exanthemata  are  commonly  found  in  bed  by  the  physician  because  they 
feel  very  ill.  The  same  is  true  of  circulatory  disturbances,  peritonitis, 
meningitis,  pneumonia,  and  acute  inflammatory  rheumatism.  It  is 
ordinarily  easy  enough  to  determine  whether  the  patient  keeps  his  bed 
on  account  of  feeling  ill,  weak,  and  perhaps  feverish,  or  on  account  of 
dyspnea,  pain,  or  other  difficulties,  which  are  increased  by  walking  about. 

THE  EXPRESSION. 

The  expression  is  of  great  diagnostic  importance,  enabling  the  skilled 
physician  to  draw  conclusions  as  to  the  subjective  feelings  and  the  men- 
tal condition  of  the  patient.  The  terms  commonly  applied  to  the  expres- 
sion— suffering,  anxious,  painful,  careworn,  uneasy,  very  ill,  agitated, 
dulled,  stupid,  flustered — are  perfectly  plain  without  further  explanation. 
Feverish  patients  present  a  characteristic  appearance  ;  sometimes  they 
have  a  peculiar  animated  look,  at  other  times  an  exceptional  depression 
of  the  mimic  faculty,  often  combined  with  glistening  eyes,  a  feverish 
redness,  and  an  increased  turgidity  of  the  skin  of  the  face.  The  facial 
expression  of  a  patient  suffering  from  dyspnea  is  quite  as  distinctive, 
dependent  upon  peculiarities  in  the  aj^pearance  of  the  skin  (cyan- 
osis, edema)  and  upon  the  mimic  elements.      The  dilatation  of  the 


24  GENERAL   CONDITION  OF  THE  PATIENT. 

nares  (see  later),  combined  with  the  open  mouth,  is  especially  character- 
istic. (See  p.  49  for  a  description  of  the  typical  fades  Hippocratica.) 
The  unusual  expression  of  tetanus,  called  the  risus  sardonicus  (sardonic 
laugh),^  has  been  variously  described.  While  the  mouth  is  distorted  as 
in  laughing,  the  upper  part  of  the  face,  especially  the  brow,  is  wrinkled, 
just  as  in  the  expression  of  trouble  or  sorrow.  Tetanus  poison  appar- 
ently contracts  the  muscles  of  the  entire  facial  territory  and  causes  a 
combined  stimulation  of  practically  antagonistic  muscles. 

MENTAL  CONDITION. 

A  patient's  facial  expression  and  his  demeanor  during  our  question- 
ing furnish  the  best  means  of  estimating  his  mental  condition. 

ACTIVE  AND  PASSIVE  POSTURE  IN  BED. 

A  critical  observer  obtains  diagnostic  points  from  noticing  the 
position  which  the  patient  assumes  in  bed.  The  less  the  general  feel- 
ings are  affected,  the  more  natural  and  unconstrained  is  his  j)Ose.  He 
tosses  about,  pushes  the  pillows  straight,  and  shifts  his  attitude  when 
one  position  has  become  uncomfortable.  This  is  called  an  active  posi- 
tion in  bed  (active  dorsal  or  lateral  posture).  On  the  contrary,  very 
weak,  helpless,  or  unconscious  patients  appear  very  differently.  Their 
attitude  is  lax,  essentially  controlled  by  the  laws  of  gravity.  Should 
such  a  patient  slide  down  against  the  footboard,  he  would  remain  lying 
there,  for  he  is  incapable  of  drawing  himself  up,  even  if  the  position 
be  very  uncomfortable  and  his  breathing  embarrassed.  This  is  called 
a  passive  position  in  bed  (passive  dorsal  or  lateral  posture). 

CONSTRAINED  ATTITUDES. 

Some  very  characteristic  postures  are  almost  diagnostic  of  certain 
diseases.  For  example  :  respiratory,  cardiac,  or  renal  affections  associ- 
ated with  much  dyspnea  prevent  a  patient  lying  upon  his  back  :  in 
the  first  place,  because  the  accessory  muscles  of  respiration  can  be  used 
to  advantage  only  in  the  sitting  posture,  with  the  spine  fixed  and  some- 
times the  arms ;  in  the  second  place  because,  if  fluid  has  accumulated  in 
the  abdominal  cavity,  the  sitting  posture  partially  relieves  the  diaphragm 
of  its  pressure ;  ^  and  finally,  because  the  influence  of  gravity  possibly 
relieves  the  venous  congestion  of  the  brain  and  of  tlie  respiratory  center 
in  particular.  With  extreme  dyspnea,  the  so-called  "orthopnea,"  a 
patient  cannot  lie  down,  but,  exhausted,  is  obliged  to  sit  erect,  bracing 
himself  with  his  elbows  and  forearms  upon  the  arms  of  his  chair  in  an 
endeavor  to  utilize  the  accessory  muscles  of  respiration  and,  if  fluid  be 
present  in  the  abdomen,  to  avoid  pressure  of  the  anterior  surface  of  the 

^  This  name  is  derived  from  "  sardone,"  a  poisonous  plant  of  the  ancients,  the  inges- 
tion of  which  produced  such  an  expression. 

^  Except,  of  course,  when  an  enormously  distended  abdomen  is  crowded  by  the  thighs- 
in  the  sitting  posture. 


POSTURE  IN  BED.  25 

thighs  upon  the  distended  abdomen.  It  is  worth  remembering  that  the 
accumulation  of  a  considerable  quantity  of  blood  in  the  veins  of  the 
lower  extremity  may  afford  some  relief  to  the  lungs  and  the  heart,  so 
that  elastic  bandages  around  the  legs,  temporarily  shutting  off  a  con- 
siderable amount  of  venous  blood,  may  enable  the  patient  to  lie  down, 
even  though  for  a  very  short  time. 

Constrained  lateral  positions  are  very  suggestive,  for  they  almost 
always  depend  upon  unilateral  affections  of  the  thoracic  viscera.  If  on 
account  of  pulmonary  infiltration  or  of  compression  by  a  pleural  effusion 
the  function  of  one  lung  is  abolished,  the  patient  usually  lies  upon  the 
affected  side,  in  order  to  afford  the  sound  lung  the  freest  possible  expan- 
sion. Should  there  be  much  pain,  such  a  position  is  generally  reversed, 
because  the  weight  of  the  body  increases  the  pain  ;  but  sometimes  when 


Fig.  1.— Case  of  cerebrospinal  meningitis.    Photograph  taken  from  above ;  patient  lying  asleep. 
Marked  retraction  of  neck,  flexion  of  thighs  and  legs  (Harlem  Hospital,  i)r.  R.  G. "Wiener). 

the  pain  depends  practically  upon  the  breathing  the  patient  will  lie 
upon  the  affected  side,  and  so  limit  the  respiratory  excursion  by  par- 
tially fixing  the  painful  side  with  the  body  weight.  In  heart  diseases, 
and  sometimes  in  health,  one  side  is  more  comfortable  than  the  other 
to  lie  on.  The  position  which  dislocates  the  heart,  the  great  vessels, 
and  the  mediastinum  most,  thereby  rendering  the  breathing  difficult, 
will  be  avoided.  -Lying  on  one  side  will  sometimes  relieve  a  patient 
who  is  perpetually  tormented  with  a  cough  when  in  the  dorsal  decubitus. 
As  one  can  easily  imagine,  in  pulmonary  cavities  with  constantly  re- 
newed secretion  certain  positions  will  aggravate  a  cough  if  the  secre- 
tions are  being  continually  poured  out  upon  the  healthy  bronchial 
mucous  membranes.  In  some  positions  the  cavity  would  become  en- 
tirely filled  before  any  overflow  would  excite  the  paroxysm  of  coughing. 


26 


GENERAL   CONDITION  OF  THE  PATIENT. 


The  latter  then  completely  empties  the  cavity,  thus  affording  the  patient 
a  temporary  rest.  The  diagnosis  of  a  cavity  would  be  strongly  sug- 
gested by  such  history. 

With  colic,  with  cardialgia,  and  sometimes  with  intestinal  obstruc- 
tion patients  generally  prefer  to  lie  upon  the  abdomen,  because  the 
tension  of  the  distended  intestines  is  diminished  or  their  position  shifted 
and  the  pain  relieved  ;  but  in  peritonitis  the  abdomen  is  so  sensitive  to 
pressure  that  the  dorsal  decubitus  is  assumed.     On  account  of  the  epi- 


FiG.  2. — Adiposity :  The  enormous  accumulation  of  fat  over  and  within  the  abdomen  simulates 

a  collection  of  ascitic  fluid. 


gastric  tenderness,  it  is  comparatively  rare  to  find  a  patient  with  a  gas- 
tric ulcer  lying  upon  the  abdomen,  unless  such  a  position  frees  the  ulcer 
from  the  contact  or  pressure  of  the  gastric  contents — e.  g.,  if  situated 
upon  the  posterior  wall.  Patients  with  lieadache  sometimes  prefer  to 
lie  upon  the  abdomen.  The  characteristic  positions  of  patients  suffer- 
ing from  cerebrospinal  meningitis  or  wry-neck  depend  upon  cramp-like 
contractions  of  certain  groups  of  muscles ;  some  peculiar  paralytic 
positions,  upon  paralyses  of  muscles. 


DEVELOPMENT  AND  STATE  OF  NUTRITION. 


27 


GAIT  AND  THE  ATTITUDE. 

An  alert,  erect  attitude  and  a  rapid  walk  usually  signify  good 
physical  condition,  while  a  stooping,  relaxed  posture  with  a  slow,  fatigued 
gait  indicates  that  the  person  is  seriously  ill  or  mentally  depressed.  (For 
a  description  of  various  characteristic  gaits  see  Examination  of  the 
Nervous  System.) 


DEVELOPMENT  AND   STATE  OF   NUTRITION. 

A  robust,  vigorous  or  muscular  physique  means  that  the  bodily  dimen- 
sions are  rather  above  the  normal,  whereas  a  weakly  or  puny  physique 
would  indicate  the  contrary.  The  subcutaneous  fatty  layer  (panniculus 
adiposus)  is  perhaps  of  even  more  importance  than  the  muscles  in  esti- 
mating the  state  of  nourishment.  The  former  varies  within  normal  limits 
in  accordance  with  the  age,  sex,  and  occupation  of  patients.  Corpulency 
is  generally  associated  with  a  weak  musculature.  Nursing  infants 
possess  an  extremely  well-developed  layer  of  fat ;  during  childhood  it 
gradually  diminishes,  and  in  the  third  or  fourth  decade  increases  again, 
while  at  old  age  it  finally  diminishes.  A  marked  tendency  to  corpu- 
lency is  often  observed  in  women  especially  after  the  menopause. 

Most  chronic  diseases  are  accompanied  by  a  noticeable  deteriora- 
tion of  the  general  nutrition.  This  is  due  either  to  lack  of  appetite, 
and,  hence,  insufficient  food,  to  defective  assimilation,  or  to  excessive 


Fig.  3.— Pronounced  emaciation  in  a  chronic  disease.    Case  of  multiple  myeloma  (New  York  City- 
Hospital). 

combustion  of  the  food  assimilated.  Emaciation  is  particularly  evident 
in  chronic 'febrile  and  digestive  diseases,  and  becomes  most  pronounced 
in  severe  and  prolonged  typhoid  fever,  in  phthisis,  in  carcinoma,  espe- 
cially esophageal  carcinoma,  and  in  certain  types  of  diabetes  mellitus. 
In  these  diseases  the  musculature  suffers  a  loss  almost  as  rapidly  as  the 
fatty  tissue.     Marked  emaciation  nearly  always  suggests  chronicity. 


28 


DEVELOPMENT  AND  STATE  OF  NUTRITION. 


BODY  WEIGHT, 

Observation  of  weight  over  a  certain  length  of  time  furnishes  an 
excellent  guide  to  the  state  of  nutrition.  Minute  cautions  in  regard  to 
the  accuracy  of  the  scales,  weight  of  diiferent  clothes,  etc.,  are  hardly 
necessary  to  enumerate.  Unless  accurately  estimated  the  weight  is  of 
no  value.  It  is  more  accurate  to  weigh  the  body  always  either  before 
or  after  eating,  since  a  hearty  meal  will  often  make  a  difference  of  one  or 
more  pounds.  General  edema  or  the  accumulation  of  fluid  in  one  of 
the  large  serous  sacs  will  considerably  increase  a  patient's  weight,  while 
free  catharsis,  diuresis  or  diaphoresis  will  rapidly  diminish  it.  Careful 
comparative  weighing  in  these  cases  furnishes  very  good  evidence  of  the 
progress  of  the  disease. 

Infants  should  be  weighed  weekly,  to  keep  track  of  their  nutrition. 
The  normal  weight  of  the  newborn  is  (females)  3000  gm.  (6  lbs.)  to 
(males)  3500  gm.  (7  lbs.)  (Uffelmann).  During  the  first  three  or  four 
days  of  life  there  is  a  physiologic  loss  of  200  to  300  gm.  (J  lb.).  Ger- 
hardt  ^  cites  the  following  table  : 


1st  month 

25  gm. 

Daily 

increase 

in    7th 

month 

15  gm 

2d 

23   " 

u 

"     8th 

11 

13    " 

3d        " 

22   " 

a 

"     9th 

" 

12    " 

4th       " 

20   " 

a 

"   10th 

a 

10    " 

5th       " 

18   " 

a 

"   11th 

u 

8    " 

6th       " 

17   " 

li 

"  12th 

a 

6    " 

Quetelet's  table  (an  extract  from  which  is  inserted  below)  does  not 
take  into  account  the  weight  of  the  clothes,  this  has  been  estimated  to 
be  in  men  about  ^  and  in  women  about  J^  of  the  total  weight;  although, 
of  course,  such  figures  must  vary  considerably  : 

Male.  Female. 

Newborn 3.1  kg.  (    6.83  lbs.)  3.0  kg.   (     6.61) 

1st  vear 9.0   "    (  19.84     "  )  8.6   "  (   18.96) 

2d   "  "          11.0   "    (  24.25     "  )  11.0   "  (  24.25) 

3d       "          12.5   "    (  27.56     "  )  12.4   "  (   27.34) 

4th     "          14.0   "    (  30.86     "  )  13.9   "  (  30.64) 

5th     "          15.4   "    (  33.95     "  15.3   "  (  33.73) 

6th     " 17.8   "    (  39.'24     "  )  16.7   "  (  36.82) 

7th     "          19.7   "    (  43.43     "  )  17.8   "  (  39.24) 

8th     "          21.6   "    (  49.62     "  )  19.0   "  (  41.89) 

9th     "          23.5   "       51.81     "  )  21.0   "  (  46.30) 

10th     "          25.2    •'    (  55.56     "  )  23.1    "  (  50.93) 

11th     "          27.0   "    (  59.52     "  )  25.5   "  (  56.22) 

13th     "          33.]    "    (  72.79     "  )  32.5   "  (  71.65) 

loth     "          41.2   "    (  90.83     "  )  40.0   "  (  88.18) 

17th     " 49.7   "    (109.57    "  )  46.8   "  (103.18) 

19th     "          57.6   "    (126.98     "  )  52.1    "  (114.86) 

20th     "          59.5   "    (131.17     "  )  53.2   "  (117.28) 

25th     "              66.2   "    (145.94     "  )  54.8   "  (120.81) 

30th     "          66.1    "    (145.72     "  )  55.3   "  (121.91) 

60th     "          61.9   "    (136.46     "  )  54.3   "  (119.71) 

70th     "           59.5   "   (141.17     "  )  51.5   "  (113.54) 

^  Gerhardt,  Lehrbuch  der  Kinderkrankheiten,  1881,  p.  2. 


BODY  WEIGHT. 


29 


MENSURATION. 


An  individual's  general  development  must  be  judged  by  comparisons 
between  his  age,  weight,  and  height.  Quetelet '  is  also  responsible  for 
the  following  table  : 


Newborn 

1st  year 

2d 

3d 

4th 

5th 

6th 

7th 

8th 

9th 
10th 
11th 
13th 
15th 
17th 
19th 
20th 
25th 
30th 
40th 
60th 
70th 


Male. 

Female. 

50.0 

cm 

.  (].8 

-i 

49.4  cm.  (1.7 

ft.) 

69.8 

(2.3 

69.0    ' 

'    (2.3 

"  ) 

79.1 

(2.7 

"  ) 

78.1    ' 

'    (2.7 

") 

86.4 

(2.10 

"  ) 

85.4    ' 

(2.10 

'M 

92.7 

(3.— 

") 

91.5    ' 

'    (3.- 

"  ) 

98.7 

(3.3 

") 

97.4    ' 

'    (3.2 

"  ) 

104.6 

(3.5 

"  ) 

103.1    ' 

'   (3.5 

") 

110.4 

(3.7 

"  ) 

108.7    ' 

'   (3.7 

"  ) 

116.2 

(3.10 

") 

114.2 

'    (3.9 

") 

121.8 

(4.0 

") 

119.6 

'    (3.11 

") 

127.3 

(4.2 

") 

124.9 

'    (4.1 

") 

132.5 

(4.4 

") 

130.1    ' 

'    (4.3 

") 

142.3 

(4.8 

") 

140.0    ' 

'    (4.7 

"  ) 

151  3 

(5.0 
f5.3 

(5.5 

148.8    "    (4.11 
154.6    "    (5.1 

"  ) 

159.4 

"  1 

165.5 

") 

157.0    ' 

'    (5.1 

"  1 

167.0 

(5.6 

"  ) 

157.8    ' 

'    (5.2 

u    \ 

168.2 

(5.6 

") 

157.4    ' 

'    (5.2 

"   ^ 

168.6 

(5.6 

") 

158.0    ' 

'    (5.2 

" ) 

168.6 

(5.6 

"  ) 

158.0 

'   (5.2 

") 

167.6 

(5.6 

") 

157.1    ' 

'    (5.2 

") 

166.0 

(5.5 

") 

155.6 

'    (5.1 

") 

Circumference  of  the  Chest. — The  chest  measurement  fur- 
nishes a  very  good  idea  of  the  state  of  development.  It  is  used  in 
many  countries  in  examining  army  recruits.  Frohlich  ^  recommends 
the  following  method  :  The  measuring  tape  is  to  be  applied  horizontally 
at  the  level  of  the  nipples  in  front  and  just  beneath  the  angles  of  the 
scapulae  behind  while  the  arms  are  held  horizontally.  The  measure- 
ments during  extreme  inspiration  and  again  during  extreme  expiration 
are  to  be  recorded,  the  difference  representing  the  chest  expansion.  He 
found  among  recruits  that  the  average  in  men  of  twenty  years  was,  for 
expiration  82  cm.  (32|  in.),  for  inspiration  89  cm.  (35f  in.),  and  the 
chest  expansion  7  cm.  (2f  in.),  and  he  attaches  considerable  diagnostic 
importance  to  these  figures,  because  he  noted  that  in  emphysema,  in 
phthisis,  and  pleural  effusions  the  circumference,  especially  during  ex- 
piration, was  increased,  while  the  chest  expansion  was  diminished,  and 
this  diminution  might  persist  for  some  time  after  the  disease  has  subsided. 
The  chest  expansion  is  diminished  if  the  costal  cartilages  become  ossified 
(the  so-called  Bryson's  sign).  This  is  often  the  case  in  exophthalmic 
goiter. 


'  Anthropometrie,  1870. 

'^  H.  Fi-olich,  Die  -Brustmessung  im  Dienste  der  Medicin,  Leipzig,  1894. 
ography  is  quoted  here. 


A  full  bibli- 


30  DEVELOPMENT  AND  STATE   OF  NUTRITION. 


CONFIGURATION  OF  THE    THORAX. 

NORMAL  SHAPE  OF  THE  CHEST. 

A  normal  chest,  such  as  one  sees  so  beautifully  illustrated  in  the 
masterpieces  of  classic  statuary,  should  be  symmetric,  the  surface  well 
rounded,  without  sharp  corners  or  depressions  ;  the  intercostal  spaces 
only  visible  between  the  lower  ribs  ;  the  subcostal  angle  about  90°  ; 
the  sternum  nearly  straight  in  profile,  without  a  decided  angle  between  the 
corpus  and  the  manubrium  ;  and  the  sternovertebral  somewhat  shorter 
than  the  transverse  diameter.  The  gradual  increase  in  the  horizontal 
diameters  of  the  thorax  should  form  a  sort  of  pyramid,  with  its  base 

below,  but  the  graduation  should  not  be  too 
marked,  and  the  shoulder  girdle,  or  in  females 
the  breast,  should  offset  this  difference.  The 
shoulders  should  be  nearly  horizontal,  the 
scapulae  lying  flat  against  the  back,  clavicles 
not  too  prominent,  and  the  supra-  and  in- 
^  fraspinous  fossae  not  too  deep. 

PATHOLOGIC   SHAPES. 

Emphysematous  Chests.  —  These 
abnormal  forms  depend  upon  an  emphy- 
sematous enlargement  of  the  lungs ;  and 
they  possess  one  feature  in  common — the 
thorax  seems  abnormally  widened  and 
\  .  J         prominent.     The   sagittal   diameter  is  gen- 

I  #  erally    increased    and    the    subcostal   angle 

^  .^\,         more    obtuse   than   in    the    normal    thorax. 

Fig.  4.-Emphyseniatous  chest     When  the  emphysema  is  diffused  over  the 
GenemiHospfS'  *^'^^''^^^^'^""     entire  lung  or  when  mostly  limited  to  the 

lower  chest,  the  thorax  looks  as  if  in  a 
normal  position  of  deep  inspiration  ;  but  when  caused  by  forced  expi- 
ration (coughing)  the  emphysema  is  situated  more  in  the  upper  chest, 
because  the  respiratory  power  acts  more  upon  the  lower  parts  of  the 
thorax.  Then  the  upper  thoracic  aperture  appears  enlarged  and  the 
so-called  "barrel  chest"  is  produced.  These  are  the  two  different 
types. 

The  Paralytic  Thorax. — Contrasted  with  the  emphysematous 
thorax,  the  so-called  paralytic  thorax  is  abnormally  flat,  long  and  some- 
times narrow  ;  the  ribs,  both  in  front  and  behind,  have  a  marked  down- 
ward direction  ;  the  intercostal  spaces  are  widened ;  the  subcostal  angle 
is  very  acute  ;  the  supra-  and  infraclavicular  fossae  are  deep  ;  the  inter- 
costal muscles  and  those  of  the  shoulder  girdle  are  feebly  developed 
(hence  the  name)  ;  and  the  shoulder  blades  project  noticeably,  like  wings, 
because  of  a  weakness  of  the  muscles,  especially  of  the  serratus  magnus. 
This  type  of  chest  is  observed  frequently  in  iveakly  or  cachectic  individ- 
uals,  very  commonly   in  phthisis.      It  was  formerly  considered  as  a 


coy  FIGURATION  OF  THE  THORAX. 


31 


predisposing  cause  of  consumption,  and  is  now  frequently  spoken  of  as 
"  the  phthisic  chest." 

Scoliotic,    Kyphotic,    and    Scoliokyphotic   Thoraces. — 

These  terms  are  applied  to  twists  and  deformities  of  the  chest  which  are 
observed  as  a  sequence  of  spinal  curvature.  They  are  often  quite  pro- 
nounced. It  is  often  difficult  to  detect  such  deformities  from  the  front ; 
but  by  noting  the  low  stature,  the  short  thorax,  and  the  marked  breadth 
of  shoulders  an  experienced  eye  can  generally  discover  them. 

Rachitic  Chests. — Rickets  is  responsible  for  many  chest  deform- 


f^ 


Fig.  5.— Paralytic  chest  (phthisis)  (Dr.  W.  H. 
Smith,  Massachusetts  General  Hospital). 


Fig.  6.— Paralytic  chest  (phthisis)  (Dr.  W.  H, 
Smith,  Massachusetts  General  Hospital). 


ities,  although  often  very  slight  ones.  Perhaps  the  most  characteristic 
is  the  keel-shaped  prominence  of  the  sternum  called  pectus  carinatum 
(pigeon  breast).  It  is  associated  with  a  compression  of  the  anterior 
diagonal  horizontal  diameter  and  an  increase  in  the  sternovertebral 
diameter  of  the  chest  (Fig.  8).  A  transverse  groove  (Harrison's  groove) 
often  marks  the  insertion  of  the  diaphragm  to  the  ribs.  The  so-called 
"  rachitic  rosary,"  a  beaded  enlargement  at  the  line  of  junction  of  the 
bony  ribs  with  their  costal  cartilages,  can  be  felt  as  well  as  seen.  It 
generally  disappears  in  later  childhood.  The  other  rachitic  deformities 
may  persist,  or  they  may  become  modified  to  a  greater  or  less  extent. 


32  DEVELOPMENT  AND  STATE  OF  NUTRITION. 

Boat-shaped  Chest  of  Syringomyelia. — Pierre  Marie  and 
Asti6  ^  described,  under  the  name  of  "  thorax  en  bateau,"  a  depres- 
sion of  the  upper  portion  of  the  anterior  chest-wall,  which,  so  far  as  we 
know,  is  only  observed  in  syringomyelia.  The  cavity  lies  in  the  median 
line,  as  if  sunk  against  the  spinal  column,  and  extends  downward  as  far 
as  the  lower  edge  of  the  pectoralis  major ;  it  may  be  as  deep  as  5  cm. 
The  atrophy  of  the  pectorals  and  of  the  other  muscles  takes  no  part  in 
producing  this  appearance. 

Funnel-shaped  Chest  and  Cobbler's  Chest. — The  true  fun- 


FiG.  7.— Right  scoliosis  (Moore). 

nel-shaped  chest  is  either  congenital  or  else  develops  in  early  infant  life, 
gradually  and  without  any  known  cause.  It  consists  of  a  funnel-shaped 
depression  of  the  lower  end  of  the  sternum,  which  frequently  reaches 
quite  deeply  into  the  interior  of  the  chest.  It  may  lead  to  circulatory 
or  respiratory  disturbances  resembling  those  observed  in  kyphoscoliosis. 
Cobblers  may  acquire  a  very  similar  deformity,  due  to  the  constant 
pressure  against  the  lower  end  of  the  sternum.  The  cobbler  type  is, 
however,  limited  to  the  inferior  portion  of  the  sternum,  or  even  to  the 
xiphoid  process  alone. 

^  Soc.  mid.  des  hdpitaux,  19,  ii.,  1897. 


CONFIGURATION  OF  THE  THORAX. 


33 


Asymmetry  of  the  Chest  Due  to  Disease  of  the  Thoracic 
or  Abdominal  Viscera. — An  expansion  or  a  contraction  of  one  chest- 
half  may  result  from  various  affections  of  the  thoracic  viscera — e.  g.,  a 
large  pleural  exudate,  a  pneumothorax,  or  even  to  a  slight  extent  a 
croupous  pneumonia.  The  alteration  may  be  general  over  one  entire  side 
or  localized.     The  affected  side  may  be  the  larger  or  the  smaller. 

A  considerable  pleural  effusion  or  a  pneumothorax  produces  an  enlargement 
of  the  affected  side  of  the  thorax,  an  obliteration  of  the  intercostal  spaces,  a  dis- 


FiG.  8.— Pigeon  breast  (Dr.  R.  C.  Cabot,  Massachusetts  General  Hospital). 

location  outward  of  the  nipple  and  of  the  scapula,  a  convexity  of  the  spine  toward 
the  affected  side,  and  an  elevation  of  that  shoulder.  The  last  two  deformities, 
both  probably  due  to  an  alteration  of  the  center  of  gravity,  make  the  patient  look 
as  if  he  were  carrying  a  weight  on  the  affected  side. 

The  lower  thorax  may  be  enlarged  by  a  decided  increase  in  the 
size  of  the  liver  or  spleen.  Such  an  enlargement  will  become  still 
more  noticeable  if  tympanites  or  ascitic  fluid  distends  the  abdomen 
enough  to  prevent  the  dropping  of  the  enlarged  liver  or  spleen.  An 
aortic  aneurism  or  an  intrathoracic  tumor  may  cause  a  localized  enlarge- 
ment of  the  thorax.  This  will  be  situated  at  the  point  of  contact  of 
the  growth  with  the  thoracic  wall.  Actual  contact  is  not,  however, 
necessary,  because,  ev^en  when  the  growth  or  aneurism  is  merely  in  close 
proximity  to  the  wall,  a  localized  bulging  will  be  caused  by  the  diminution 


34 


DEVELOPMENT  AND  STATE   OF  NUTRITION. 


in  the  intrathoracic  negative  pressure — e.  g.,  an  aortic  aneurism,  even 
when  covered  by  the  lung,  will  cause  a  local  prominence.  Neither  does 
a  pleural  effusion  need  to  be  under  positive  pressure,  as  is  so  commonly 
supposed,  in  order  to  enlarge  the  affected  side  of  the  <ihest.  (See  what 
is  said  upon  dislocation  of  organs  by  exudations,  p.  79.)  Cardiac 
enlargements  and  pericardial  effusions  give  rise  to  a  precordial  bulging. 
The  lower  thorax  will  be  quite  uniformly  and  decidedly  expanded  by 
any  marked  increase  in  the  contents  of  the  abdomen — e.  g.,  meteorism, 
ascites,  or  large  ovarian  tumors. 


Fig.  9.— Rickets:  Note  the  size  and  shape  of  head  (see  p.  19),  the  rosary,  Harrison's  groove, 
kyphosis,  prominent  belly,  bowing  of  legs,  and  the  enlargement  of  wrists  (Dr.  W.  L.  Stowell, 
Randall's  Island  Hospital). 

Chronic  indurative  processes  in  the  lung — e.g.,  chronic  pneumonia 
with  or  without  bronchiectasis,  chronic  tuberculosis — are  apt  to  cause  a 
unilateral  contraction  of  the  thorax,  sometimes  including  the  entire  half 
of  the  chest.  The  coincident  pleuritic  contraction  may  be  partly  respon- 
sible for  the  deformity.  After  the  absorption  of  a  pleuritic  effusion  it 
is  very  common  to  find  a  retraction  of  the  affected  side  of  the  chest 
instead  of  the  previous  enlargement.  This  is  due  to  the  fact  that  the 
lung,  incased  in  thick  fibrous  adhesions,  has  been  compressed  so  long 
that  it  can  never  again  expand  fully,  and  that  the  pleuritic  adhesions 
tend  to  contract  and  draw  the  thorax  in.     These  pulmonary  and  pleu- 


CONFIGURATION  OF  THE  THORAX. 


35 


ritic  conditions  are,  of  course,  very  commonly  combined.  When  the 
contraction  of  one  side  of  the  chest  is  very  decided,  the  scapula,  clav- 
icle, and  the  neighboring  soft  parts  are  plainly  depressed ;  the  nipple 
and  the  shoulder  then  approach  the  median  line,  and  the  spinal  column 
presents  a  curvature  with  a  concavity  toward  the  affected  side.  The 
corresponding  dislocations  of  the  thoracic  viscera  will  be  discussed  under 
Topographic  Percussion.  Noticeable  increase  in  the  depth  of  the  supra- 
or  infraclavicular  fossae  suggests  a  retraction  of  the  apices,  and  is  there- 
fore an  early  and  important  sign  in  pulmonary  tuberculosis. 

Inspection  reveals  these  chest  deformities  more  accurately  than  direct  measuring 
with  the  tape  ;  probably  because  the  eye  notes  differences  not  only  in  the  size  of 


Fig.  10.— Funnel-shaped  chest  (Dr.  R.  0.  Cabot,  Massachusetts  General  Hospital). 

the  chest,  but  in  the  extent  of  the  respiratory  excursions.  The  latter  are,  of  course, 
always  diminished  on  the  affected  side.  The  extent  of  the  respiratory  excursion  is 
the  surest  way  to  decide  whether  a  given  deformity  is  due  to  an  enlargement  of  one 
side  or  a  contraction  of  the  other  side.  Another  reason  why  measuring  with  the 
tape  is  apt  to  be  inaccurate  in  pleuritic  effusions  is  this:  The  lower  end  of  the  ster- 
num is  generally  dislocated  to  the  affected  side,  so  that  the  middle  line  of  the 
sternum  forms  an  acute  angle  with  the  true  median  line  of  the  body.  Therefore, 
measuring  from  the  middle  of  the  spinal  column  to  the  middle  of  the  sternum  is 
not  accurate.  We  should  measure  to  a  plumb  line  dropped  fi'om  the  middle  of  the 
jugulum  (ligne  du  cordon). 

Woillez's  cyrtometer  is  a  practical  instrument  for  measuring  and  picturing  chest 
deformities,  and  is  rather  better  than  the  ordinary  tape  ;  but  as  a  matter  of  fact  a 
narrow  lead  band,  about  the  thickness  of  a  lead  pencil,  is  more  convenient  than  the 
specially  devised  instrument.  It  can  be  accurately  applied  to  the  chest-wall  at  one 
level  and  removed  without  altering  its  shape  ;  a  tracing  can  then  be  made  upon 
paper  and  mea.surements  taken.     Such  tracings  are  sometimes  very  instructive  in 


36 


DEVELOPMENT  AND  STATE   OF  NUTRITION. 


following  the  course  of  an  obstinate  pleurisy.     (For  the  discussion  of  more  compli- 
cated apparatus,  the  reader  is  referred  to  the  references  cited  below.  ^) 


Fig.  11.— Scoliosis  and  asymmetry  of  the  thorax:  Patient  with  fibroid  phthisis  of  left  lung; 
left  chest  smaller  than  right;  left  shoulder  (affected  side)  higher  than  right;  left  scapula  nearer 
the  spine ;  dorsal  spine  concave  to  left ;  lumbar  spine  with  a  compensatory  convexity  to  left  (New 
York  CityHospital). 

SIZE   AND  SHAPE   OF  THE  HEAD. 

The  horizontal  circumference  of  the  skull  in  the  newborn  is  normally 
40  cm.,  at  the  end  of  the  first  year  45  cm.,  and  at  puberty  50  cm. 
(Striimpell). 

During  the  first  eight  or  nine  months  the  large  fontanel  slightly  increases  in 
size  ;  about  the  tenth  month  it  begins  to  diminish,  and  at  the  sixteenth  month  it 
should  be  closed. 

'  F.  Schenk,  "  Zur  Aetiologie  der  Skoliose."  Vortrag,  gehaUen  in  der  Chir.  Section 
der  58.  Versamnilung  deutsclier  Naturforscher  und  Aerzte  zu  Strassburg  i.  E.  Berlin. 
Verlag  von  H.  Heinicke.  C.  Hiibscher,  "  Redresseur  und  Messapparat."  Ein  Beitrag 
zur  Therapie  der  fixierten  Skoliose.  BeitrLige  zur  klinischen  Chirurgie,  redigiert  von  P. 
Bruns,  vol.  xiii.,  part  1. 


SIZE  AND  SHAPE  OF  THE  HEAD. 


37 


Hydrocephalus  may  be  either  congenital  or  acquired  early  in  life.  The  skull  is 
enlarged,  and  most  of  the  bones  are  separated  by  broad  sutures  and  fontanels,  i 
The  cranium  looks  like  a  big  bladder,  tapering  downward.     The  orbital  roofs  are 


Fig.  12. — Hydrocephalus:  Note  size  and  shape  of  the  head  as  compared  with  the  face;  the 
prominence  of  eyes  and  overhanging  orbital  roof;  marked  talipes  equinovalgus  of  left  foot 
(Dr.  W.  L.'Stowell,  Randall's  Island  Hospital). 


projected  downward,  causing  the  eyes  to  look  downward  in  a  very  characteristic 
fashion;  and  the  face  is  diminutive  in  comparison.  The  cranial  bones  are  very 
thin,  and  when  pressed  upon  crackle  like  parchment. 

Rachitis  is-  characterized  by  a  peculiar  malformation  of  the  skull.  Although 
the  longitudinal  and  transverse  diameters  are  approximately  normal,  the  cranium 
has  a  distinctive  appearance,  due  to  the  prominent  frontal  and  parietal  eminences 
and  to  the  vertical  position  of  the  occipital  bone,  forming  the  square-shaped  head 
(tete  carree).  The  large  fontanel  may  remain  patent  into  the  third,  fourth  or  even 
the  sixth  year,  and  the  sutures  a  correspondingly  long  time.  The  thinned  areas  of 
bone  over  the  cranium,  and  especially  over  the  occipital  bone,  will  furnish  the 
same  parchment-crackling  described  above.* 

^  The  horizontal  circumference  may  be  as  much  as  .50  cm.  in  the  first  month  of  life. 
'Special  Pathology  must  be  consulted  for  a  description  of  the  deformities  of  the  face 
in  acromegaly  and  of  the  asymmetry  in  hemiatrophia  facialis  progressiva. 


38  EXAMINATION  OF  THE  SKIN. 


EXAMINATION    OF  THE   SKIN. 

An  examination  of  the  skin  should  not  be  restricted  to  cutaneous 
diseases  alone,  because  in  diseases  of  the  internal  organs  we  meet  with 
all  manner  of  changes  in  the  skin,  which  can  be  appreciated  by  the 
sense  of  sight  or  by  that  of  touch. 

COLOR  OF  THE  SKIN. 

The  normal  fleshy  tint  of  the  skin  is  due  to  the  color  of  the  blood 
shining  through  the  epidermis  and  the  superficial  layers  of  the  cuticle. 
The  color  of  the  skin  may  be  modified,  both  physiologically  and  patho- 
logically, by  (1)  a  quantitative  increase  or  decrease  in  the  amount  of 
flesh  color ;  (2)  a  qualitative  change  due  to  abnormal  pigmentation. 
The  first  is  better  observed  in  the  face  ;  the  second,  in  other  parts  of 
the  body,  where  the  normal  flesh  color  is  not  so  prominent.  Many 
qualitative  variations,  occasioned  by  abnormal  pigmentation,  are,  how- 
ever, determined  better  over  paler  uncovered  areas. 

QUALITATIVE   CHANGES  OF  THE  FLESH  COLOR. 

The  intensity  of  the  flesh  color  depends  upon  (1)  the  intensity  of 
the  blood  color ;  (2)  upon  the  amount  of  blood  contained  in  the  ves- 
sels ;  (3)  upon  the  thickness  of  the  layers  of  skin  covering  the  vessels. 
Any  one  of  these  three  factors  may  vary  and  so  cause  alterations  in  the 
flesh  color  of  more  or  less  diagnostic  importance. 

PALLOR. 

Pallor  Depending:  upon  Oligochromemia. — A  pale  face  pre- 
supposes anemia,  or  a  diminution  of  the  coloring  power  of  the  blood 
(oligochromemia) — that  is  to  say,  a  qualitative  alteration  of  the  blood. 
For  we  do  not  recognize  any  real  quantitative  diminution  ("  blood  pov- 
erty "  of  the  Germans)  except  that  which  occurs  after  a  profuse  hemor- 
rhage, and  this  is  rapidly  made  up  by  reabsorption  of  lymph  and  water, 
thus  causing  again  the  condition  of  oligochromemia.  As  we  shall  see 
later  on,  pallor  is  a  very  uncertain  guide  in  the  diagnosis  of  oligochro- 
memia. 

Pallor  without  Oligochromemia. — It  is  impossible  to  diag- 
nose anemia  from  pallor  alone.  A  careful  blood-examination  (see  Sec- 
tion on  p.  659)  is  absolutely  essential  in  order  to  avoid  the  mistake  of 
diagnosing  anemia  in  a  patient  with  normal  blood  simply  because  his 
face  is  pale  ;  or  of  reassuring  a  patient  with  red  cheeks  whose  hemoglobin 
percentage  is  only  50. 

Aside  from  oligochromemia,  the  causes  of  pallor  of  the  face  are 
numerous — e.  g.,  many  people  absolutely  well,  without  a  symptom  or 
sign  of  disease,  are  abnormally  pale.  The  only  way  to  explain  such 
pallor,  providing,  of  course,  the  conjunctival  and  mucous  membranes 
are  not  also  pale,  is  to  assume    either  an  abnormal  opacity  of  the 


COLOR  OF  THE  SKIN.  39 

epidermis  or  a  scanty  supply  of  blood-vessels  in  the  face.  During  the 
course  of  an  illness  a  patient  sometimes  gradually  becomes  paler  and 
paler,  and  although  the  hemoglobin  percentage  remains  normal,  the 
physician,  unless  he  examines  the  blood,  will  certainly  consider  the 
condition  one  of  oligochromemia.  Here  we  must  suppose  that  the 
pallor  is  due  either  to  a  diminution  of  the  total  amount  of  blood, 
or  that  the  skin  contains  less  blood  than  normally  as  a  result  of 
morbid  changes  in  the  circulation.  As  suggested  above,  except  in 
severe  hemorrhages,  we  know  no  way  of  determining  that  there  is  a 
diminution  in  the  total  amount  of  blood  as  compared  to  the  weight 
of  the  body,  so  we  must  content  ourselves  with  the  second  explanation  ^ 
— an  alteration  in  the  circulation.  The  latter  is  all  the  more  probable 
in  connection  with  certain  other  symptoms — e.  g.,  weakness  of  the  pulse, 
slight  grade  of  cyanosis  (see  p.  40  et  seq.),  dilatation  of  the  external  cuta- 
neous veins,  slight  dizziness,  malaise,  general  physical  debility,  etc.  It 
is  difficult  to  determine  whether  the  diminished  amount  of  blood  in  the 
small  arteries  and  capillaries,  which  is  certainly  the  cause  of  the  pallor, 
depends  upon  an  alteration  in  the  cardiac  activity  or  in  the  vasomotor 
control.  A  low  blood-pressure  is  associated  with  pallor  if  entirely 
dependent  upon  diminished  cardiac  activity,  the  vasomotor  tonus  re- 
maining constant ;  but  if  the  small  arteries  dilate,  pallor  does  not  result. 
High  blood-pressure  is  characterized  by  a  marked  pallor,  provided 
there  is  a  very  decided  vasomotor  contraction. 

A  closer  study  of  the  connection  between  a  normal  hemoglobin  per- 
centage and  this  pallor  would  be  of  some  service  for  careful  treatment ; 
because  so  long  as  every  pale  patient  is  considered  anemic,  as  is  unfor- 
tunately too  often  the  case  in  practice,  we  shall  not  progress  very  far 
toward  proper  therapy.  Affections  of  the  stomach,  heart  disease,  and 
phthisis,  although  associated  with  pallor,  often  show  a  normal  blood. 
All  such  conditions  will,  of  course,  lead  later  on  to  oligochromemia. 

The  temporary  pallor  caused  by  nausea,  collapse,  or  violent  psychical 
impressions  practically  comes  under  the  head  of  an  alteration  in  circula- 
tion, being  due  partly  to  vasomotor,  partly  to  cardiac,  influences. 

ABNORMAL  REDNESS   OF  THE  SKIN  OF  THE  FACE. 

If  the  above  conditions  which  produce  pallor  are  reversed,  an  abnor- 
mal redness  of  the  skin  will  result.  A  hemoglobin  percentage  as 
high  as  120,  although  very  rare,  may  be  responsible  for  an  increased 
color.  We  -do  not  know  as  yet  whether  there  is  such  a  condition 
as  true  plethora ;  v.  Recklinghausen  thinks  there  is,  and  so  explains 
the  appearance  of  full-blooded  people.  In  many  cases  such  an  ap- 
pearance is  caused  by  an  abnormally  thin  or  transparent  skin  ;  in  others 
by  a  local  increase  in  the  amount  of  blood  sent  to  the  face.  The 
so-called  "  rosy  chlorotics "  are  supposed  to  possess  blood-vessels  of 
abnormal  transparency.      In  all  such  cases  an  examination  of  the  blood 

^  Although  it  seems  probable  that  extreme  emaciation  is  associated  with  a  diminution 
in  the  amount  of  blood,  it  has  never  been  proved  that  this  diminution  is  out  of  propor- 
tion to  the  loss  of  body  weight. 


40  EXAMINATION  OF  THE  SKIN. 

is  absolutely  essential  before  a  diagnosis  of  oligochromemia  can  be  made. 
A  suggestion  is,  however,  often  obtained  by  comparing  the  pallor  of  the 
conjunctivae  with  the  rosy  hue  of  the  cheeks. 

People  who  spend  most  of  the  day  out  of  doors,  and  especially  those 
who  are  exposed  to  all  sorts  of  weather,  generally  acquire  a  ruddy  face 
from  the  constant  increase  of  blood  in  the  exposed  portions. 

Alcoholics  are  usually  flushed  on  account  of  the  dilating  influence 
of  alcohol  upon  the  vessels.  Minute  dilated  radicals  may  also  be 
seen  just  underneath  the  epidermis,  or  an  acne  rosacea,  which  is 
so  frequent  in  drinkers.  As  is  well  known,  this  same  peculiarity  is 
often  observed  in  perfectly  healthy  individuals,  in  whom  it  is  difficult 
to  determine  any  cause.  Fever  produces  a  characteristic  redness, 
ordinarily  combined  with  some  puffiness  and  moisture  of  the  skin  of 
the  face.  The  lax  condition  of  the  muscular  coat  of  the  vessels  is 
apparently  responsible.  This  is  evident  in  a  sphygmographic  trac- 
ing. The  flush  of  fever  is  most  noticeable  in  the  cheeks,  especially 
when  contrasted  with  a  pallor  such  as  is  observed  in  tubercular  patients- 
(so-called  hectic  flush).  Psychical  excitement,  shame,  violent  physi- 
cal exertion,  external  applications  of  heat  to  the  skin  (baths,  insola- 
tion), the  inhalation  of  nitrite  of  amyl,  or  a  moderate  grade  of  atropin- 
or  opium-poisoning,  all  cause  a  flushing  of  the  face  from  vasomotor 
influences.  The  reddening  in  these  cases  may  spread  to  the  neck  and 
to  the  upper  part  of  the  trunk.  Poisoning  with  carbon  monoxid 
ordinarily  produces  a  very  intense  redness  of  the  face,  which  is  sup- 
posed to  be  due  to  an  alteration  of  the  blood.  The  latter,  however,^ 
contains  so  little  carbon  monoxid  that  it  is  even  difficult  to  determine 
it  with  the  spectroscope,  so  that  the  explanation  is  unsatisfactory. 

Hemicrania  and  some  afi^ections  of  the  cervical  sympathetic  some- 
times cause  a  unilateral  redness  of  the  face,  which  is  commonly  asso- 
ciated with  a  unilateral  pupillary  change.  The  redness  of  the  face 
associated  with  various  cutaneous  diseases  and  the  acute  exanthemata 
need  not  be  discussed. 

CYANOSIS. 

By  this  term  is  meant  a  bluish  tinge  of  the  skin  and  mucous  mem- 
branes which  depends  upon  the  poverty  of  the  capillary  blood  in  oxygen 
and  its  abnormal  richness  in  carbon  dioxid.  Since  it  is  even  a  deeper 
blue  than  ordinary  venous  blood,  we  must  assume  in  explanation  some 
peculiarity  in  the  skin-covering. 

General  Cyanosis. — Two  chief  factors  take  part  in  the  produc- 
tion of  general  cyanosis  : 

(1)  Insufficient  oxidation  of  the  blood  in  the  lungs,  so  that  the 
arterial  blood  in  the  capillaries  is  poor  in  oxygen  and  therefore  dark. 

(2)  Obstruction  to  the  venous  return,  so  that  the  veins  are  dilated, 
the  skin  contains  more  venous  blood  than  normally,  the  current  is  slug- 
gish, and  the  blood  is  charged  with  more  carbonic  acid. 

With  true  general  cyanosis  the  bluish  tinge  will  naturally  be  more 
pronounced  in  certain  body  parts — i.  e.,  there  are  certain  points  of  pre- 
dilection.    The  face,  especially  the  cheeks,  lips  and  ears,  shows  cyanosis 


COLOR   OF  THE  SKIN,  41 

very  plainly,  on  account  of  the  first  of  the  two  factors,  because  here 
the  color  shows  through  more  plainly ;  the  feet  and  the  toes,  the  fingers 
and  the  finger-nails,  on  account  of  the  second  of  the  two  factors  (the 
venous  stasis),  the  parts  in  question  being  so  remote  from  the  chest. 
The  nose  and  the  knees,  too,  often  show  cyanosis  very  noticeably. 

General  cyanosis  will  therefore  appear  in  any  respiratory  or  circula- 
tory affection.  These  two  systems  are  so  intimately  related  and  so 
dependent  one  upon  the  other  that  if  the  cyanosis  is  very  pronounced 
we  should  naturally  attribute  it  to  an  interference  with  both  respiration 
and  circulation,  no  matter  which  is  primarily  affected. 

The  following  disturbances,  primarily  respiratory,  cause  cyanosis : 
Any  aflPection  preventing  the  free  entrance  of  air  to  the  lungs — e.  g., 
retropharyngeal  abscess  ;  croup  ;  pseudocroup  ;  edema  or  spasm  of  the 
glottis  ;  paralysis  of  the  inferior  laryngeal  nerve  ;  tumor  of  the  larynx  ; 
foreign  bodies  in  the  pharynx,  larynx,  trachea  or  bronchi ;  any  kind  of 
tracheal  stenosis,  as  by  goiter  or  other  tumors ;  strangulation ;  bronchi- 
tis ;  bronchial  asthma,  etc. 

Affections  which  diminish  the  amount  of  breathing  surface  of  the 
lungs — e.  g.,  emphysema ;  all  varieties  of  pulmonary  infiltration  ;  ate- 
lectasis ;  compression  of  the  lungs  by  an  exudation  or  by  pneumothorax. 
In  this  connection  it  is  interesting  to  note  that  in  pulmonary  consump- 
tion the  cyanosis  does  not  reach  as  high  a  grade  as  the  amount  of 
breathing  surface  involved  would  lead  us  to  expect.  This  is  probably 
because  the  emaciated  body  contains  less  blood  and  needs  less  oxygen, 
so  that  what  remains  of  the  healthy  lung  tissue  is  nearly  sufficient  to 
aerate  the  diminished  amount  of  blood. 

All  affections  which  influence  the  activity  of  the  respiratory  muscles  : 
paralyses  and  atrophies  of  the  muscles  of  respiration  (bulbar  paralysis, 
etc.)  ;  as  well  as  spasms  (tetanus,  epilepsy) ;  further,  any  affection  caus- 
ing pain  enough  to  inhibit  respiration. 

In  all  these  disturbances  the  arterial ization  of  the  blood  in  the  lungs 
is  primarily  affected,  and  later  on  some  venous  congestion  results  because 
the  circulation  lacks  the  help  of  the  pumping  action  of  respiration. 

The  following  disturbances,  primarily  circulatory,  cause  cyanosis  from 
congestion  : 

Uncompensated  cardiac  affections  ;  valvular  lesions  and  affections  of 
the  heart  muscle ;  arteriosclerotic  and  nephritic  changes  ;  strains  upon 
the  heart ;  pericarditis,  etc.,  as  well  as  paralysis  of  the  vasomotors. 

Mitral  defects,  both  those  of  insufficiency  and  those  of  stenosis,  even 
when  compensated,  cause  a  certain  degree  of  cyanosis.  This  is  respira- 
tory in  nature,  and  depends  upon  the  increased  pressure  in  the  pulmonary 
circulation,  upon  the  resulting  rigidity  and  brown  induration  of  the 
lungs,  and  upon  the  accompanying  bronchial  catarrh,  all  of  which  im- 
pede the  respiration. 

The  cyanosis  of  congenital  heart  disease  is  often  more  pronounced  than 
in  any  other  condition.  It  depends  upon  venous  congestion,  or  upon 
the  admixture  of  arterial  with  venous  blood,  or  upon  both.  (See  section 
upon  Congenital  Heart  Lesions.) 


42  EXAMINATION  OF  THE  SKIN. 

The  cyanosis  which  is  caused  by  vasomotor  j^aralysis  depends  upon 
a  dilatation  of  the  small  vessels  (the  smallest  arteries,  capillaries  and 
smallest  veins).  It  differs  from  tlae  other  types  of  general  cyanosis  in 
a  lack  of  distention  of  the  larger  veins,  aud  in  the  peculiar  grayish- 
blue  color  of  the  entire  surface  of  the  body  without  the  localization  at 
certain  points  of  predilection,  which  is  so  characteristic  of  the  other 
forms.      (See  the  following  section.) 

Certain  poisons,  notably  antifebrin  and  nitrobenzol,  turn  the  blood  xery  dark  by 
changing  the  hemoglobin  into  methemoglobin.    This  is  not  a  true  cyanosis,  althougli 

the  body  surface  is  blue. 

Cyanosis  from  I^ocal  Causes. — Localized  areas  of  the  skin  may 
become  cyanotic  without  any  disturbance  of  the  general  circulatory  or 

respiratory  system.  Either  a  local  venous  congestion  from  compression 
or  thrombosis  of  large  or  small  veins,  or  else  some  vasomotor  disturb- 
ance, will  be  found  to  be  responsible.  Examples  of  the  latter  variety 
are  the  cyanosis  of  the  hands,  feet  and  ears  produced  by  the  local  action 
of  cold,  the  cyanosis  of  paralyzed  extremities,  of  the  hands  and  feet  of 
hysteric  individuals,  and  occasionally  of  perfectly  healthy  individuals. 
In  the  hysteric  cyanosis  is  frequently  combined  with  edema  (oedeme 
bleu  des  hysteriques). 

This  purely  vasomotor  cyanosis  evidently  depends  upon  a  degree  of  vascular 
dilatation  sufficient  to  produce  stagnation  fi-om  inadequate  vis  a  iergo.  The  process 
may  be  compared  to  a  running  stream  which,  from  the  lack  of  a  definite  river-bed, 
becomes  a  swamp.  One  might  think  that  such  a  dilatation  of  the  vascular  system, 
by  diminishing  the  resistance,  would  assist  the  current.  In  this  case,  however,  the 
current  would  not  flow  uniformly  over  so  wide  a  territory,  but  much  more  rapidly 
by  the  centrally  directed  paths,  while  practically  stagnant  at  the  borders.  The 
bright-scarlet  spots  which  the  writer  has  frequently  observed  scattered  through  the 
blue  of  vasomotor  cyanosis  furnish  a  jiroof  of  the  accuracy  of  this  theory'.  They 
correspond  to  areas  of  increased  capillary  current. 

A  cvanosis  of  similar  origin  appears  in  certain  inflammatory  processes.  When 
extreme  it  is,  of  course,  an  unfavorable  sign. 

Cyanosis  of  the  skin  is  naturally  associated  with  increased  loss  of  heat,  so  that 
cyanotic  parts  generally  feel  cold. 

ICTERIC  COLORATION  OF  THE  SKIN   (JAUNDICE). 

Icterus  is  the  peculiar  pathologic  yellow  discoloration  of  the  skin 
and  mucous  membranes,  caused  by  bile  pigment  or  some  of  its  deriva- 
tives. The  ordinary  form  (obstructive  icterus)  depends  upon  a  total  or 
a  partial  occlusion  of  the  bile  duct,  so  that  instead  of  being  emptied 
into  the  intestine,  some  or  all  of  the  bile  is  absorbed  and  stains  the 
various  tissues — e.  g.,  the  skin  and  the  mucous  membranes.  This  dis- 
coloration varies  in  tint  from  a  pale  lemon  yellow  to  a  dark  brown, 
olive  green  or  almost  black.  The  darker  shades  (melasicterus)  always 
signifv  an  obstruction  of  long  duration.  They  are  caused  either  by  a 
great  excess  of  pigment  accumulated  in  the  skin  or  by  a  transformation 
of  the  original  bile  pigment  to  darker  shades. 

Icterus  is  usually  first  noticed  in  the  conjunctiva  of  the  sclera  and 
upon  the  unexposed  body  parts,  which  are  covered  with  but  a  thin  layer 


COLOR   OF  THE  SKIN.  43 

of  epidermis  and  are  only  slightly  pigmented.  After  the  obstruction 
has  persisted  for  a  short  time  the  skin  of  the  face  and  the  mucous 
membrane  of  the  mouth  share  in  the  discoloration.  Pressure  of  the 
finger,  by  diminishing  the  amount  of  blood,  sometimes  makes  the  yellow 
of  a  mild  icterus  plainer.  Because  the  gums  are  normally  so  pale  they 
show  icterus  before  the  rest  of  the  mouth-lining.  Unless  very  intense, 
jaundice  cannot  be  appreciated  by  artificial  light. 

In  looking  for  icterus  we  generally  begin  by  examining  the  conjunctivae.  We 
should  remember  that  the  yellowish  color  of  the  subconjunctival  fat,  so  pro- 
nounced in  cachectic  individuals  and  in  drunkards,  is  sometimes  mistaken  for  icte- 
rus. The  distribution  of  this  fat  is  largely  hmited  to  the  neighborhood  of  the  folds 
in  the  mucous  membrane,  so  that  a  careful  examination  of  the  tightly  drawn  con- 
junctiva nearer  the  cornea  generally  prevents  a  mistake.  Pinyueculce,  j^eculiar 
formations  of  colloid  degenerated  connective  tissue  which  contain  yellow  pigment, 
are  situated  within  the  palpebral  folds  on  either  side  of  the  cornea.  They  may  be 
another  source  of  confusion. 

Certain  races  and  some  individuals  exhibit  a  yellowish  tint  of  skin,  which  a 
beginner  might  confuse  with  a  faint  jaundice ;  but  a  careful  examination  of  the 
conjunctiva  would  prevent  this  mistake. 

The  yellowish  discoloration  in  picric  acid  poisoning  can  be  easily  differentiated 
from  icterus  by  the  history,  etc.,  as  well  as  by  the  urinary  examination. 

Bile  pigment  occurs  in  the  urine  and  sweat  of  icteric  individuals.  Yellowish 
stains  upon  the  linen  sometimes  attract  a  patient' s  attention  before  he  has  observed 
the  yellow  color  of  his  skin.  The  saliva  is  for  the  most  part  unaffected.  The  feces 
become  pale  and  more  or  less  clay-colored  on  account  of  the  lack  of  bile.  The 
absorption  of  certain  biliary  salts  with  the  biliary  pigment  produces,  at  least  in 
fresh  cases,  a  slowing  of  the  pulse  and  considerable  itching  of  the  skin. 

Although  obstructive  jaundice  arises  most  frequently  from  a  catarrh 
of  the  biliary  passages,  it  may  depend  upon  serious  changes  in  the  liver 
itself — e.g.,  cirrhosis,  carcinoma,  abscess,  etc. 

Another  type  of  jaundice,  which  differs  from  the  obstructive  by  the 
fact  that  the  feces  are  unaffected  (i.  e.,  of  normal  color),  depends  upon 
very  imperfectly  understood  causes. 

Icterus  neonatorum  belongs  to  this  type.  The  old  idea  was  that  the  drying  up 
of  the  blood-current  in  the  umbilical  vein  after  birth  caused  a  sufficient  lowering 
of  the  pressure  in  the  portal  vein  to  enable  the  bile  pigment  to  pass  from  the  liver 
into  the  portal  vein.  Quincke^  and  Schreiber^  defend  Peter  Frank's  theory  of 
the  cause  of  jaundice  in  the  newborn.  Frank  argued  that  the  bilirubin  absorbed 
from  the  meconium,  instead  of  being  stored  up  in  the  liver  for  further  use,  escapes 
directly  into  the  general  circulation  by  way  of  the  ductus  venosus  arantii.  This 
duct  generally  remains  open  for  a  short  time  after  birth.  One  argument  in  favor 
of  this  theory  is  the  fact  that  icterus  neonatorum  occurs  most  frequently  in  prema- 
ture infants. 

The  cause  of  the  jaundice  which  is  not  infrequently  observed  in  infectious  dis- 
eases (pneumonia,  pyemia  and  yellow  fever)  is  not  perfectly  clear;  it  probably  de- 
pends upon  the  absorption  of  bile  pigment  from  the  liver.  It  has  been  claimed 
that  a  catarrh  of  the-  biliary  passages,  due  to  the  general  venous  congestion,  is 
responsible  for  the  jaundice  in  pneumonia,  but  microscopic  examinations  of  the 
liver  tissues  in  such  cases  have  shown  that  the  bile  ducts  were  normal.  Stag- 
nation and  reabsorption  of  bile  from  the  lack  of  the  usual  rhythmic  pressure 
exerted  by  the  diaphragm  upon  the  liver  has  been  cited  as  another  explanation 
of  the  icterus  in  pneumonia.      If  jaundice  occurred  only  with  pneumonia  which 

^Arch.f.  exper.  Path.,  vol.  xix.,  p.  34  et  seq.  ^Berlin,  klin.  Woch.,  1895,  No.  25. 


44  EXAMINATION  OF  THE  SKIN. 

involved  the  lower  right  lobe,  this  theory  might  seem  more  plausible.  Experience 
in  acute  yellow  atrophy  of  the  liver  has  shown  that  under  some  circumstances  a 
parenchymatous  degeneration  of  the  liver  without  any  biliary  obstruction  may  be 
the  cause  of  a  reabsorption  icterus,  so  that  it  does  not  seem  impossible  that  a  simi- 
lar process,  which  is  not  so  well  understood,  may  be  the  cause  of  the  icterus  in 
pneumonia,  pyemia  and  yellow  fever.  Liebermeister  created  an  expression  to  em- 
body this  idea  in  the  term  "acatectic"  icterus  {kutex^i-v,  to  hold  back)  or  diffusion 
icterus. 

The  term  hematogenous  icterus  was  formerly  applied  to  all  these  cases  of  obscure 
jaundice  as  well  as  to  that  found  after  jjoisoning  by  ether,  chloral,  chloroform, 
potassium  chlorate,  arsenious  acid  or  toluylendiamin.  It  was  assumed  that  the 
biliary  or  other  pigment  was  formed  in  the  circulatory  system  from  the  coloring- 
matter  of  the  blood,  more  especially  because  most  of  these  poisons  are  capable  of 
destroying  the  red  corpuscles.  More  accurate  experiments  in  the  poisoning  of 
arsenious  acid  and  toluylendiamin  have  proved  that  the  yellow  pigment  is  formed 
from  an  alteration  of  the  hemoglobin  of  the  red  corpuscles  into  bile  pigment;  but 
within  the  liver,  not  in  the  blood  itself.  This  excessive  accumulation  of  biliary 
pigment  can  be  demonstrated  microscopically  in  the  capillary  bile  ducts,  and  a  part 
of  it  is  absorbed.  Again,  it  was  shown  that  in  some  cases  of  poisoning  the  destruc- 
tion of  red  corpuscles  was  so  extensive  that  the  liver  was  incapable  of  altering  all 
the  hemoglobin  to  bile  pigment,  so  that  a  part  of  it  had  to  be  eliminated  as  such 
in  the  urine.  These  results  explain  the  connection  so  frequently  observed  between 
icterus  and  other  cases  of  hemoglobinuria.  It  is  therefore  advisable  to  distinguish 
from  the  diffusion  icterus  just  described  all  these  cases  of  hematoheptogenous  or 
pleiochromic  icterus,  and  to  include  under  the  latter  term  only  those  in  which  we 
can  demonstrate  a  destruction  of  the  red  corpuscles,  or  a  hemoglobinuria. 

This  modern  conception  of  hematoheptogenous  jaundice  has  obviated  the  neces- 
sity w^hich  formerly  existed  of  distinguishing  between  hematogenous  and  heptoge- 
nous  jaundice  by  the  presence  of  biliary  acids  in  the  latter  and  their  absence  in  the 
former.  Such  a  distinction  was,  however,  unnecessary,  because  cases  of  obstructive 
jaundice  sometimes  present  no  biliarj'  acids  in  the  urine,  and,  conversely,  biliary 
acids  are  sometimes  found  in  perfectly  healthy  individuals. 

So  far  we  have  assumed  that  the  pigmentation  which  occasions 
jaundice  is  real  bile  pigment — i.  e.,  bilirubin.  In  most  cases  this  sup- 
position is  correct,  for  bilirubin  can  be  demonstrated  in  the  urine. 
But  there  are  numerous  other  cases  in  which  only  urobilin  (hydrobili- 
rubin)  can  be  found.  The  latter  have  been  designated  as  urobilin  icterus 
— i.  e.,  icterus  due  to  the  deposition  of  the  urobilin  in  the  skin.  But  it 
is  probable  that  such  an  assumption  is  unnecessary,  and  that  as  a  matter 
of  fact  the  urobilin  excreted  in  the  urine  is  derived  from  bilirubin  in 
the  tissues :  for,  in  the  first  place,  urobilin  possesses  a  very  much 
slighter  coloring  power  than  bilirubin  ;  in  the  second  place,  the  serum 
in  cases  of  urobilin  icterus  contains  bilirubin  ;  in  the  third  place,  a  con- 
siderable amount  of  urobilin  may  be  found  in  the  urine  of  a  healthy 
person  who  does  not  show  a  trace  of  jaundice ;  and,  finally,  Leube  has 
demonstrated  bilirubin  in  the  sweat  of  patients  with  so-called  urobilin 
icterus.  The  term  should  therefore  be  limited  to  cases  in  which  urobilin 
alone  is  excreted  in  the  urine,  whereas  the  supposition  that  any  yellow- 
ish discoloration  of  the  skin  can  arise  from  urobilin  is  probably  erro- 
neous. Such  a  type  of  icterus  is  generally  of  a  very  mild  grade.  It 
is  observed  especially  in  cirrhosis  of  the  liver  and  in  the  early  stages  of 
ordinary  jaundice. 


COLOR   OF  THE  SKIN.  45 

ABNORMAL  PIGMENTATION   OF   THE  SKIN. 

Pigmentation  of  the  skin,  as  is  well  known,  varies  a  great  deal 
within  physiologic  limits.  It  is  most  pronounced  in  brunets,  and  more 
marked  upon  the  exposed  body  parts  of  anyone — e.  g.,  face  and  hands, 
as  well  as  about  the  genitals  and  the  anus,  in  the  axillae,  on  the  nipples, 
and  in  the  linea  alba.  During  pregnancy  the  pigmentation  is  generally 
markedly  increased  about  the  areolae  of  the  nipples  and  in  the  linea 
alba,  and,  besides,  areas  of  irregular  mottling  may  appear  upon  the  face 
or  other  body  parts — the  so-called  "chloasma  uterinum"  (chloasma 
gravidarum,  masque  des  femmes  enceintes). 

Ephelides  or  freoMes  can  scarcely  be  called  pathologic  pigmentation. 
Their  distribution  upon  the  face  and  hands,  especially  in  blonds,  and 
their  frequent  disappearance  during  the  winter,  is  well  known  to  every- 
one. 

Itching  cutaneous  diseases  often  leave  behind  a  permanent  pigmenta- 
tion, due  to  the  scratching.  The  characteristic  arrangement  of  this 
pigmentation  in  streaks,  as  well  as  the  history,  always  points  to  its 
origin.  It  is  often  decidedly  marked  between  the  shoulder  blades  in 
individuals  who  have  suffered  from  body  lice,  because  these  insects  seem 
to  have  a  preference  for  the  folds  of  the  shirt  in  this  region.  The  so- 
called  "vagabonds'  disease/'  sometimes  presenting  a  very  dark-brown 
color  (due  to  serious  and  persistent  investment  with  all  sorts  of  vermin 
and  constant  scratching,  as  well  as  partially  to  accumulation  of  dirt), 
might  in  rare  instances  be  confused  with  Addison's  disease. 

Melanosarcoma,  and  especially  melanosarcomatosis,  is  accompanied  by 
a  diffuse  gray  to  black  discoloration  of  the  skin,  and  by  the  excretion 
of  melanin  in  the  urine.      (See  Examination  of  the  Urine.) 

Pulmoiuiry  tuberculosis  is  sometimes  associated  with  a  decided 
brownish  coloration  of  the  face  or  of  the  entire  body.  Measles  occa- 
sionally leaves  behind  traces  of  its  existence,  in  the  shape  of  brownish 
pigmented  spots,  whose  form  and  arrangement  are  sufficiently  characteris- 
tic for  recognition.  3Iustard  plasters,  blisters,  JBaunscheidtismus,  produce 
a  localized  pigmentation  which  is  sometimes  permanent. 

Morbus  Addisoni  causes  a  smoky-gray  to  a  bronze  discoloration  of 
the  skin,  which  is  the  most  important  diagnostic  symptom.  Other 
associated  symptoms  are  :  well-marked  digestive  disorders — e.  g.,  dys- 
pepsia, vomiting,  diarrhea  ;  certain  nervous  symptoms  ;  and  a  gradually 
increasing  cachexia.  The  pigmentation  usually  appears  first  upon  areas 
where  the  pigment  of  the  skin  is  normally  intensified,  such  as  the  face, 
hands,  axillae,  etc.,  also  wherever  there  is  any  friction  upon  the  skin, 
such  as  the  waist-line  or  around  the  neck.  At  first  a  pale  smoky  gray, 
the  discoloration  deepens  to  a  bronze  brown,  resembling  the  color  of  a 
mulatto,  and  tiny  spots  of  an  intense  brown  or  even  black  color  are  ob- 
served scattered  over  this  uniformly  brown  background.  The  mucous 
membranes  are  involved  as  well  as  the  skin,  and  although  not  so  com- 
monly observed  in  the  conjunctivae,  a  few  grayish  j^atches  upon  the  buccal 
membrane,  especially  just  inside  the  lips  and  cheeks,  are  rather 
characteristic  of  Addison's  disease.     In  well-marked  examples  of  this 


46  EXAMINATION  OF  TEE  SKIN. 

disease  the  only  parts  exempt  from  pigmentation  are  the  palms  of  the 
hands,  the  soles  of  the  feet,  and  the  nails.  To  distinguish  this  affection 
from  melasicterus,  the  urine  should  be  tested  for  bile  pigment ;  it  is  in- 
variably present  in  the  latter.  The  mucous  membranes  of  the  mouth 
should  also  be  examined  for  pigmentation  spots ;  they  are  commonly 
present  in  the  former.  The  patient's  history  and  his  general  condition 
will  clinch  the  diagnosis.  The  pigmentation  which  is  occasionally 
observed  in  pulmonary  tuberculosis  may  be  a  source  of  error,  especially 
since  patients  afflicted  with  Addison's  disease  often  suffer  from  pulmo- 
nary tuberculosis  as  well.  The  selection  of  the  mucous  membranes,  the 
progressive  nature  of  the  pigmentation,  as  well  as  the  entire  symptom- 
complex  in  morbus  Addisoni,  usually  facilitate  a  distinction. 

It  is  well  to  caution  the  reader  that,  although  this  pigmentation  of  the  mucous 
membranes  is  one  of  the  most  characteristic  signs  in  morbus  Addisoni,  an  identical 
appearance  is  sometimes  observed  in  perfectly  healthy  indi^■iduals. 

Hepatic  cirrhosis  and  some  of  the  other  liver  diseases  occasionally 
exhibit  a  peculiar  brownish  discoloration  of  the  skin,  which  differs  from 
icterus  in  being  rather  more  of  a  dirty -gray  shade  and  somewhat  spotted 
in  arrangement.  The  absence  of  bile  pigment  in  the  urine  and  of  a 
yellowish  tinge  in  the  conjunctivae  will  prevent  any  mistake.  The  cause 
of  this  pigmentation  is  as  yet  undetermined,  but  since  the  description  of 
bronzed  diabetes  its  occurrence  has  acquired  a  certain  importance.  Dia- 
bete  bronzee,  first  described  by  the  French,  presents  a  combination  of 
diabetes,  hepatic  cirrhosis,  and  pigmentation  of  the  skin.  In  the  cases 
observed  by  the  author  there  was  no  pigmentation  of  the  mucous  mem- 
branes, nor  any  of  the  intense  brownish-black  spots  of  pigment  so  char- 
acteristic of  Addison's  disease.  The  presence  of  sugar  in  the  urine,  the 
demonstration  of  cirrhosis  of  the  liver  without  icterus,  and  the  lack  of 
the  characteristic  symptom-complex  of  Addison's  disease  will  ordinarily 
very  readily  determine  a  diagnosis. 

The  continued  administration  of  silver  or  arsenic  preparations  is 
sometimes  responsible  for  a  dark  pigmentation  of  the  skin.  Argyria 
depends  upon  the  deposition  of  metallic  silver,  not  only  in  the  internal 
organs,  but  also  in  the  skin  and  mucous  membranes.  It  may  look  like 
Addison's  disease,  but  is  not  associated  with  any  symptoms  of  illness. 
Besides,  the  nails  are  discolored  as  well  as  the  rest  of  the  integument. 
To-day  silver  nitrate  is  employed  so  little  in  the  therapy  of  nervous 
diseases  that  this  form  of  pigmentation  is  of  very  rare  occurrence. 
Arsenic  melanosis  is  very  much  more  difficult  to  distinguish  from  Addi- 
son's disease,  for  the  small  dark  spots  scattered  about  in  the  diffuse 
pigmentation,  the  involvement  of  the  mucous  membranes  of  the  mouth, 
and,  in  fact,  all  the  peculiarities  of  Addison's  disease  have  been  observed 
to  follow  the  persistent  use  of  arsenic.  The  pigmentation  itself  seems  to 
be  derived  from  the  blood-coloring  matter.  A  further  difficulty  in  dif- 
ferential diagnosis  depends  upon  the  fact  that  the  arsenic  has  generally 
been  employed  for  some  cachectic  condition — e.  g.,  pernicious  anemia — 
so  that  the  accompanying  history  will  not  always  solve  the  difficulty.  If 
the  pigmentation  diminishes  after  the  arsenic  has  been  stopped,  as  in  a 


MOISTURE  OF  THE  SKIN;  SWEAT  EXCRETION.  47 

case  observed  by  the  author,  the  diagnosis  could  be  made  with  proba- 
bility. We  must  acknowledge,  however,  that  even  very  small  doses  of 
arsenic  sometimes  cause  arsenic  melanosis,  and  that  stopping  the  drug 
does  not  always  diminish  the  pigmentation. 

The  reader  is  referred  to  text-books  upon  skin  diseases  for  the 
consideration  of  the  numerous  cutaneous  affections  accompanied  by  pig- 
mentation— e.g.,  nevus  jAgmentosus,  lentigo,  albinismus  partialis  and 
universalis,  vitiligo  and  jjoliosis. 

MOISTURE  OF  THE  SKIN;    SWEAT  EXCRETION. 

An  abnormally  dry  skin  will  be  observed  in  any  condition  where 
the  amount  of  water  absorbed  by  the  digestive  organs  is  limited,  or 
where  a  large  amount  of  water  is  removed  from  the  body  in  some  other 
way  than  by  means  of  the  sweat  glands — e.  g.,  profuse  diarrhea,  excessive 
vomiting,  digestive  diseases  with  diminished  absorption,  diabetes  melli- 
tus  and  insipidus,  chronic  nephritis  with  polyuria,  marked  edema  of 


Fig.  13. — Crystals  of  nitrate  and  oxalate  of  urea  obtained  from  deposits  upon  the  skin 

(after  Leube). 

the  skin,  etc.  An  increased  production  of  sweat  is  observed  in  certain 
fevers,  especially  in  acute  articular  rheumatism,  acute  nephritis,  and 
epidemic  sudamina. 

The  excretion  of  sweat  is  one  of  nature's  methods  of  cooling  the 
body,  both  under  physiologic  and  under  pathologic  conditions.  When 
the  temperature  in  any  febrile  affection  drops  rapidly,  whether  spontane- 
ously or  under  the  influence  of  drugs,  a  profuse  sweat  usually  accompa- 
nies the  fall — e.  g.,  at  the  crisis  of  pneumonia,  at  the  drop  of  temperature 
in  malaria,  arid  during  the  third  week  of  typhoid  fever,  when  the  tem- 
perature begins  to  remit.  The  hectic  sweats  of  phthisis,  which  are  so 
annoying  and  prognostically  serious,  coincide  with  the  fall  of  temperature. 
They  usually  occur  at  night  or  in  the  early  morning.  In  some  patients, 
to  be  sure,  they  are  independent  of  any  fever  and,  just  as  is  the  increased 
pulse-rate,  are  merely  a  symptom  of  tuberculous  intoxication.  They 
are  generally  associated  with  a  sense  of  considerable  weakness,  probably 
connected  with  the  vascular  relaxation  from  the  loss  of  water,  for  copi- 
ous draughts  of  water  sometimes  counteract  it. 

We  may  mention  the  sweating  produced  by  pilocarpin,  by  ammonium  acetate, 
and  by  most  antipyretic  measures,  by  hot  baths  and  hot  drinks.  Salvia,  atropin, 
agaricin,  camphoric  acid  and  sulphonal  check  the  sweat  secretion. 


48  EXAMINATION  OF  THE  SKIN. 

In  certain  types  of  nephritis,  interference  in  renal  activity  is  asso- 
ciated with  an  increased  production  of  sweat,  and  sometimes  with  the 
deposition  of  crystalline  scales  of  urea  upon  the  skin  (Fig.  13),  par- 
ticularly of  the  face.  To  recognize  these  crystals,  the  deposit  should 
be  scraped  oif  upon  a  glass  slide,  dissolved  in  dilute  nitric  or  oxalic 
acid,  and  then  allowed  to  evaporate.  Crystals  of  sodium  chlorid  are 
often  found  instead  of  urea.  As  a  general  rule,  especially  with  much 
edema,  nephritis  cases  are  associated  with  a  diminution  in  the  sweat 
production. 

The  sweat  in  jaundice  may  be  colored  yellow.  In  other  conditions  different 
colors  have  been  noted,  although  not  explained  (chromidrosis).  Blue  sweat  has 
been  described,  and  is  probably  due  to  the  gro'n'th  of  the  Bacillus  pyocyaneus  in 
the  skin.  Naturally,  variously  colored  underclothes  may  be  a  cause  of  coloring  the 
sweat,  especially  since  the  use  of  anilin  dyes  has  become  so  universal.  Bloody  sweat 
(hemidrosis)  is  exceedingly  rare,  though  it  has  undoubtedly  been  observed. 

SWELLING  AND  EDEMA  OF  THE  CUTANEOUS  AND 
SUBCUTANEOUS  TISSUES. 

Swelling  or  turgidity  of  the  skin  depends  upon  an  increase  in  the 
amount  of  fluid  contained  in  its  tissue — i.  e.,  of  the  blood  and  lymph. 
Increased  turgidity  accompanies  plethora,  fever,  and  all  conditions  asso- 
ciated with  an  increased  supj)ly  of  blood  to  the  skin,  or  with  circulatory 
excitement.  Diminished  turgidity  accompanies  all  conditions  associated 
with  a  diminished  amount  of  fluid  in  the  skin — e.  g.,  cachexia,  and 
an  impoverishment  of  general  watery  elements  of  the  body.  Increased 
turgidity  presents  an  increased  fulness,  a  rounded  outline  of  the  surface  ; 
it  obliterates  the  lines,  especially  of  the  face,  and  is  generally  combined 
with  a  deepening  of  the  fleshy  tint.  Diminished  turgidity  is  character- 
ized by  sharper  outlines  of  the  parts  and  by  a  pallor.  With  the  poverty 
in  fluid  the  skin  loses  some  of  its  elasticity,  and  the  wrinkles  and  lines 
of  the  face  are  emphasized. 

Anasarca,  general  dropsy  or  edema  of  the  skin,  means  the  pathologic 
increase  of  fluid  in  the  lymph  spaces  and  subcutaneous  tissues.  The 
difference  between  edema  and  turgidity  is  one  of  degree.  Despite  the 
increase  of  fluid,  the  elasticity  of  the  skin  is  diminished  in  edema, 
as  is  evidenced  not  by  the  wrinkles,  but  by  the  so-called  pitting  of  the 
skin  to  pressure. 

Edema  always  indicates  an  obstruction  to  the  flow  of  lymph,  vrith 
some  lack  of  proportion  between  its  influx  and  exit,  so  that  an  equi- 
librium is  obtained  only  after  the  high  pressure  has  distended  the 
meshes  of  the  tissues. 

ALTERATIONS  IN  THE  CXJTANEOUS  TURGIDITY  OF  THE  SKIN. 
Almost  all  the  appearances  which  the  laity,  or  we  as  physicians,  desig- 
nate by  the  terms  "run  down,"  "worn  out,"  etc.,  depend  upon  altera- 
tions in  the  turgidity  of  the  skin.  Worry,  excessive  fatigue,  fever, 
collapse,  exophthalmic  goiter,  all  these,  which  mar  the  beauty  of  a  face, 
depend  upon  alterations  in  the  turgidity  of  the  skin.     In  emaciation, 


CUTANEOUS  AND  SUBCUTANEOUS  TISSUES.  49 

pallor,  cyanosis,  edema,  there  is  more  than  turgidity  responsible  for  the 
appearances.  Diminution  in  turgidity  plus  depression  of  the  mimic 
faculty  is  responsible  for  the  characteristic  facial  expressions  of  the 
moribund,  and  for  the  so-called  fades  Hippocratica  accompanying  intes- 
tinal obstruction,  peritonitis,  cholera,  etc.  In  the  latter  the  features 
seem  sunken  ;  the  wrinkles  and  lines  of  the  face  more  pronounced ;  the 
nose  sharp ;  the  eyes  fallen  deep  into  their  sockets ;  the  skin  is  cool, 
even  cold,  and  damp  with  cold  sweat ;  while  the  color  is  pale  and  dusky 
with  cyanosis.  In  diminished  turgidity  the  wrinkles  are  very  plainly 
marked  on  the  trunk,  especially  in  cholera  morbus  or  "cholera  infantum,'* 
where  the  organism  has  been  deprived  of  so  much  water.  Oftentimes 
in  cachexia,  where  the  subcutaneous  fat  is  also  diminished,  the  wrinkles 
become  even  more  marked.  A  certain  grade  of  diminished  turgidity 
is  a  physiologic  accompaniment  of  advanced  age  and  senility. 

EDEMA. 

Edema  presents  a  plump  swelling,  and  a  tense,  shiny  appearance  of 
the  surface  of  the  skin  ;  it  obliterates  the  wrinkles,  the  hollows,  and  the 
normal  bony  prominences.  When  the  edema  suddenly  disappears,  the 
epidermis  exhibits  fine  lines  and  creases  and  perhaps  scales  off.  When 
quite  fresh,  edema  often  imparts  an  increased  transparency  to  the  skin. 
Over  certain  regions,  especially  the  thighs  and  abdomen,  transparent 
lines  or  streaks  may  appear,  following  the  grain  of  the  skin  and  resem- 
bling striae  gravidarum.  These  lines  may  remain  permanently,  even 
after  the  disappearance  of  the  edema.  They  are  due  to  a  stretching 
and  distention  of  the  connective  tissues  and  lymph  spaces.  Very  pro- 
nounced edema,  especially  over  areas  exposed  to  considerable  mechani- 
cal irritation,  may  be  associated  with  the  formation  of  blebs  and  blisters 
in  the  external  layers  of  the  epidermis.  If  these  burst  or  are  opened 
artificially  a  thin  fluid  will  ooze  from  microscopic  openings  of  the  inner 
surface,  sometimes  persisting  quite  indefinitely.  As  is  natural,  the 
danger  of  infecting  these  tiny  lacerations  is  considerable,  and,  of  course, 
serious. 

Edematous  skin  is  usually  pale  because  the  blood-vessels  are  com- 
pressed by  the  pressure  of  the  lymph,  and  the  same  amount  of  blood 
must  be  spread  over  a  greater  area.  Inflammatory  edema  and  edema 
associated  with  cyanosis  are  exceptions  to  this  rule. 

Pitting  of  the  skin  is  quite  essential  for  the  diagnosis  of  edema.  It 
is  due  to  a  loss  of  the  cutaneous  elasticity,  from  the  distention  of  the 
meshes  of  the  tissues  by  the  lymph.  Where  the  skin  is  very  elastic  and 
easily  stretched,  as  on  the  face  or  prepuce,  the  imprint  of  the  finger  may 
vanish  almost  immediately.  Children's  skin  is  so  much  more  elastic 
than  adults'  that,  even  over  other  parts,  pitting  may  sometimes  be 
wanting.  Again,  brawny  edema  which  has  persisted  for  some  time  may 
pit  with  difficulty,  because  there  is  a  certain  amount  of  connective-tissue 
growth.  We  notice  this  particularly  in  inflammatory  edema  and  in  the 
chronic  edema  of  the  lower  extremities,  which  is  sometimes  converted 
to  elephantiasis. 


50  EXAMINATIOX  OF  THE  SKIN. 

Edema  may  be  classified  etiologically  into  four  varieties  : 

1.  Edema  from  venous  obstruction,  where  it  mav  be  combined  'with, 
other  transudations,  especially  into  the  serous  cavities. 

2.  Edema  from  hydremic  plethora,  where  hydrops  may  be  present 
elsewhere. 

3.  Edema  from  inflammation. 

4.  Edema  from  angioneurotic  disturbances. 

Obstructive  Bdema,  or  Bdema  from  Congestion. — It  is 
by  no  means  clear  whether  the  decisive  factor  in  producing  this  type  of 
edema  is  a  diminished  power  of  lymph  absorption  upon  the  part  of  the 
beginning  veinules,  due  to  an  excess  of  pressure  in  the  veins  [e.  g.,  local 
congestion),  or  whether  it  is  an  excessive  formation  of  lymph,  due 
to  an  increased  capillary  pressure.  In  any  general  circulatory  conges- 
tion we  must  also  take  into  account  the  obstruction  in  the  lymphatic 
circulation  occasioned  by  the  back  pressure  in  the  large  lymphatic  ducts 
which  empty  into  venous  trunks.  The  relations  between  these  differ- 
ent factors  in  obstructive  edema,  and  the  influence  of  prolonged  impair- 
ment of  the  vessel-walls  by  the  disturbed  circulation,  merit  further 
research. 

Any  affection  of  the  heart  or  of  the  lungs  which  will  produce  cyan- 
osis from  congestion  may  also  produce  obstructive  edema  (see  p.  41). 
The  edema  begins  and  becomes  most  intense  in  the  body  parts  most 
remote  from  the  heart  and  most  influenced  by  gravity — e.  g.,  the  hands, 
the  feet,  and,  in  the  recumbent  posture,  the  loins.  It  only  appears  very 
late  in  the  face  except  under  some  conditions,  not  very  well  understood, 
which  probably  depend  upon  vasomotor  phenomena.  The  influence  of 
gravity  upon  the  distribution  of  the  edema  becomes  very  evident  with 
change  of  posture — e.  g.,  ambulatory  patients  will  suffer  from  edematous 
feet ;  but  upon  going  to  bed  the  edema  soon  disappears  from  the  extremi- 
ties and  appears  in  the  region  of  the  loins.  Lying  upon  one  side  for  a 
considerable  time  will  distribute  the  edema  to  that  side  of  the  body,  and, 
if  a  hydrothorax  be  present,  will  make  it  more  marked  upon  that  side. 
When  the  obstruction  is  local  the  edema  will,  of  course,  be  confined  to  the 
region  supplied  by  the  obstructed  veins. 

A  fluid  exudation  in  the  abdominal  cavity,  due  to  portal  obstruc- 
tion (cirrhosis,  thrombosis)  or  to  a  chronic  affection  of  the  peritoneum 
(tuberculosis),  will  sometimes  compress  the  vena  cava  inferior  or  the 
common  iliac  veins,  and  so  give  rise  to  an  edema  of  the  lower  extremi- 
ties. To  decide  the  true  nature  of  this  symptom-complex  is  often  very 
difficult,  for  both  ascites  and  edema  of  the  lower  extremities  may  be 
co-ordinated  sequences  of  some  general  obstruction  located  in  the  thorax. 
The  onset  will  sometimes  permit  a  differentiation.  If  the  abdomen 
swelled  before  the  legs,  the  cause  will  undoubtedly  be  one  of  the  above- 
mentioned  affections  of  the  abdominal  cavity  ;  if  the  legs  swelled  before 
the  abdomen,  the  cause  will  undoubtedly  be  some  general  circulatory 
disturbance. 

Hydremic  l^dema. — Magnus'  experimental  researches  ^  indicate 

^Arch.f.  exper.  Path.,  vol  xlii.,  1899. 


PLATE  U 


Haygarth's  nodosities.    Case  of  arthritis  deformans  (Dr.  J.  M.  Jackson,  Massacliusetts  General 

Hospital). 


Heberden's  nodes  in  artliritis  deformans  (New  York  City  Hospital). 


Heberden's  nodes  and  ulnar  deformity.    Case  of  arthritis  deformans  (New  York  City  Hospital). 


CUTANEOUS  AND  SUBCUTANEOUS  TISSUES.  51 

that  hydremic  plethora — i.  e.,  an  increased  volume  of  the  blood  due  to 
retention  of  its  water — may  be  the  cause  (although  not  the  only  one)  of 
edema  and  of  other  transudations  if  the  vessel-walls  are  coincidently 
damaged.  This  latter  condition  occurs  in  renal  disease  from  the  reten- 
tion of  the  urinary  solids.  In  this  sense  much  of  the  edema  of  renal 
affections,  and  the  edema  occurring  in  chronic  wasting  diseases,  and  in 
the  anemias  of  the  most  variable  type  are  all  to  be  attributed  to  hydremic 
plethora  from  retention  of  water.  Nevertheless,  circulatory  disturbances 
are  so  often  combined  with  these  diseases  that  the  edema  must  then 
depend  partly  upon  the  resulting  venous  congestion  as  well  as  upon  the 
hydremic  plethora  and  the  injury  to  the  vessels.  As  a  result  of  experi- 
mental investigations  we  may  say  that  pure  hydremia — i.  e.,  a  watery 
blood  without  any  increase  in  its  volume  or  without  injury  to  the  vessel- 
walls — does  not  cause  edema. 

Hydremic  plethoric  edema,  as  contrasted  with  the  variety  due 
to  congestion,  is  practically  independent  of  the  influence  of  gravity  and 
of  the  distance  of  the  affected  part  from  the  heart.  Its  location  seems  to 
depend  upon  some  peculiar  arrangement  of  the  lymphatics  in  the  different 
parts  of  the  body.  Nephritic  edema  (in  acute  and  subacute  nephritis) 
is  a  typical  example  of  this  selective  action,  appearing  generally  in  the 
face,  and  especially  about  the  eyelids.  Edema  localized  in  this  way  is 
very  suggestive  of  the  diagnosis  of  nephritis.  The  more  chronic  types 
of  nephritis  (contracted  kidney),  however,  rarely  exhibit  any  edema  until 
quite  late  in  the  disease,  and  then  it  usually  begins  in  the  feet,  because 
the  hypertrophied  heart,  unable  to  maintain  the  circulation  against  the 
obstacles  in  the  kidneys  and  at  the  periphery,  begins  to  flag.  In  other 
words,  in  these  very  chronic  cases  of  nephritis  dropsy  is  generally  of 
cardiac  origin. 

The  absence  of  cyanosis  is  another  characteristic  of  purely  hydremic 
edema. 

Purely  hydremic  plethoric  edema  is  generally  very  rare  except  in 
acute  and  subchronic  cases  of  nephritis.  Almost  all  cachectic  conditions, 
such  as  grave  anemia  and  carcinoma,  frequently  exhibit  a  swelling  about 
the  ankles  as  the  first  sign  of  a  disturbance  in  the  circulation,  so  that, 
despite  the  common  impression  that  it  is  due  to  water  retention,  the 
edema  is  not  purely  hydremic,  but  of  a  mixed  type. 

Inflammatory  Hdema. — From  the  diagnostic  point  of  view,  the 
only  importance  inflammatory  edema  has  is  in  pointing  to  some  deep- 
seated  inflammation.  It  must  be  attributed  to  the  saturation  of  the 
neighborhood  of  an  inflammatory  area  with  the  fluid  components  of  the 
exudation  (Samuel). 

It  is  of  more  interest  to  the  surgeon  than  to  the  clinician.  Although  so  rarely 
present,  it  is  important  in  suggesting  the  purulent  nature  of  an  underlying  pleuritic 
effusion.  In  acute  articular  rheumatism  the  inflammatory  edema  about  the  joints 
is  quite  as  important  as  the  effusion  in  the  joint  itself.  Inflammatory  edema  may 
aid  the  surgeon  in  recognizing  a  deep  suppuration,  as  in  purulent  perforative  ap- 
pendicitis, liver  abscess,  etc.  Here  it  would  depend  upon  adhesions  which  connect 
the  inflammatory  focus  with  the  skin. 


52  EXAMINATION  OF  THE  SKIN. 

Angioneurotic  Bdema. — Under  this  heading  are  included  certain 
rare  types  of  edema  of  the  face  or  of  other  areas  of  the  skin.  Some  of 
them  are  combined  with  analogous  conditions  in  the  mucous  membranes 
(laryngeal,  bronchial,  gastric  or  intestinal).  Apparently  idiopathic,  we 
have  as  yet  no  clear  notion  of  the  mechanism  of  their  origin,  except 
that  they  appear  and  disappear  suddenly,  and  are,  therefore,  credited 
with  a  dependence  upon  the  nerves  of  the  vessels. 

A  similar  conception  is  held  of  the  edema  observed  in  nervous  affec- 
tions— e.g.,  the  edema  in  polyneuritis  and  the  localized  edema  in  urticaria. 
The  latter  consists  in  the  formation  of  rapidly  appearing  wheals.  (See 
Examination  of  the  Nerves.)  The  blue  edema  of  the  hysteric  is  usually 
included  under  angioneurotic  edema  (see  p.  42). 

It  is  difficult  to  classify  the  general  edema  which  occurs  without 
nephritis  in  certain  infectious  diseases,  especially  in  scarlet  fever  and 
diphtheria,  as  well  as  that  appearing  after  the  injection  of  diphtheric 
antitoxin,  and  that  after  the  employment  of  potassium  iodid. 

EMPHYSEMA  OF  THE  SKIN. 

This  is  due  to  the  presence  of  gas  (generally  air)  in  the  meshes  of 
the  subcutaneous  tissues.  Upon  mere  inspection,  emphysema  of  the 
skin  resembles  edema.  Palpation,  however,  over  emphysematous  regions 
produces  a  peculiar  crackling,  audible  as  well  as  palpable.  It  is  due  to 
the  movement  of  bubbles  of  air  in  the  tissues.  Percussion  elicits  a 
tympanitic  note.      (See  Percussion.) 

In  very  rare  instances  the  gas  is  developed  in  the  skin  by  the  activity 
of  gas-producing  bacteria — e.  g.,  in  glanders  and  in  malignant  edema. 
In  most  cases  air  j^enetrates  the  subcutaneous  tissues  from  the  rupture  of 
some  air-containing  organs  or  from  some  external  wound.  The  most 
frequent  source  is  through  the  mediastinal  connective  tissue,  resulting 
from  an  ulcerative  destruction  of  the  esophageal  wall  (carcinoma)  or 
from  a  rupture  of  the  pulmonary  alveoli  (following  coughing  or  exter- 
nal trauma).  The  emphysema  will  then  be  first  noted  at  the  lower  part 
of  the  neck  or  over  the  manubrium.  In  a  patient  with  a  tracheotomy 
wound,  air  may  be  forced  under  the  skin  by  a  fit  of  coughing.  The 
chief  diagnostic  significance  of  cutaneous  emphysema  is  its  dependence 
upon  the  rupture  of  some  air-containing  viscus.  If  the  source  persists, 
the  entire  body  surface  may  be  swollen  ;  but  ordinarily  the  air  is  readily 
absorbed  and  the  cutaneous  emphysema  disappears. 

CUTANEOUS   HEMORRHAGES. 

Hemorrhages  into  the  skin  appear  as  spots  of  variable  size,  at  first 
red,  later  violet  to  black,  gradually  changing  to  green  and  yellow,  and 
finally  disappearing.  These  changes  in  color  are  due  to  the  alterations 
in  the  blood-pigment.  In  contrast  to  hyperemic  spots,  cutaneous  hemor- 
rhages do  not  disappear  under  pressure.  They  are  not  usually  elevated 
except  in  certain  types  of  purpura,  where  the  epidermis  may  be  raised 
like  a  bleb.     Absorption  of  the  hemorrhagic  spots  usually  begins  in  the 


C  UTA  NEO  US  HEM  ORBHA  G  ES. 


53 


center.  When  small,  pin-point  in  size,  they  are  called  ecchymoses  or 
petechise. 

Cutaneous  hemorrhages  occur  : 

1.  From  trauma  (ordinary  black-and-blue  spots).  The  ecchymoses 
caused  hj  flea  bites  (purpura  pulicosa)  belong  to  this  group  and  may  be 
mistaken  for  a  form  of  ]>urpura.  They  are,  however,  unlike  purpura, 
found  most  abundantly  upon  the  trunk.  They  frequently  exhibit  the 
bite-mark  as  a  dark  spot  in  the  center  of  the  hemorrhage,  and  when 


Fig.  14.— Emphysema  of  left  breast  and  chest-wall,  due  to  broken  ribs  (Massachusetts 
General  Hospital). 


fresh  they  are  surrounded  by  a  hyperemic  zone,  the  color  of  which  will 
disappear  upon  pressure. 

2.  Spontaneously  in  all  severe  cachexias  and  infections  which  are 
associated  with  a  hemorrhagic  diathesis  ;  particularly  as  a  characteristic 
symptom  in  the  various  types  of  purpura,  in  grave  anemias,  especially 
in  pernicious  anemia,  leukemia  and  scurvy,  in  acute  yellow  atrophy  of  the 
liver,  in  phosphorus-poisoning,  in  ulcerative  endocarditis,  in  pyemia,  and 
in  the  terminal  stages  of  certain  cases  of  jmlmonary  tid:>erculosis. 

3.  In  the  hemorrhagic  forms  of  the  ac^ide  exanthemata, :  scarlet 
fever,  measles,  small-pox.    These  are  notoriously  more  serious  and  critical 


54 


EXAMINATION   OF  THE  SKIN. 


than  the  ordinary  types,  especially  in  "  black  small-pox/'  where  the 
hemorrhage  occurs  in  the  interior  of  the  pustules ;  and  still  more  so  in 
that  rare,  very  fatal  form,  "  purpura  variolosa,"  where  extensive  cuta- 
neous hemorrhages  occur  without  the  formation  of  any  rash.  But  there 
are  some  cases  of  measles  and  scarlet  fever  which  are  not  much  more 
serious  than  the  ordinary  cases,  although  they  are  shown  to  be  hemor- 
rhagic, by  the  fact  that  the  coloration  of  the  rash  does  not  entirely 


Fig.  15.— Purpura  (New  York  City  Hospital). 

disappear  upon  pressure,  and  that  even  into  the  convalescence  slight 
remains  of  the  rash  still  show  as  a  pigmentation. 

Erythema  nodosum  (contusiformi)  not  infrequently  simulates  bruises 
of  the  skin,  presenting  rather  extensive  cutaneous  hemorrhages  upon 
the  extensor  surface  of  the  extremities. 

4.  From  marhed  venous  stasis,  especially  when  accompanied  by 
severe  paroxysms  of  cough,  which  suddenly  increase  the  congestion — 
e.g.,  jjertussis — where  hemorrhages  in  the  mucous  membranes,  particu- 
larly in  the  conjunctivae,  are  not  uncommon. 


PLATE  2. 


Purpura  (New  York  City  Hospital). 


COLLATERAL  CIRCULATION  IN  THE  SKIN. 


55 


COLLATERAL  CIRCULATION  IN  THE  SKIN. 

A  visible  distention  of  veins  or  arteries  in  the  skin  often  suggests 
some  deep-seated  obstruction  to  the  circulation — e.  g. : 

I.  The  collateral  circulation  (arterial),  when  the  aorta  is  occluded  at 
the  isthmus.      (See  Congenital  Heart  Diseases.) 

II.  The  collateral  circulation   (venous)   upon  the  anterior  thoracic 
wall.     This  is  of  some  importance  in  diagnosing  mediastinal  or  pulmo- 


FiG.  16. — Collateral  circulation  iu  the  abdominal  wall  (New  York  City  Hospital). 

nary  tumors,  which  compress  the  big  veins  within  the  chest,  especially 
the  vena  cava  superior  and  inferior.  Here  the  intercostal  and  internal 
mammary  veins  dilate  and  furnish  a  channel  of  communication  between 
the  two  vena  cavse  when  either  one  is  occluded. 

III.  The  very  striking  collateral  circulation  in  the  abdominal  wall 
caused  by  thrombosis  of  both  iliac  veins  or  of  the  vena  cava  inferior 
(Fig.  17).  The  blood  from  the  lower  extremities,  and  even  from  the 
kidneys,  reaches  the  thorax  by  way  of  distended  tortuous  veins,  which 
are  arranged  longitudinally,  and  are  more  pronounced  upon  the  sides 
than  upon  the  front  of  the  abdomen.     This  selection  of  the  sides  of 


56 


EXAMINATION  OF  THE  SKIN. 


the  abdomen  is  of  some  importance  in  distinguishing  this  form  of  ob- 
struction from  the  next. 

TV.  The  collateral  circulation  caused  by  obstruction  of  the  portal 
veins  (cirrhosis  of  the  liver  or  portal  thrombosis,  Fig.  18).  In  the  latter 
case  it  is  furnished  by  anastomoses  between  the  tiny  veins  at  the  root  of 
the  mesentery  and  those  of  the  peritoneal  covering  and  suspensory  liga- 
ments of  the  liver,  even  sometimes  by  a  patent  vena  umbilicalis.      In 


Fig.  17.— Collateral  circulation  in  thrombosis  of  the  vena  cava  inferior. 

this  latter  type  of  anastomosis  the  distended  veins  of  the  abdominal 
wall  are  apt  to  be  very  characteristically  arranged  about  the  navel, 
forming  the  so-called  "  caput  meduste." 

Figs.  17  and  18  illustrate  the  diagnostic  distinction  between  the 
distention  of  the  abdominal  wall  veins,  due  in  the  one  case  (Fig.  17)  to 
obstruction  in  the  vena  cava,  and  in  the  other  case  (Fig.  18)  to  obstruc- 
tion in  the  portal  system.     Numerous  exceptions  make  this  distinction 


COLLATERAL  CIRCULATION  IN  THE  SKIN. 


57 


less  valuable  for  diagnostic  purposes — e.  g.,  when  ascites  follows  portal 
stasis  the  presence  of  the  fluid  in  the  peritoneal  cavity  will  naturally 
produce  a  secondary  obstruction  in  the  vena  cava,  and  the  veins  of  the 
sides  of  the  abdomen  will  also  become  distended. 

In  any  of  these  cases  of  collateral  venous  circulation  it  is  always 
important  to  determine  the  direction  of  flow  of  the  venous  blood.    This 


Fig.  18.— Collateral  circulation  in  thrombosis  of  the  portal  vein  or  in  hepatic  cirrhosis. 


is  readily  done,  particularly  when  the  valves  of  the  veins  are  intact,  by 
emptying  the  blood  from  the  vein  by  means  of  pressure  with  the  fingers, 
and  then,  when  the  pressure  is  removed,  by  watching,  first  at  one  end 
and  then  at  the  other  end  of  the  vein,  to  see  from  which  direction  the 
blood  comes  first.  If  there  are  no  valves  or  if  the  valves  are  incompe- 
tent this  test  is  valueless,  because  the  blood  would  stream  back  with 
equal  rapidity  from  either  end. 


58  EXAMINATION  OF  THE  SKIN. 

A  very  fine  dendritic,  irregular  enlargement  of  the  thoracic  skin 
veins  is  often  observed  in  all  chronic  affections  of  the  lungs  and  pleurae, 
especially  when  adhesions  are  present  between  the  two  pleural  surfaces. 
It  probably  represents  a  collateral  circulation  between  the  lung  and  skin. 
In  the  very  chronic  forms  of  phthisis  it  is  observed  frequently,  and  then 
quite  often  in  the  supraspinous  fossa. 

Nearly  twenty  years  ago  the  writer  described  a  zone  of  small  dilated 
skin  veins  which  are  arranged  dendritically  and  extend  in  the  form  of  a 
band  about  1  to  3  cm.  broad  along  the  anterior  lower  border  of  the 
lung  and  over  the  superficial  cardiac  dulness.^  It  has  no  especial  path- 
ologic significance,  because  it  is  also  observed  in  perfectly  healthy  indi- 
viduals ;  but  clinically  it  represents  a  rough  picture  of  the  position  of  the 
lung  borders.  It  may  be  situated  either  within  or  without  the  pulmo- 
nary margins,  but  is  generally  nearby,  unless  modified  in  some  fashion,  as 
by  pleural  adhesions.  Percussion-results  prove  that  a  low  position  of 
this  zone  corresponds  to  emphysema  of  the  lungs. 

It  is  very  difficult  to  explain  the  appearance  of  this  zone  of  vessels,  but,  with- 
out question,  it  is  due  to  a  difference  in  pressure  between  the  inside  and  the  outside 
of  the  chest-wall.  Suppose  we  take  the  region  where  the  zone  of  vessels  marks  the 
internal  pulmonary  hepatic  boundarj\  Above  the  intrathoracic  pressure  is  negative, 
and  below  the  intra-abdominal  pressure  is  positive,  which,  of  com-se,  in  and  of  itself 
explains  nothing.  Respiration,  however,  alters  the  pressure  relations  (see  p.  7  7,  et  seq. ). 
It  produces  a  distinctive  change  of  shape  in  the  chest-wall,  as  evidenced  by  the  normal 
sinking  in  of  the  lower  intercostal  spaces  and  by  the  so-called  diaphragm  phenom- 
enon. Both  these  conditions  furnish  an  inspiratory,  localized,  girdle-shaped  depres- 
sion of  the  ch'^st-wall,  which  must  occasion  a  rhythmic  obstruction  to  the  venous 
blood-current,  because  the  supei-ficial  veins  of  the  part  are  compressed  by  the  ex- 
ternal atmospheric  pressure.  Now  it  is  conceivable  that  this  rhythmic  constriction 
may  give  rise  to  an  area  of  small  distended  veins.  Perhaps  a  similar  explanation 
would  account  for  the  formation  of  the  zone  which  suiTOunds  the  heart,  because 
evidently  similar  differences  in  pressure  exist  at  that  portion  of  the  chest-wall  against 
which  the  heart  beats  and  at  that  portion  against  wdiich  the  lung  rests.  In  fact,  one 
oftentimes  sees  an  inspiratoiy  depression  surrounding  the  cardiac  area,  quite  similar 
to  that  about  the  margin  of  the  lung.  Local  variations  in  pressure  caused  by  the 
maximum  distention  of  the  heart,  and  its  minimum  size  dtu'ing  systole,  would  also 
influence  the  circulation  in  the  thoracic  wall.  Paroxysms  of  coughing  were  formerly 
considered  to  be  the  most  important,  if  not  the  sole,  cause  of  this  vascular  distention. 
They  probably  do  exert  a  considerable  influence,  because  during  a  cough  the  strong 
positive  pressm-e  from  the  inside  causes  a  marked  congestion  of  the  subplem-al  and 
subperitoneal  veins.  This  in  turn  reacts  upon  certain  cutaneous  veins  which  are 
connected  with  the  subserous  veins,  and  the  congestion  will  be  marked  along  the 
lines  of  attachment  of  the  diaphragm.  The  latter,  to  a  certain  extent,  acts  as  a 
watershed  for  the  venous  blood,  flowing  upward  and  downward.  Everyone  wdth  a 
cough  does  not  present  this  zone  of  veins,  so  that  we  must  assume  as  another  factor 
in  its  origin  a  certain  indefinite  abnormal  distensibihty  of  the  smallest  vessels.  As 
a  matter  of  fact,  it  is  found  oftenest  in  such  patients  as  exhibit  a  similar  tendency 
to  the  formation  of  dendritic  venous  dilatations  in  other  parts  of  the  skin. 

^  Ueber  das  Vorkommen  und  die  diagnostische  Bedeutung  einer  Zone  ektasierter  fein- 
ster  Hautgef  asse  in  der  Nahe  der  unteren  Lungengrenze,  Corr.-Bl.  f.  Schw.  Aerzte,  1885. 


TROPHIC  AFFECTIONS  OF  THE  SKIN. 


59 


TROPHIC   AFFECTIONS   OF  THE   SKIN. 

The  so-called  "  decubitus  "  and  the  trophic  disturbances  accompany- 
ing nervous  aifectious  will  be  considered  later  under  Examination  of 
the  Nervous  System. 

Clubbed  fingers,  the  peculiar  swellings  of  the  terminal  phalanges 
of  the  fingers,  are  observed  in  congenital  heart  disease,  in  chronic  pul- 
monary diseases,  most  frequently  in  bronchiectasis  and  empyema  (hence 
the  name  empyema  fingers),  and  less  often  in  phthisis.  The  deformity 
may  develop  within  a  few  weeks,  and  then  disappear  again  when  the 
causal  disease  has  decidedly  improved.     In  the  more  chronic  cases  even 


Fig.  19.— Clubbed  fingers:  Chronic  phthisis  (New  York  City  Hospital). 

the  bones  share  in  the  deformities.  The  tendons  are  also  affected,  though 
less  decidedly.  As  yet  we  have  little  accurate  information  in  regard  to 
the  mode  of  oriofin. 


ACUTE   EXANTHEMATA;   CUTANEOUS  DISEASES;  DER- 
MATITIS  MEDICAMENTOSA. 

Although  the  scope  of  this  book  does  not  include  the  subject  of  skin 
diseases  and  the  acute  exanthemata,  it  seems  fitting,  from  the  standpoint 
of  diagnosis,  to  descril)e  the  rash  of  typhoid  fever,  herpes  febrilis,  miliaria, 
and  the  medicinal  eruptions. 


60 


EXAMlSATIOy   OF  THE  SKIN. 


ROSE  SPOTS   (Roseola). 

These  are  small,  round,  very  slightly  elevated,  hvperemic,  rose-red 
spots,  varying  in  size  from  that  of  a  pin-head  to  that  of  a  small  pea. 
They  appear  after  the  beginning  of  the  second  week  of  typhoid  fever. 
They  are  sparingly  scattered  over  the  abdomen,  more  rarely  over  the 
chest,  back,  and  lower  extremities.  Though  most  marked  at  the  height 
of  the  fever,  they  may  persist  throughout  the  whole  duration,  and  even 
after  convalescence.     Eelapses  are  frequently  accompanied  by  a  fresh 


Fig.  20.— Skiagraph  of  hand  of  patient  with  clubbed  fingers  (New  York  City  Hospital). 

crop  of  spots.  Their  hyperemic  nature  is  shown  by  their  immediate 
disappearance  under  the  pressure  of  the  finger,  only  to  reappear  instantly 
when  the  pressure  is  removed.  From  the  rash  of  acne,  rose  spots  are 
diiferentiated  by  the  ab.sence  of  a  decided  center.  This  tip  in  acne  is 
caused  by  some  cutaneous  gland  or  hair  follicle,  or  by  a  suppuration 
starting  in  one  of  them.  The  opening  of  a  cutaneous  gland  or  hair 
follicle  only  rarely  is  found  occupying  the  center  of  a  rose  spot,  or  a 
vesicle  tipping  the  center.  In  doubt  we  can  generally  find  in  a  case 
of  typhoid  fever  other  absolutely  characteristic  rose  spots  elsewhere  upon 


PLATE  3. 


Typhoid  spots  (rose  spots)  in  the  region  of  the  umbilicus  (natural  size). 


A 


Rose  spots  in  a  case  of  typhoid  fever,  showing  distribution  upon  the  trunk.    The  three  spots 
upon  the  face  are  rather  unusual. 


ACUTE  EXANTHEMA TA , 


61 


the  abdomen.  The  spots  usually  pass  through  a  cyclic  development, 
ripening  in  the  course  of  two  or  three  days  and  then  fading  aNvay, 
Avhile  in  the  meantime  new  spots  have  sprung  up  in  other  places.  In  a 
doubtful  case  it  is  often  advisable  to  mark  out  with  a  skin  pencil  the  few 
spots  that  appear,  in  order  to  observe  them  carefully  at  each  visit.  For 
although  rose  spots  may  never  appear  during  the  entire  course  of  some 
few  cases  of  typhoid  fever,  the  positive  evidence  of  this  peculiar  rash  is 
perhaps  the  safest  diagnostic  sign  of  the  disease.     (See  Plate  3.) 


HERPES   FEBRILIS. 


This  consists  of  a  group  of  vesicles,  J  to  2  cm.  in  diameter,  situated 
upon  a  slightly  inflamed  base.  The  watery  content  of  each  vesicle 
rapidly  becomes  purulent  and  turbid,  and  the  vesicle  then  either  bursts 
or  dries  up,  leaving  an  irregular  scaly  crust  upon  a  somewhat  reddened 


Fig.  21.— Herpes  cervicalis :  Cerebrospinal  meningitis  (Dr.  E.  G.  Cutler,  Massachusetts 

General  Hospital). 

background.  Although  they  may  appear  anywhere  upon  the  face,  nose, 
cheek,  lip,  or  ear,  they  develop  most  frequently  on  the  outer  edge  of  the 
lip.  According  to  their  position  they  are  called  herpes  labialis,  facialis, 
nasalis,  frontalis,  and  auricularis.  The  eruption  generally  appears  at 
the  beginning  of  febrile  diseases  ;  rarely  in  the  latter  stages.  It  is  most 
common  in  those  fevers  with  a  rapid  onset,  particularly  in  croupous 
pneumonia. 

[Howard  ^  has  very  recently  been  able  to  demonstrate  in  two  cases 

of  labial  and  nasal  herpes  and  herpes  of  the  body  occurring  in  acute 

lobar  pneumonia  pathologic  changes  in  the  posterior-root  ganglia,  the 

Gasserian  ganglia,  and  the  skin.     The  changes  are  apparently  identical 

'Howard,  Am.  Jour.  Med.  ScL,  Feb.,  1903. 


"62  EXAMINATION  OF  THE  SKIN. 

with  those  shown  by  Head  and  Carpenter  ^  to  be  invariably  associated 
with  herpes  zoster. 

From  evidence  available  at  the  present  date,  it  is  probable  that 
lesions  identical  in  character  and  similarly  localized  are  present  in  the 
herpes  of  other  infectious  diseases,  arid  in  the  light  of  our  present 
knowledge,  that  the  lesions  of  the  sensory  ganglia,  nerves,  and  skin  are 
due  to  the  action  of  the  soluble  toxins  of  various  micro-organisms. — Ed.] 

Herpes  is  very  rarely  observed  in  typhoid  fever.  There  is  a  certain  type 
of  slight  ephemeral  fever,  with  nothing  objective  to  be  discovered  except 
the  increased  temperature  and  herpes,  which  is  termed  febris  herpetica. 
Herpes,  as  a  rule,  is  considered  a  favorable  prognostic  sign.  Our  ex- 
perience in  the  use  of  streptococcus  toxin  in  the  treatment  of  malignant 
tumors  proves  that  herpes  febrilis  depends  upon  a  toxic  action.  It  is 
common  in  malaria,  cerebrospinal  fever,  and  meat-poisoning;  and 
therefore  a  sign  of  some  value  in  the  diagnosis  of  these  affections  from 
typhoid. 

MILIARIA   (PRICKLY  HEAT);  SUDAMINA. 

Under  this  head  are  included  various  eruptions  of  tiny  vesicles 
developing  most  frequently  upon  the  abdomen  and  chest  and  usually 
associated  with  profuse  perspiration.  It  is  generally  supposed  that  this 
eruption  is  due  to  the  plugging  of  the  orifices  of  the  sweat  glands  with 
swollen  epithelium  and  to  the  formation  of  small  retention  cysts,  some 
of  which  may  be  associated  with  a  slight  inflammatory  reaction  in  the 
neighborhood.     Three  main  types  are  to  be  distinguished  : 

Miliaria  crysfallina  (sudamina ;  crystal  rash) :  absolutely  transpar- 
ent vesicles,  resembling  a  dew  drop  and  without  reddened  base. 

Miliaria  alba :  vesicles  with  slightly  turbid  contents  upon  a  faintly 
reddened  base. 

Miliaria  rubra :  small  red  papules  with  a  faintly  developed  vesicle 
in  the  center.     This  type  is  apt  to  itch. 

Miliaria  vesicles  are  generally  situated  close  together. 

DERMATITIS    MEDICAMENTOSA   (DRUG  ERUPTION). 

Numerous  medicinal  agents  have  the  peculiarity  of  exciting  in  certain 
individuals  eruptions  which  resemble  urticaria,  measles  or  even  scar- 
let fever.  The  rash  generally  fades  promptly  and  disappears  when  the 
drug  is  omitted.  Examples  of  such  drugs  are  most  of  the  antipyretics, 
especially  antipyrin,  antifebrin,  phenacetin  ;  not  infrequently  sodium 
salicylate  ;  many  preparations  of  balsams — e.  g.,  balsam  of  copabia ;  and 
mercury  used  externally,  or,  in  rare  cases,  internally.  The  injection  of 
antitoxin  produces  an  eruption  resembling  urticaria,  measles  or  scarlet 
fever  very  closely.  lodid  of  potash  is  apt  to  produce  a  rash  which  may 
closely  resemble  erythema  multiformi  or  to  bring  out  a  purulent  acne- 
like eruption  which  may  be  confounded  with  syphilis  or  small-pox.  The 
prolonged  administration  of  considerable  doses  of  bromid  of  potash  fre- 
quently causes  an  eruption  very  much  like  acne.  It  is  usually  localized 
^  Head  and  Carpenter,  Brain,  1900,  Part  III. 


OTHER   CUTANEOUS  MANIFESTATIONS.  63 

upon  the  face  and  chest,  and  an  experienced  observer  generally  distin- 
guishes it  by  its  marked  nodular  infiltration  and  bluish  appearance.  It 
may  develop  into  suppurating  sores  covered  with  crusts  which  resemble 
chancroids,  and  which  persist  in  the  resemblance  even  microscopically 
by  exhibiting  a  marked  overgrowth  of  epithelium. 

OTHER  CUTANEOUS  MANIFESTATIONS  IMPORTANT 
FROM  THE  DIAGNOSTIC  STANDPOINT. 

Striae. — The  striae  caused  by  the  stretching  of  the  skin  in  edema, 
their  resemblance  to  strise  gravidarium,  and  their  persistence  for  some 
time  after  the  edema  has  disappeared  or  even  permanently,  have 
already  been  noted  on  page  49.  Similar  striae  may  appear  from  the 
rapid  accumulation  or  disappearance  of  the  subcutaneous  fat.  Any 
cause  which  rapidly  increases  the  size  of  the  abdomen,  such  as  preg- 
nancy or  the  growth  of  tumors,  may  produce  these  striae. 

Desquamation. — In  cachexia  and  emaciated  conditions  one  fre- 
quently observes  a  diffuse  bran-like  scaliness  covering  the  skin  of  the 
trunk  and  extremities  (pityriasis  tabescentium).  A  characteristic  lam- 
ellar desquamation  of  the  skin,  usiially  most  conspicuous  upon  the 
palmar  surfaces  of  the  feet  and  hands,  occurs  after  scarlet  fever ;  a 
characteristic  bran-like  desquamation,  after  measles  ;  a  more  crust-like 
desquamation,  after  small-pox  ;  and  a  flaky  desquamation,  after  ery- 
sipelas. 

F'liruiiculosis,  as  a  complication  of  some  general  disorder,  such  as 
diabetes,  is  of  diagnostic  interest  to  clinicians  ;  otherwise,  it  concerns 
only  skin  specialists. 

Scars. — The  forms  of  various  scars  may  be  of  some  importance  in 
considering  the  past  history  of  a  patient — e.  g.,  marks  of  vaccination,  of 
small-pox,  of  furunculosis,  of  carbuncle,  of  lupus,  of  inguinal  buboes,  of 
tubercular  glands,  and  the  bean-shaped  scars  of  serpiginous  syphilides. 
Unfortunately  even  a  slight  scar  very  rarely  persists  to  show  the  site  of 
the  primary  sore  of  syphilis.  Surgical  operations,  various  therapeutic 
measures,  such  as  moxas,  cautery,  venesections,  leeches,  Baunscheidtis- 
mus,  and  epispastics,  and  wet-cupping  leave  behind  permanent  charac- 
teristic scars.  They  may  be  important  in  marking  the  dates  of  previous 
illness. 


DETERMINATION  OF  THE  BODY  TEMPERATURE. 

Physicians  in  ancient  times  recognized  as  a  principal  symptom  of 
fever  an  increase  in  the  temperature  of  the  blood.  But  the  amount 
of  fever  was  measured  by  the  acceleration  of  the  pulse.  About  the 
middle  of  the  last  century  Traube,  v.  Biirensprung,  and  Wunderlich 
perfected  the  methods  for  taking  the  body  temperature,  considering  it 
one  of  the  essential  points  to  be  observed  in  an  examination.     Since 


64  DETERMINATION  OF  THE  BODY  TEMPERATURE. 

their  time  the  tendency  has  been  to  consider  that  an  increase  of  the 
body  temperature  is  the  essential  sign  of  fever. 

The  classical  symptoms  of  fever  include,  in  addition  :  weakness, 
malaise,  anorexia,  thirst,  digestive  and  psychic  disorders,  rapid  breath- 
ing, alteration  in  the  amount  of  urinary  excretion,  and  especially  "  con- 
sumption of  the  body." 

Some,  though  not  all,  of  the  above-mentioned  symptoms  may  be 
produced  by  an  artificial  overheating  of  the  body.  Certain  of  them, 
however,  by  no  means  run  parallel  to  the  increase  of  temperature ;  for 
sometimes,  either  with  or  without  antipyretics,  the  temperature  may 
drop  without  any  especial  imj^rovement  in  the  other  symptoms.  Hence, 
an  increase  of  body  temperature  is  the  most  important  and  constant  ac- 
companiment of  what  we  call  fever,  and  to-day  the  terms  are  used  inter- 
changeably. But  still  we  must  not  neglect  the  associated  phenomena 
of  the  febrile  system-complex  in  determining  the  severity  of  an  attack, 
because  they  are  partly  independent  of  the  temperature,  and  are  some- 
times much  more  important  than  the  amount  of  temperature  increase. 

Before  the  use  of  thermometers  physicians  estimated  the  temperature 
by  the  sense  of  touch.  Though  generally  this  is  a  perfectly  satisfactory 
method  of  telling  whether  or  not  fever  is  present,  many  mistakes  may 
arise.  The  hand  appreciates  only  the  temperature  of  the  skin.  This  is 
not  always  parallel  to  the  internal  temperature  of  the  body  or  of  the 
blood ;  because  the  skin  temperature  evidently  depends  not  only  upon 
the  temperature  of  the  blood,  but  also  upon  the  amount  of  blood  in  the 
skin  at  a  given  time,  as  well  as  upon  the  conditions  of  heat  radiation. 
For  example,  during  a  chill  the  cutaneous  temperature  is  sometimes  dimin- 
ished as  a  result  of  a  contraction  of  the  peripheral  vessels,  while  the  blood 
temjjerature,  as  shown  by  the  thermometer,  is  increased.^  Conversely, 
the  cutaneous  temperature  of  perspiring  patients  seems  increased,  pro- 
vided evaporation  and  subsequent  cooling  is  prevented  by  their  being 
wrapped  up,  because  the  skin  contains  an  increased  amount  of  blood. 
Yet  the  internal  temperature  need  not  be  raised.  These  possible  sources 
of  error  make  it  plain  that  thermometers  are  essential  for  the  accurate 
determination  of  the  temperature  relations.  Nevertheless,  palpation  of 
the  skin  is  of  some  value  in  disclosing  the  condition  of  the  cutaneous  cir- 
culation. It  is  oftentmies  accurate,  provided  that  evaporation,  chill,  and 
profuse  perspiration  can  be  excluded.  Perhaps  the  best  place  for  such 
palpation,  when  the  patient  is  in  bed,  is  the  back  ;  for  there  the  tem- 
perature must  be  nearly  the  same  as  that  of  the  blood.  In  spite  of  a 
high  temperature,  the  skin  need  not  feel  very  hot  to  the  physician's 
hand  if  the  room  temperature  is  low  and  the  skin,  as  well  as  the  blood 
itself,  has  been  cooled  by  the  surrounding  air.  This  is  a  point  especially 
to  be  remembered  for  the  diagnosis  of  ambulatory  typhoid. 

^  According  to  Liebermeister,  fever  depends  npon  an  alteration  in  the  temperature 
regulation.  Either  heat  production  or  heat  radiation,  one  or  both,  are  affected.  This 
view  has  been  supported  by  more  recent  experiments  (Hildebrandt,  Stern,  and  othei-s). 
During  a  chill  it  is  supposed  that  the  cutaneous  temperature  is  not  diminished  actually, 
but  only  relatively,  com])ared  with  the  internal  temperature,  and  that  the  cutaneous 
sensibility  in  response  to  this  relation  replies  by  the  excitation  of  a  sensation  of  chilliness. 


METHOD   OF  TAKING   TEE  TEMPERATURE.  65 


THE  THERMOMETER. 

The  thermometer  carried  by  practising  physicians  is  a  mercury  in- 
strument, subdivided  in  England  and  America,  according  to  the  Fahren- 
heit scale,  from  95°  to  115°,  and  on  the  Continent,  according  to  the  Cel- 
sius scale,  from  20°  to  45°.  To  convert  Fahrenheit  into  Celsius  and 
vice  versa  : 

A°  Celsius  =  (f  a  +  32)°  Fahrenheit,  or 

A°  Fahrenheit  =  (a  —  32)  |°  Celsius. 

A  variety  of  small  clinical  thermometers  can  be  obtained  in  America 
or  in  ^England  (perhaps  the  best  are  the  English  make).  They  are  very 
accurate,  so  that  an  explanation  of  the  method  of  correcting  and  tabu- 
lating their  errors  is  hardly  necessary.  [The  one-minute  Hick's  max- 
imum clinical  thermometer,  furnished  with  a  prismatic  lens  to  magnify 
the  column  of  mercury,  is  perfectly  satisfactory. — Ed.]  The  cylindric 
is  ordinarily  more  convenient  than  the  old-fashioned  spheric  bulb. 
The  so-called  "  maximum  "  thermometers  in  most  common  use  to-day 
require  vigorous  shaking  to  ])ush  the  mercury  down  below  the  normal 
point.  Then  the  mercury  remains  at  whatever  height  it  may  reach  until 
shaken  down  again. 

METHOD  OF  TAKING  THE  TEMPERATURE, 

The  temperature  is  ordinarily  taken  by  placing  the  bulb  of  the  ther- 
mometer beneath  the  side  of  the  tongue  and  instructing  the  patient  to 
keep  the  lips  tightly  closed  during  the  necessary  interval  (one  to  five 
minutes).  In  some  cases  it  may  be  necessary  to  obtain  the  temperature 
in  the  axilla,  and,  whenever  in  doubt,  in  the  rectum  or  vagina.  It  is 
hardly  necessary  to  caution  a  physician  to  be  most  careful  in  disinfecting 
the  thermometer  after  each  time  it  is  used. 

In  many  of  the  hospitals  in  Germany  they  employ  a  large  thermom- 
eter, leaving  it  in  the  axilla  from  fifteen  to  twenty  minutes.  With 
comatose,  stupid  or  violently  delirious  patients  or  with  patients  suffering 
from  severe  dyspnea  or  from  nasal  obstruction  sufficient  to  impede 
breathing,  the  temperature  must  be  taken  in  the  rectum  or  vagina. 

[The  ordinary  one-minute  clinical  thermometer  is  sufficiently  accurate 
when  used  in  the  mouth,  and  absolutely  so  in  the  rectum. — Ed.] 

In  any  case  the  temperature  should  be  measured  at  least  twice  a  day, 
and  under  many  conditions  every  two  to  four  hours.  When  the  morn- 
ing and  evening  temperatures  are  taken,  the  morning  commonly  repre- 
sents the  temperature  between  7  and  9  o'clock,  and  the  evening  between 
4  and  6  o'clock,  which  furnishes  a  practical  maximum  and  minimum 
without  disturbing  the  patient's  sleep  (see  pp.  66  and  68).  The  tem- 
perature is  ordinarily  indicated  upon  temperature  charts  ruled  either  for 
every  two  hours  or  merely  for  morning  and  evening.  The  normal 
line  is  generally  printed  more  deeply  or  in  another  color.  (See  Figs. 
28  and  29  for  a  convenient  method  of  indicating  night  and  day  tem- 
peratures.) 

5 


6^  DETERMINATION  OF  THE  BODY  TEMPERATURE. 

The  temperature  curve  alone  sometimes  suffices  to  make  a  diagnosis 
with  considerable  certainty  ;  as,  for  instance,  in  typhoid  fever,  pneumo- 
nia, chronic  tuberculosis,  malaria,  and  suppurative  processes.  Even  a 
single  estimation  of  the  temperature  will  often  throw  considerable  light 
upon  the  diagnosis.  Simulation  may  be  excluded  if  there  is  decided 
fever. 

THE  NORMAL  BODY  TEMPERATURE. 

The  normal  temperature  is  0.2°  to  0.5°  C.  (0.4°-l°  F.)  higher 
in  the  rectum  or  vagina  than  in  the  axilla,  von  Barensprung  gives 
the  following  figures  as  the  normal  mean  in  the  axilla  at  the  various 
ages  : 

First  10  days 37.75°  C.  (99.95°  F.). 

Up  to  puberty 37.43°  C.  (99.37°  F.). 

15  to  20  years 37.19°  C.  (98.94°  F.). 

21  to  70      "      36.85°  C.  (98.93°  F.). 

80  years 37.26°  C.  (99.07°  F.). 

These,  of  course,  are  the  daily  averages.  The  daily  variation  of 
temperature  in  a  normal  person  is  shown  in  Fig.  22.     The  minimum  of 


Hours  of  the 
day. 


iHHBBBBBBHBBBBBBBBBBBBWBBBBBBBI 

S9| 


■■■■■■■■■■■a  ■■■■■■■■■■■■■■■■  ■■■■■■■■■■■■■■SS'S'SSBBBSB! 
■■■■■■■■■■■■■■■■■■■■■■■■■■■■■■■■■■■■■■■■■■■■■■■■■■B55SS 
■■^■■^■■■■■■■■■■■■■■■^■■■■■■— ■■■■■■;■■■■■■■■■■  ■»■■■■■■■ 

Fig.  22.— Daily  curve  of  the  normal  body  temperature  (Liebermeister). 

temperature  is  observed  in  the  first  few  hours  after  midnight ;  its  first 
maximum  is  reached  during  the  forenoon,  generally  between  9  and  10 
o'clock ;  it  falls  again  before  the  midday  meal,  rises  and  reaches  a  sec- 
ond, the  proper  maximum,  some  time  between  5  and  8  o'clock  in  the 
evening;  it  then  begins  to  fall  till  the  first  minimum  is  reached.  The 
periodicity  of  the  normal  temperature  curve  probably  depends  primarily 
upon  the  change  between  waking  and  sleeping.  At  least  there  have 
been  numerous  examples  of  people  accustomed  to  reversing  the  day, 
sleeping  in  the  daytime  and  working  in  the  night,  in  whom  the  temper- 
ature variation  is  reversed. 

Food  and  physical  exercise  influence  the  temperature.  Mountain- 
climbing,  for  example,  has  raised  the  temperature  in  normal  individuals 
as  high  as  40°  C.  (104°  F.).  The  temperature  of  the  external  air  has 
some  effect  upon  the  body  temperature.  Sometimes  just  before  a  thun- 
der shower  a  slight  rise  has  been  noted  in  normal  individuals.  Lieber- 
meister's  chart  shows  that  the  daily  variation  amounts  to  1°  C.  (1.8°  F.), 
comparing  the  absolute  maximum  and  minimum,  but  to  not  more  than 
0.5°  C  (0.9°  F.)  comparing  the  difference  between  the  morning  temper- 


FEBRILE  TEMPERATURES.  67 

ature  at  8  or  9  o'clock  and  the  evening  temperature  at  5  o'clock.^  An 
evening  temperature  of  37.4°  C.  (99.32°  F.)  is  within  physiologic 
limits ;  although  in  consumptives  it  would  probably  correspond  to  a 
rectal  temperature  of  38°  C  (100.4°  F.),  and  so  indicate  fever. 

[Unless  otherwise  stated  these  temperatures  are  mouth  temperatures. 
—Ed.] 

FEBRILE  TEMPERATURES, 

Wunderlich  has  computed  the  following  fever  scale  : 

I.  Normal  temperatures,  37.0°-37.4°  C.  (98.6°-99.3°  F.). 
II.  Subfebrile  temperatures,  37.4°  -38.0°  C.  (99.3°-! 00.4°  F.). 
III.   Febrile  temperature  : 

(«)  Slight  fever,  38.0°-38.4°  C.  (100.4°-101.1°  F.). 

(6)  Moderate  fever,  38.5-39.0°  C.  (101.3°-102.2°  F.)  in  the 

morning  to  39.5°  C  (103.1°  F.)  in  the  evening, 
(c)  Considerable  fever,  up  to  39.5°  C.  (103.1°  F.)  in  the 

morning  to  40.5°  C.  (104.9°  F.)  in  the  evening. 
{d)  High  fever,  above  39.5°  C.  (103.1°  F.)  in  the  morning 
and  above  40.5°  C.  104.9°  F.)  in  the  evening. 
Hyperpyrexia. — Very    unusual     temperatures,  41°    or    42°    C. 
(105.8°   or  107.6°  F.)  are  spoken  of  as  hyperpyrexia.     Teale's  case 
(injury  to  the  spine  and  recovery)  is  the  highest  recorded  temperature, 
50°  C.  (122°  F.).     At  the  Insel  Hospital,  Berne,  a  patient  with  typhoid 
fever,   who  subsequently    recovered,  once  exhibited   a  temperature  of 
45°  C  (113°  F.).     Similar  cases  are  quoted  in  literature  as  medical 
curiosities.     A  temperature  above  42°  C.  (107.6°  F.)  is  rare  to-day, 
because  we  now  have  at  our  command  more  efficient  means  of  combat- 
ting fever. 

Stern  has  recently  given  to  the  term  hyperpyrexia  a  general  pathologic  signifi- 
cance, limiting  it  to  those  cases  in  which  the  heat  regulating  apparatus  is  insuffi- 
cient, in  contradistinction  to  febrile  temperatures  where  the  regulating  apparatus  is 
capable  of  preventing  a  further  increase  or  an  undue  cooling-off.  Hyperpyrexia 
includes,  therefore,  the  excess  of  temperature  added  to  fever  by  insufficient  heat 
radiation.  We  do  not  really  know  in  every  case  whether  fever  is  injurious  or  bene- 
ficial; but  it  is  evident  that  hyperpyrexia  is  a  dangerous  surplus  of  heat,  and  therefore 
to  be  controlled  therapeutically.  Stern  considers  that  true  fever  may  be  distinguished 
clinically  from  hyperpyrexia  by  the  fact  that  when  the  temperature  of  a  patient  with 
fever  is  reduced  hj  means  of  a  cold  bath  a  reaction  takes  place  directly  (chilliness, 
shivering),  whereas  no  such  reaction  occurs  in  hyperpyrexia,  nor  does  the  patient 
experience  any  discomfort.  However,  we  may  still  consider  almost  any  excessive 
temperature  under  the  heading  of  hyperpyrexia. 

PROGNOSTIC  SIGNIFICANCE  OF  HIGH  TEMPERATURES* 

Although  a  certain  significance  can  be  attributed  to  the  height  of  the 
temperature,  we  must  be  very  guarded  in  making  the  prognosis  of  a 
disease,  and  not  assume  that  every  high  fever  is  necessarily  fatal.  In 
general  a  typhoid   fever  with  a  high  temperature  curve  is  more  severe 

^  Debcynski,  ref.  in  Hermann's  Handhuch  der  Phyaiohgie,  1882,  vol.  TV.,  p.  323. 
Further,  U.  Mosso :  Experienze  fatte  per  invertire  le  oscillazioni  diurne  della  terapera- 
tura  neiruomo  sano.     Laboratorio  di  fisiologia  nella  R.  Universita  di  Torino,  7th  ed. 


68  DETERMINATION  OF  THE  BODY  TEMPERATURE. 

than  one  with  a  low  range,  and  in  the  same  patient  an  increase  of  tem- 
perature generally  coincides  with  some  more  serious  condition  or  with  a 
complication.  The  bearing  of  a  certain  height  of  temperature  upon  the 
prognosis  varies  greatly  in  different  diseases.  In  malarial  fever,  for 
example,  the  temperature  may  be  extremely  high  without  rendering  the 
prognosis  more  serious ;  or  again,  quite  innocent  throat  affections  in 
children  are  responsible  for  temperatures  of  40°  C.  (104°  F.)  or  more. 
Unverricht  ^  has  published  a  collection  of  abnormally  high  tempera- 
tures in  which,  nevertheless,  recovery  followed. 

THE  FEVER   COURSE, 

DAILY  VARIATIONS  OF  THE  FEVER;   THE  FEBRILE  TYPE. 

The  daily  course  of  temperature  in  any  case  of  fever  lasting  one  or 
more  davs  is  usually  much  the  same  as  in  healthy  individuals.  If  the 
curve  pictured  upon  page  66  were  elevated  one  or  two  degrees  throughout 
it  would  correspond  accurately  enough  to  the  daily  variation  of  many  a 
fever.  But  in  numerous  febrile  diseases  the  maximum  or  minimum 
point  may  appear  at  a  different  time ;  for  example,  the  maximum 
point  may  occur  in  the  forenoon  or  at  midday.  Again,  the  daily  vari- 
ations may  be  much  greater  than  in  a  normal  individual,  or  in  the 
morning  the  patient's  temperature  may  be  normal  and  in  the  evening 
elevated  two  or  three  degrees.  It  is  therefore  evident  that  to  obtain  the 
accurate  temperature  of  a  patient  with  fever  we  must  not  be  content 
w^ith  measuring  the  temperature  at  morning  and  night  alone,  but  take  it 
at  regular,  shorter  periods,  such  as  once  in  two  hours  or  once  in  four  hours. 
An  irregular  fever  is  often  first  discovered  by  taking  the  temperature  at 
an  unusual  time ;  for  example,  late  at  night.  A  very  good  indication 
of  the  amount  of  fever  is,  of  course,  the  patient's  feelings ;  he  generally 
feels  worse  when  he  has  most  fever. 

Various  types  are  distinguished  according  to  the  variation  of  the 
fever  during  the  day.  In  prolonged  or  continued  fevers  the  daily  oscil- 
lations rarely  vary  more  than  in  a  normal  individual — /.  e.,  not  more 
than  1°  C.  (1.8°  F.).  In  remittent  fevers  the  daily  variation  is  more 
than  1°  C.  (1.8°  F.).  In  intermittent  or  interrupted  fevers  the  daily 
minimum  is  normal  or  below  normal.  Since  malaria  is  now  so  com- 
monly called  intermittent  fever,  it  is  perhaps  advisable  to  designate  this 
type  as  interrupted  fever. 

COURSE  OF  FEVER  FOR  LONGER  PERIODS ;  COURSE  OF  FEVER  EST 
A  RESTRICTED  SENSE  OF  THE  WORD;  THE  FEVER  CURVE 
IN  DIFFERENT  DISEASES. 

The  fever  type,  meaning  more  particularly  the  daily  variations,  is  of 
less  diagnostic  importance  than  the  so-called  course  of  fever  or  fever 
curve,  including  a  longer  period  of  observation. 

'^  Unverricht,  "  Ueber  das  Fieber."  Sammlung  klinischer  Vortrdge,  No.  159,  p.  724, 
1896,  Breitkopf  and  Hlirtel. 


THE  FEVER   COURSE. 


69 


EPHEMERAL  VARIETIES    OF   FEVER    (SINGLE-DAY   FEVERS)    (FEBRICULA). 

Ordinarily  these  are  either  well-known  infections  whose  nature  is  shown 
partly  by  the  objective  examination,  partly  by  the  prevalence  of  an  epidemic  of 
similar  cases,  but  which  run  an  abnormally  rapid  or  abortive  course  ;  or  else  slight 
infections  of  some  unknown  origin,  or  else  are  caused  by  temporary  digestive 
disorders,  or  else  due  to  some  nervous  influence,  such  as  hysteria  or  mental  excite- 
ment ;  children,  as  is  well  known,  exhibit  a  rise  of  temperature  from  very  insig- 
nificant causes  ;  in  the  beginning  of  an  ephemeral  fever  a  diagnosis  is  almost 
impossible — so  that  the  height  that  the  temperature  reaches  will  often  cause  appre- 
hension. 

Under  this  heading  is  included  the  fever  which  appears  after  catheterization, 
whose  origin  we  do  not  perfectly  understand,  and  the  brief  fever  following  asejjttG 
operations.  The  latter  is  to  be  explained  by  purely  psychic  influences,  such  as 
anxiety  as  to  the  result  of  the  operation,  by  the  toxic  action  of  the  chloroform,  or 


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of  the  antiseptics  employed,  and  by  the  absorption  of  the  relatively  harmless  secre- 
tion of  the  wound,  etc.  Where  the  consistence  of  the  blood  is  altered  by  some 
therapeutic  interference,  such  as  transfusion  of  blood  or  of  salt  solution,  we  often 
observe  fevers  of  similar  slight  import.  In  such  cases  the  origin  may  dej^end  upon 
some  slight  infection  or  upon  fermentative  intoxication.  In  any  case  these  rises 
of  temperature  are  generally  transitory  and  innocent. 

Notwithstanding  these  numerous  types  of  ephemeral  fever  no  careful  physician, 
in  any  febrile  attack,  will  neglect  a  most  carefiil  search  for  some  objective  explana- 
tion or  some  evidence  of  infection. 


FEVER  CURVE  OF  CROUPOUS   PNEUMONIA  AND    ERYSIPELAS;    CRISIS  AND 

LYSIS. 

There  are  a  number  of  diseases  with  continued  fever  in  which  the  course  of  the 
temperature  is  suflSciently  characteristic  to  furnish  the  diagnosis.  Croupous  pneu- 
monia is  one  of  these.     It  is  generally  ushered  in  with  a  chill,  and  within  a  few 


70 


DETERM I  NATION  OF  THE  BODY  TEMPERATURE. 


hours  by  a  rapid  rise  of  temperature — 39°  to  40°  C.  (102.2°-104°  F.)— although 
shortly  before  the  chill  the  patient  had  been  feehng  apparently  well.  The  fever 
persists  with  but  slight  variation  for  several  days  (5  to  9  days),  and  then  subsides 


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as  rapidly  as  it  developed,  usually  accompanied  by  a  profuse  perspiration.  This 
sudden  drop  in  the  temperature,  so  characteristic  of  pneumonia,  is  called  the  crisis. 
Lysis,  in  contradistinction,  signifies  a'  gradual  drop  of  temperature  during  two  or 
three  days.     The  latter  is  rarely  observed  in  croupous  pneumonia,  but  very  com- 


THE  FEVER  COURSE. 


71 


monly  in  many  other  febrile  diseases.  A  protracted  crisis  is  a  transitional  type 
between  the  two.  An  interrupted  crisis  is  a  critical  drop  of  temperature  interrupted 
by  a  transitory  rise,  A  pseudocrisis  is  one  in  which  a  critical  fall  is  rapidly  followed 
by  a  rise  and  persistence  of  the  fever.  A  decided  rise  of  temperature  associated 
■with  a  marked  disturbance  of  the  patient's  general  condition,  the  so-called  per- 
turbatic  critica,  sometimes  precedes  the  crisis.  All  of  these  conditions  may  be 
variously  combined  in  pneumonia  (Fig.  23).  So  far  as  the  fever  is  concerned, 
erysipelas  resembles  it  veiy  closely. 

THE    COURSE    OF   TYPHOID    FEVER. 
The  temperature  of  typhoid  fever  is  characterized  by  a  gradual  stepladder-like 
onset,  so  that  each  evening  it  reaches  a  little  higher  point  than  the  evening  before. 


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Initial  fever.  Eruptive  fever. 

Fig.  25. — Fever  curve  in  measles. 


The  initial  stage  lasts  four  to  seven,  days ;  it  is  followed  by  a  period  of  continued 
high  temperature  without  much  of  any  diurnal  variation,  the  so-called  fastigium, 
(seven  to  ten  days) ;  and  then  by  a  period  of  remittent  fever,  the  amphibolic  stage, 


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Fig.  26.— Temperature  curve  in  scarlet  fever. 


72  DETERMINATION  OF  THE  BODY  TEMPERATURE, 


ios° 


40* 


3S« 


Initial  rise.  Suppuration  temperature. 

Fig.  27. — Temperature  curve  in  small-pox. 


in  whicli  the  diurnal  variations  are  very  marked,  often  with  a  difference  of  several 
degrees.    This  lasts  five  to  ten  days  and  merges  into  the  de/ervescing  stage,  which  is  as 


Fig.  28.— Temperature  in  intermittent  quotidian. 


gradual  as  the  initial  rise.     The  chart  on  page  70  (Fig.  24)  shows  this  peculiar 
temperature  curve  better  than  we  can  describe  it. 


THE  FEVER   COURSE. 


73 


TEMPERATURE    CURVE    OF    MALARIAL    FEVER. 

The  curve  of  malarial  fever  (Figs.  28  and  29)  is  characterized  by  a  critical  rise 

and  fall  of  the  temperature  every  two  or  three  days,  associated  with  the  other 

symptoms  of  an  acute  disease.     In  typic  cases  the  patient  feels  quite  well  during 

the  interval ;  the  rise  of  temperature  occurs  very  suddenly,  is  accompanied  by  a 


marked  chill,  and  is  followed  later  by  a  sudden  drop  and  a  profuse  perspiration. 
The  various  types  are  named  quotidian,  tertian,  and  quartan  fever.  As  a  rule,  in 
malaria  the  attacks  repeat  themselves  at  exactly  the  same  hour.  Numerous  excep- 
tions do,  however,  occur ;  in  the  anticipating  variety,  the  attack  of  fever  appears 
a  little  earlier  each  day  ;  in  the  postponing  variety,  a  little  later  each  day. 


74 


DETERMINATION  OF  THE  BODY  TEMPERATURE. 


CURVE  IN  RECURRENT  FEVER. 

As  in  malaria  so  in  relapsing  fever  the  temperature  curve  consists  of  a  number 
of  individual  attacks.  Each  attack  and  each  interval,  however,  persist  for  several 
days  in  recurrent  fever  (Fig.  30).  The  relapses  may  be  repeated  several  times,  but 
finally  become  shorter  and  less  severe,  until  complete  defervesence  takes  place. 

RELAPSES. 

In  any  acute  infectious  disease  there  may  be  a  recrudescence  of  the  specific 
symptoms,  and  especially  of  the  fever,  after  convalescence  has  apparently  begun. 
Such  recrudesences  are  most  common  in  typhoid.     They  should  not,  of  course,  be 


4    5    6    7 


Days  of  Fever. 

8    9    10  11  12  13  14  15  Ifi  17  18  19  20 


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First  apyrexia.  First  relapse.        Second  apyrexia. 

FiG.  30.— Temperature  of  recurreut  fever  (Wunderlich). 

confused  with  the  individual  attacks  in  febris  recurrens  or  malaria,  nor  with  any 
complication  of  the  original  disease  ;  as,  e.  g.,  an  otitis  in  measles  or  scarlet  fever. 


HECTIC  FEVER. 

This  is  the  typic  fever  of  chronic  tuberculosis.  It  generally  persists  a  con- 
siderable length  of  time  and  is  of  a  remittent  or  interrupted  character,  mth  sud- 
den rises  and  falls.  The  minimum  temperature  is  usually  in  the  morning  and  the 
maximum  in  the  evening,  or  the  opposite  type  may  occur — inverted  hectic  fever. 
A  two-hour  chart  exhibits  a  very  irregular  course,  with  many  slight  rises  and  lalls 
throughout  the  day. 

PUS.  OR    SUPPURATIVE  FEVER  t  ERRATIC   CHILLS    IN  PYEMIA,  ULCERATIVE 
ENDOCARDITIS,  AND  GALL-STONES ;  CHILLS  IN  INFARCTIONS. 

Though  often  resembling  the  chart  of  hectic  fever,  that  of  suppura- 
tion is  generally  more  irregular  in  the  time  and  the  degree  of  the  exacer- 
bations. 

In  pyemia  the  fever  frequently  occurs  in  very  intense  paroxysms, 
accompanied  by  severe  chills  resembling  malaria,  except  that  they  are 
more  irregular.     Closely  related  to  these  so-called  erratic  chills  of  py^- 


SUBNORMAL  TEMPERATURES. 


75 


mia  are  the  chills  which  appear  in  ulcerative  endocarditis  and  in  gall- 
stone affections.  Non-purulent  infarctions  are  associated  with  a  similar, 
though  a  less  pronounced,  chill. 


ATYPICAL  FEVER. 


In  some  diseases  there  is  no  type  to  the  temperature  course,  so  that, 
although  the  clinical  picture  is  sufficiently  constant,   the  temperature 


Days  of  Fever. 
4         5         6         7 


103 


\OZ 


101 


100 


-39' 


38' 


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-36° 


Fig.  31.— Hectic  fever  in  phthisis. 


chart  alone  would  furnish  very  little  information  of  the  nature  of  the 
disease.     Examples  are  diphtheria  and  septic  -processes. 


SUBNORMAL  TEMPERATURES. 

These  are  quite  as  important  clinically  as  febrile  temperatures. 
"VVunderlich  considers  anything  below  36.25°C.  (95.25 °F.)  a  sub- 
normal temperature. 

Marked  depressions  of  temperature  are  noted  : 

1.  In  the  prolonged  action  of  intense  cold.^  A  temperature  of  27°  C. 
(80.6  °F.),  as  in  a  case  of  freezing,  is  not  necessarily  fatal. 

2.  Following  a  pronounced  critical  fall  of  temperature  in  fever. 
After  the  crisis  in  pneumonia  the  temperature  often  drops  to  34°  or 
35°  C.  (93.2°  or  95°  F.). 

3.  In  so-called  "  collapse,"  where  there  is  a  sudden  fall  in  the  temper- 
ature. This  occurs  in  very  sick  patients  (especially  those  with  fever),  and 
is  associated  with  marked  weakness,  numbness,  rapid  pulse,  profuse  per- 

'  Compare  Glaser,  "  Ueber  Vorkommen  und  Ui-sachen  abnormale  niedriger  Korpertem- 
peraturen,  Inauguraldissertation,"  Bern,  1878;  and  Janssen-Quincke,  "  Ueber  subnormale 
Korpertemperaturen,"  D.  Arch.  J.  klin.  Med.,  vol.  liii.,  p.  247. 


76 


DETERMINATION  OF  THE  BODY  TEMPERATURE. 


spiration,  etc.  The  crisis  in  pneumonia  is  sometimes  mistaken  for  a 
collapse.  The  pulse,  however,  in  the  latter  is  weak  and  rapid  ;  whereas 
in  the  former  it  remains  of  good  strength,  and  diminishes  in  frequency 
proportionally  to  the  fall  in  the  temperature.  Collapse  is  a  precursor 
of  death.  The  accompanying  symptoms  are  usually  attributed  to  crit- 
ical weakness.     Vasomotor  inhibition  may  also  be  a  factor. 

4.  Sometimes  after  a  severe  hemorrage;  in  chronic  heart  and  lung 
diseases,  which  lead  to  imperfect  aeration  of  the  blood  (cyanosis),  and 


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; 

.". 

,'\ 

< 

,•" 

,■' 

.-■ 

\ 

/ 

i 

1 

I 

1 

1 

1 

• 

1 

1 

-'"'■^ 

1 

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1 

1 

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1 

1 

Fig.  32.— Pulse,  temperature,  and  respiration  in  collapse. 


therefore  to  insufficient  oxidation  of  the  various  processes  throughout  the 
body  ;  further,  in  chronic  wasting -diseases  (carcinoma  of  the  esophagus), 
where  metabolism  is  reduced  to  a  minimum;  m  sclerema  neonatorum; 
and  finally  in  mentally  afflicted  patients,  especially  of  the  melancholic 
type. 

Prolonged  subnormal  temperatures  accompanying  such  conditions  as 
are  mentioned  above  always  indicate  a  grave  diminution  of  the  metab- 
olism or  some  equally  serious  disturbance  of  the  heat  regulation. 


CHARACTER   OF  THE  RESPIRATION.  11 


CHARACTER  OF  THE  RESPIRATION. 

FREQUENCY  OF  RESPIRATION  UNDER  PHYSIOLOGIC 

CONDITIONS. 

Hutchinson  quotes  the  normal  respiratory  frequency  in  adults  as 
between  16  and  24,  or  about  1  to  every  4  pulse-beats.  Quetelet  gives 
for  the  newborn  an  average  of  44,  for  the  iive-year  old  child  26,  respi- 
rations to  the  minute. 

It  is  a  good  plan  to  count  the  respirations  while  apparently  feeling 
the  pulse,  because  the  patient's  attention  might  otherwise  modify  the  rate. 
For  greater  accuracy,  the  number  of  respirations  should  be  counted  dur- 
ing an  entire  minute. 

Physical  exertion  will  increase  the  rate  of  respiration  ;  lying  down 
or  sleep  will  diminish  it  somewhat.  A  stomach  distended  by  food 
and  drink  increases  the  rapidity  of  the  respiration  because  the  dia- 
phragm excursion  is  thereby  somewhat  limited.  Irritation  of  the  skin 
may  increase  or  diminish  the  rate  of  respiration.  Psychic  or  sensory 
impressions,  movements,  clearing  the  throat,  eating,  drinking,  or  smok- 
ing will  alter  the  rapidity  of  the  respiration.  Before  considering  that 
a  certain  rate  of  respiration  is  pathologic  we  must  therefore  bear  in  mind 
all  these  physiologic  variations. 

NORMAL  TYPES  OF  BREATHING. 

The  distention  of  the  lungs  with  air  takes  place  partly  by  means  of 
raising  the  ribs  and  sternum  and  rotating  the  former  outward  and  up- 
ward, and  partly  by  depressing  the  diaphragm.  Although  in  every- 
body both  these  factors  take  part  in  the  movement  of  respiration,  yet 
one  or  the  other  is  apt  to  be  more  prominent,  thus  producing  a  more 
costal  or  a  more  diaphragmatic  (i.  e.,  abdominal)  type  of  breathing. 
Women  commonly  breath  costally  ;  men,  costo-abdominally.  This  selec- 
tion, which  seems  to  depend  upon  the  formation  of  the  chest,  is  naturally 
very  suitable  during  pregnancy,  when  the  diaphragmatic  excursions  are 
interfered  with.     A  child's  breathing  is  essentially  costal. 

PATHOLOGIC  VARIATIONS  IN  THE  TYPE  OF 
RESPIRATION. 

Either  the  costal  or  the  diaphragmatic  element  may  be  implicated 
and  so  alter  the  type  of  respiration. 

I/imitation  of  Diaphragmatic  Breathing. — The  excursions 
of  the  diaphragm  may  be  impeded  by  some  mechanical  interference  with 
its  descent — e.  g.,  by  a  paralysis  of  its  muscular  structure  ;  by  an  ab- 
normal flattening  of  its  vault  (in  certain  types  of  emphysema) ;  by  pain- 
ful breathing ;  by  any  increase  in  the  abdominal  contents — i.  e.,  preg- 
nancy, meteorism,  abdominal  tumors,  ascites.  Any  inflammation  in  the 
vicinity  of  the  diaphragm — e.  g.,  pleurisy,  pericarditis,  peritonitis — will 


78  CHARACTER   OF  THE  RESPIRATION. 

limit  the  excursions  of  the  diaphragm,  partly  on  account  of  the  pain 
and  partly  from  a  slight  paralysis  of  the  muscle  fibers  of  the  dia- 
phragm (especially  in  diffuse  peritonitis,  on  account  of  the  disturbances 
in  the  circulation  following  the  inflammation).  Actual  diaphragmatic 
paralysis  occurs  in  viultiple  neuritis,  in  progressive  muscular  atrophy,  etc. 
In  any  of  the  above  instances  the  costal  breathing  may  appear  to  be  in- 
creased at  the  expense  of  the  abdominal  effort. 

I/imitation  of  Costal  Breathing-. — Costal  respiration  may  be 
interfered  with  in  a  mechanical  way  by  extensive  ossification  of  the  costal 
cartilages  (ankylosis  of  the  articulations  of  the  ribs  in  arthritis  deformans, 
etc.).  Under  such  conditions  the  costal  type  in  women  and  children  and 
the  costo-abdominal  type  in  men  may  become  purely  abdominal. 

DIAPHRAGM  PHENOMENON  AND  ALLIED  APPEAR- 
ANCES (LITTEN'S  SIGN), 

Litten  ^  called  attention  to  this  almost  forgotten  sign,  analyzed  a  series  of  cases, 
determined  its  practical  significance,  and  named  it  the  "  diaphragm  phenomenon." 
(Plate  4).  It  consists  of  a  horizontally  placed  shadow  observed  with  inspiration  near 
the  lower  pulmonary  edge,  most  constantly  anterolaterally,  but  occasionally  running 
in  a  ring  around  the  whole  chest.  This  shadow  seems  to  slip  downward,  corresponding 
to  the  inspiratory  descent  of  the  pulmonary  margin,  as  shown  by  percussion.  It  is 
very  fittingly  named,  because,  as  a  matter  of  fact,  it  is  the  most  distinctly  visible 
evidence  of  the  depression  of  the  diaphragm.  Normally,  the  moving  shadow 
begins  above  in  the  sixth  intercostal  space,  descends  with  superficial  inspiration 
one  to  one  and  one-half  intercostal  spaces,  and  with  deep  inspiration  two  to  three 
spaces.  It  intersects  the  ribs  at  an  acute  angle.  To  show  it  most  distinctly,  the 
patient  should  lie  as  flat  as  possible  (without  extra  support  for  his  head)  and  with 
his  feet  toward  the  window,  so  that  the  region  between  the  sixth  rib  and  the  costal 
margin  is  lighted  obliquely.  The  observer  should  stand  between  the  patient's  feet 
and  the  window,  with  his  eye  at  a  distance  of  3  or  4  feet  and  at  an  angle  of  about 
45  degrees  with  the  lower  thorax.  Provided  the  patient  breathes  deeply  and  the  light, 
although  not  necessarily  strong,  slants  sufiiciently,  the  phenomenon  is  generally  plain. 
Even  a  candle  light  may  be  sufiicient,  but  a  very  difluse  light  is  unfavorable.  There 
is  no  corresponding  expiratory  sign.  The  flattening  of  the  lower  intercostal  spaces 
fi-om  below  upward  during  expiration  is  of  quite  different  significance. 

The  explanation  of  Litten' s  sign  is  comparatively  simple.  As  the  diaphragm 
in  its  descent  begins  to  peel  off  from  the  thorax  and  both  widens  and  deepens  the 
complimentary  pleural  sinus,  it  exerts  a  suction  upon  the  intercostal  spaces  just 
below  the  margin  of  the  lung.  This  produces  the  shadow.  It  is  evident  that  no 
analogous  process  will  occur  during  expiration,  because  the  elevation  of  the 
diaphragm  is  regulated  only  by  the  elastic  retraction  of  the  lung.  In  health, 
particularly  in  lean  individuals,  the  diaphragm  phenomenon  is  a  nearly  constant 
•appearance.  Marked  development  of  fat  or  muscle  or  edema  of  the  thoracic  wall 
will  prevent  its  appreciation,  and  even  under  perfectly  physiologic  conditions  it 
may  be  sought  for  in  vain.  Its  presence  proves  that  at  the  particular  place  where 
it  is  observ'ed  the  diaphragm  and  the  lung  lie  against  the  thoracic  wall,  both  freely 
movable;  its  absence  points  to  the  opposite  conclusion.  Therefore  it  cannot  be 
made  out  opposite  pneumonic  infiltrations  nor  in  those  places  in  pleurisy  where  the 
exudation  is  situated,  or  where  the  lung  is  adherent  to  the  chest,  nor  in  hydro-  or 
pneumothorax,  etc.  Litten  has  called  attention  to  the  fact  that  this  sign  is  of  great 
value  in  differentiating  an  empyema  from  a  subphrenic  abscess;  it  is  absent  in  the 

"^  DeuUch.  med.  Woch.,  1892,  No.  13.  Das  Zwerchfellphanomen  und  seine  Bedeu- 
tung  fill-  die  Praxis,  Deutsche  Aerztezeitung,  1895,  No.  1.  Verhandl,  dea  Cony.f.  inn. 
Med.,  1895. 


PLATE  4. 


V  P'i}K^"u«'^  P^P°°^f"0P  (Litten's  sign),  from  a  patient  with  fibroid  phthisis  of  left  Inn?  fXew 
lorK  Lity  Hospital),     ihe  linear  shadow  has  been  emphasized  in  the  reproduction  of  the  photo- 

«^^i:  -f'"'',.^'/'^'"''''^"-— ^'nte  the  height  of  the  shadow  and  the  slight  concavity  of  the  abdomen 
correspondini,'  to  the  respiratory  phase. 

-•  a'^''''''""  -'^««/J"'a<''-'«  — ^'at■e  the  descent  of  the  linear  shadow  and  the  slight  change  of  con- 
tour ot  abdomen  corresponding  to  the  respiratory  phase. 

3.  Deep  Impiratiou.—yote  the  further  descent  of  the  linear  shadow  and  the  rigid  abdomen 
corresponding  to  the  respiratory  phase. 

Although  the  arti.st  has  intensified  the  shadow  in  the  reproduction,  the  excursion  of  tlie  rio-ht 
lung  and  right  side  of  the  diaphragm  were  so  pronounced  in  this  patient  that  the  distance 
oetween  the  shadows  in  the  extreme  positions  of  respiration  was  greater  than  has  been  repre- 
sented. The  patient  s  left  lung  was  practically  useless  :  hen<.'e  the  abnormal  extent  of  the  right 
lung  s  excursion.  " 


.    INSPIRATORY  RETRACTION  OF  THE  CHEST.  79 

former  but  present  in  the  latter.  ^  Under  some  conditions  the  diaphragm  phenomenon 
may  facilitate  a  distinction  between  pneumothorax  and  diaphragmatic  hernia.  A 
broken  or  irregular  shadow  is  said  to  point  to  partial  adhesions  of  the  diaphragm  to 
the  thorax-wall.  The  extent  of  the  diaphragm  phenomenon  will  furnish  some  idea 
as  to  the  excursion  of  the  lung  in  emphysema  and  phthisis.  Paralysis  of  pai-ts  sup- 
plied by  the  phrenic  nerve  is  associated  with  an  absence  of  the  diaphragm  phenom- 
enon. Since  this  sign  is  by  no  means  absolutely  constant  in  healthy  individuals, 
it  is  evident  that  its  absence  upon  one  side  alone  is  much  more  important  than  upon 
both  sides. 

We  must  be  careful  not  to  confuse  the  diaphragm  phenomenon  with  two  other 
conditions  which  exhibit  shadows  in  the  same  area — viz.,  the  visible  depression  of 
the  lower  ribs  with  expiration  and  the  retraction  of  the  lower  intercostal  spaces 
with  inspiration. 

The  former,  being  expiratory,  is  easily  differentiated  from  the  diaphragm  phe- 
nomenon ;  but  the  latter,  being  inspiratory,  is  more  difficult  to  distinguish.  The 
lower  intercostal  spaces  situated  along  the  attachment  of  the  diaphragm  are  under 
a  positive  intra-abdominal  pressure  when  the  latter  is  in  a  position  of  expiration, 
whereas  they  are  exposed  to  a  negative  intrathorax  pressure  when  the  diaphragm 
is  depressed  by  inspiration,  and  therefore  they  are  retracted  in  the  same  way  as  the 
diaphragm.  The  physiologic  retraction  of  the  lower  intercostal  spaces  as  a  whole 
will  thus  present  a  descending  shadow  easily  to  be  confounded  with  the  Litten  sign, 
but  a  careftil  observation  will  detect  the  difference.  The  shadow  of  the  Litten  sign 
is  linear,  passing  through  the  intercostal  spaces  as  a  line,  while  the  shadow  of  the 
physiologic  retraction  of  the  intercostal  spaces  is  more  diffiise,  each  space,  one  after 
another,  becoming  shaded  in  toto.  Very  often  also  the  descending  character  of  the 
inspiratory  retraction  cannot  be  recognized  at  all,  because  the  diaphragm  in  its  con- 
traction exerts  a  suction  upon  those  intercostal  spaces  from  which  it  has  not  yet 
separated.  A  further  distinction  is,  that  an  exactly  opposite  movement  from  below 
upward  takes  place  during  expiration — i.  e. ,  an  expiratory  bulging.  This  does  not 
occur  in  the  diaphragm  phenomenon. 

The  depression  in  stenosis  of  the  air  passages,  and  the  essentially  identical 
peripneumonic  retraction,  differ  from  this  physiologic  retraction  in  that  the  appear- 
ances are  very  much  more  marked  in  the  former,  affect  the  ribs  as  well,  and  are  not 
confined. to  the  intercostal  spaces  in  the  territory  of  the  diaphragm. 

ASYMMETRIC  RESPIRATION  AND  PATHOLOGIC    INSPI- 
RATORY RETRACTION  OF  THE  CHEST. 

An  obstruction  to  respiration  which  affects  but  one  lung  will  cause 
asymmetric  breathing ;  the  diseased  side  will  make  a  less  extensive  ex- 
cursion and  will  also  lag  somewhat  behind  the  healthy  side.  The  con- 
ditions which  may  give  rise  to  such  a  unilateral  limitation  of  breathing 
are :  the  various  types  of  pulmonary  infiltration  (pneumonia,  phthisis, 
tumors) ;  pleurisy  with  effusion  or  pleurisy  merely  with  the  formation 
of  fibrous  bands  and  tough  adhesions  ;  and  pericarditis  with  -effusion. 
Asymmetric  respiratory  excursions  may  be  appreciated  by  inspection, 
but  they  will  oftentimes  be  much  better  appreciated  by  palpation.  With 
one  hand  placed  upon  each  side,  the  examiner  can  at  the  same  time 
appreciate  an  asymmetry  of  the  chest  contour.  The  chest,  half  of  whose 
mobility  is  diminished,  may  be  either  expanded  or  contracted,  as  ex- 
plained upon  p.  34  et  seq. 

Compare  p.  86  e^  seq.  for  the  occurrence  of  inspiratory  retraction  in 

'  It  is  well,  however,  not  to  lay  too  much  stress  upon  this  statement,  because,  althoug:h 
cases  have  been  demonstrated,  we  can  as  yet  scarcely  be  sure  that  the  diaphragmatic 
movement  is  not  sometimes  impeded  by  a  subphrenic  abscess. 


r 


80  CHARACTER   OF  THE  RESPIRATION. 

the  jugulum  (suprasternal  fossa),  epigastrium,  and  flanks  with  stenosis 
of  the  upper  air  passages. 

But  similar  local  retractions  occur  without  any  stenosis  over  parts  of 
the  lung  area  where  the  normal  inspiratory  distention  of  the  lung  is 
prevented  by  atelectasis  or  by  infiltration.  This  retraction,  especially 
when  it  occurs  quickly  and  violently  (as  with  dyspnea),  is  due  to  the 
variation  in  the  inspiratory  negative  pressure  within  the  interior  of  the 
chest,  which  draws  in  the  more  expansible  portions  of  the  lung  along 
with  the  overlying  portions  of  the  chest  wall  under  the  influence  of  the 
external  atmospheric  pressure.  AVe  see  this  particularly  well  marked 
in  the  catarrhal  pneumonia  of  children,  whose  soft  and  more  flexible 
chests  favor  the  retraction.  It  is  called  a  " peripneumonic  retraction  " 
or  a  " pjerijmeumonic  groove."  It  is  usually  situated  in  the  lateral  and 
anterior  region  of  the  chest  along  the  lower  lung  border,  even  when  the 
pneumonia  is,  as  usual,  situated  in  the  back.  This  probably  depends 
upon  the  fact  that  the  stiif  infiltration  located  in  the  back  interferes 
mechanically  to  a  certain  extent  with  the  excursions  of  the  lung  margins 
at  the  sides  and  in  the  front,  and  that  the  anterior  and  lateral  portions 
of  the  chest  are  especially  flexible.  Peripneumouic  retractions  are, 
however,  sometimes  observed  posteriorly,  near  the  inferior  pulmonary 
margin.  The  direct  pull  of  the  diaphragm,  just  as  in  stenosis  of  the 
upper  air  passages,  may,  in  addition  to  these  mechanical  factors,  help  to 
create  a  peripneumouic  depression  (see  p.  87).  The  epigastrium  and 
the  jugulum,  too,  may  be  retracted  in  a  similar  way  in  pneumonia,  so  that 
in  small  children  the  diagnosis  of  croup  is  not  infrequently  suggested. 
The  inspiratory  stridor,  and  hoarseness  of  the  voice  and  of  the  cough  in 
the  latter  ordinarily  facilitate  a  distinction,  Peripneumouic  retraction 
must  not  be  confounded  with  the  normal  inspiratory  depression  of  the 
lower  intercostal  spaces,  the  explanation  and  differentiation  of  which 
have  been  discussed  upon  page  7S  et  seq. 

D.  Gerhardt^  has  recently  called  attention  to  another  cause  of  inspirator}'  re- 
traction of  the  lower  thoracic  margin.  Besides  the  diaphragm's  well-known  eflfect 
upon  the  inferior  surface  of  the  lung,  Ducherme  demonstrated  that  by  resting  on 
the  abdominal  contents  and  moving  over  the  parts  contained  in  its  vault,  as  over  a 
roller,  it  has  in  inspir.-ition  the  action  of  lifting  the  margin  of  the  thorax.  If  this 
decided  elevation  of  the  lower  ribs  is  prevented  by  immobility  of  the  costal  articula- 
tions or  by  the  horizontal  jjosition  of  the  ribs,  as  in  some  emphysematous  chests,  or 
by  the  lack  of  any  firm  point  of  attachment  of  the  abdominal  contents  in  enteroptosis, 
then  during  inspiration  the  contraction  of  the  diaphragm  will  depress  the  chest- 
wall  inward. 

ABNORMALITIES    IN    FREQUENCY    AND    RHYTHM    OF 
THE    RESPIRATION  fnot  Including  Dyspnea). 

Alterations  in  the  frequency  of  respiration  depend  for  the  most  part 
upon  difficulties  of  pulmonary  aeration  or  upon  increased  demands  upon 
the  lung,  and  will  therefore  be  considered  and  explained  with  the  symp- 
tom-complex of  dyspnea  in  the  following  chapter.     Only  in  very  rare 

^Zeit.f.  klin.  Med.,  1896,  vol.  xxx.,  Nos.  1  and  2. 


ABNORMALITIES  IN  FREQ  UENCY  AND  RHYTHM  OF  RESPIRA  TION.  81 

instances  are  changes  in  the  frequency  of  breathing  independent  of 
dyspnea. 

To  this  group  belongs  the  diminution  of  respiratory  frequency 
(oligopnea)  found  in  certain  conscious  states,  especially  in  severe  brain 
affections  (meningitis,  hemorrhage,  or  in  tumors  of  the  brain) ;  uremia ; 
diabetic  coma ;  severe  infections ;  some  cases  of  poisoning ;  and  in  a 
similar  way  in  the  final  agony.  Irregularity  of  the  respiration  may 
be  noted  as  well  in  any  one  of  these  conditions.  Unquestionably 
these  disturbances  are  distinctly  dependent  upon  an  alteration  in  the 
function  of  the  respiratory  center. 

Either  one  of  two  very  characteristic  types  of  pathologic  breathing, 
each  one  associated  with  a  change  in  the  rhythm,  may  arise  under  ex- 
actly similar  conditions  instead  of  the  slowed  respiration  just  mentioned. 
These  are  the  so-called  Biot's  or  meningeal  and  the  Cheyne-Stokes 
respiration. 

Biot's  respiration,  especially  common  in  meningitis,  may  also 
occur  in  other  cerebral  disorders  and  in  other  grave  general  conditions. 
It  is  characterized  by  very  decided  pauses  in  the  breathing,  which  last 
from  several  seconds  to  half  a  minute  or  longer.  They  are  more  or  less 
periodic,  but  at  times  repeat  themselves  irregularly.  It  is  a  phenomenon 
of  grave  prognostic  significance. 

Cheyne-Stokes  respiration  is  characterized  by  similar  long 
pauses  in  the  breathing.  It  differs,  however,  from  the  above  by  the  fact 
that  the  breathing  begins  very  slowly  and  superficially  after  the  pause, 
gradually  increases  in  depth  and  intensity  to  a  maximum,  diminishes 
again,  and  finally  stops  entirely,  thus  producing  another  respiratory 
pause.  It  is,  therefore,  a  distinctly  periodic  type  of  respiration.  It  occurs 
under  similar  conditions  to  the  Biot's  meningeal  respiration,  especially 
in  grave  affections  of  the  brain,  of  the  respiratory  and  of  the  circulatory 
organs,  and  quite  frequently  in  arteriosclerosis  and  chronic  nephritis. 
Although  more  frequently  observed  in  the  unconscious,  it  is  not  uncom- 
mon even  when  consciousness  is  maintained,  especially  in  patients  with 
chronic  respiratory  or  circulatory  disorders.  In  these  affections  con- 
sciousness oftentimes  oscillates  with  the  respiration,  is  periodically 
obliterated  during  the  pause,  and  returns  again  when  respiration  is 
resumed.  There  are  other  phenomena  more  or  less  characteristic.  During 
the  pause  in  the  breathing  the  rate  of  the  pulse  may  be  decidedly  slowed, 
its  tension  may  be  altered,  and  the  pupils  may  be  contracted.  Very  often, 
though  by  no  means  always,  patients  have  a  subjective  sense  of  dyspnea 
during  the  period  of  increasing  respiration  ;  and  if  unconscious  during 
the  pause,  they  are  awakened,  as  they  express  it,  by  a  sensation  of  suf- 
focation or  dyspnea.  Cyanosis  usually  accompanies  the  onset  of  the 
•dyspnea,  and  it  may  sometimes  even  increase  with  the  augmentation  of 
the  breathing.  With  some  patients  Cheyne-Stokes  respiration  occurs 
only  during  sleep.  Medicinal  doses  of  morphin  usually  intensify  the 
phenomenon  and  may  even  originate  the  condition.  Generally  speaking 
the  prognostic  significance  is  very  grave,  although  not  invariably  fatal. 
According  to  the  severity  of  the  causal  condition,  the  symptom  is  either 


82  CHARACTER   OF  THE  RESPIRATION. 

a  transitory  sign  which  rapidly  disappears,  or  else  one  directly  preceding; 
death.  Only  in  cardiac  or  renal  disease  has  it  ever  been  observed  to 
persist  for  some  months. 

The  explanation  of  Cheyue-Stokes  respiration  is  still  not  wholly 
agreed  upon.  It  is  indisputable  that,  like  meningeal  breathing,  it  de- 
pends upon  a  diminished  excitability  of  the  respiratory  center.  This 
seems  to  be  the  only  part  of  the  explanation  beyond  a  doubt.  Traube's 
original  theory  assumed  that  the  symptom  arises  when  the  excitability 
of  the  respiratory  center  is  so  decidedly  diminished  by  the  insufficient 
supply  of  oxydized  blood  resulting  from  the  circulatory  disturbance  that,, 
at  a  certain  moment  coinciding  with  the  first  breathing  pause,  there  is  no 
longer  a  sufficient  physiologic  stimulus  to  arouse  the  respiratory  move- 
ments. With  the  cessation  of  respiration  the  blood  becomes  still  more- 
decidedly  venous.  This  irritates  the  respiratory  center  intensely,  so  that,, 
despite  its  diminished  susceptibility,  breathing  begins  again.  This  in 
turn  diminishes  the  venous  character  of  the  blood,  and  the  breathing 
gradually  becomes  weaker  in  proportion  to  the  oxidation  of  the  blood. 

Traube's  explanation  does  not  make  it  very  clear  why  the  breathing 
increases  gradually  nor  why  the  second  respiration  is  stronger  and  deeper 
than  the  first.  For  as  soon  as  breathing  begins,  the  venous  character  of  the 
blood  must  immediately  lessen  the  respiratory  center's  irritation,  and  so 
the  second  respiration  should  be  weaker.  Traube  explains  that  the 
first  breath  is  so  diminutive  that  it  cannot  afPect  the  venous  character 
of  the  blood,  and  so  cannot  lessen  the  irritation  to  the  respiratory  center  ;. 
but  that,  on  the  contrary,  the  irritation  increases  despite  the  return  of 
breathing,  until  it  (the  irritation)  reaches  a  maximum.  Such  a  hypothesis 
will  explain  the  peculiarity  that  the  patient  appears  most  cyanotic  and 
complains  most  of  the  subjective  sensation  of  dyspnea  during  the  period 
of  increasing  respiration.  Another  objection  to  Traube's  explanation 
is  that  after  an  improved  supply  of  oxygenated  blood  has  once  restored 
the  respiratory  center's  normal  excitability,  there  is  no  apparent  reason 
for  the  breathing's  fading  away  again.  If  we  believe  with  Traube  that 
the  respiratory  center's  asphyxia  is  the  sole  cause  of  its  diminished  ex- 
citability, the  objection  cannot  be  answered.  If,  however,  we  regard 
the  diminished  excitability  as  entirely  or  partially  independent  of  the 
circulatory  disturbance  and  more  self-dependent,  the  objection  loses  its 
force.  Evidently,  then,  if  the  blood  is  better  aerated,  the  intense  irri- 
tant to  the  respiratory  center  will  be  removed,  although  the  latter's 
sensibility  has  not  been  improved.  Hence,  the  breathing  will  gradually 
diminish  in  frequency  in  proportion  to  the  improvement  in  the  oxidation 
of  the  blood. 

With  these  modifications,  Traube's  theory  seems  plausible  enough. 
Partly  on  account  of  the  difficulties  mentioned  above,  numerous  other 
'explanations  of  Cheyne-Stokes  respiration  have  been  advanced.  We 
will  only  mention  two  of  these  which  are  the  most  generally  known — 
viz.,  Filehne's  and  Rosenbach's. 

Filehne's  hypothesis,  beginning  with  the  pause  in  respiration,  as- 
sumes that  the  venous  condition  of  the  blood  irritates  the  vasomotor 


DYSPNEA.  83 

centers  and  so  produces  a  spasm  of  the  cerebral  vasomotors.  There- 
fore the  respiratory  center,  whose  irritability  has  already  been  reduced, 
becomes  anemic.  This  anemia  acts  as  a  further  irritant  to  respiration. 
As  soon  as  the  breathing  has  again  oxygenated  the  blood  sufficiently,  the 
vasomotor  spasm  vanishes,  but  the  respiratory  stimulus  is  not  sufficient 
to  induce  breathing,  hence  the  pause  reappears.  Filehne's  theory  is  more 
complicated  than  Traube's ;  the  same  objections  apply  to  it ;  and  more 
accurate  investigations  seem  to  have  completely  disproved  any  such  re- 
lationship between  the  vasomotor  system  and  Cheyne-Stokes  breathing. 

Rosenbach  maintains  that  the  periodicity  of  this  type  of  breathing 
results  simply  from  an  abnormal  fatigue  of  the  respiratory  center,  but 
that  this  fatigue  should  not  be  confused  with  a  diminished  irritability. 
The  center  is  active  for  a  time,  works  against  a  gradually  increasing 
difficulty,  finally  stops  entirely,  and  begins  its  activity  again  only  after 
the  pause  has  to  some  extent  recuperated  its  powers.  It  seems  doubt- 
ful whether  we  can  assume  that  such  recuperation  of  the  respiratory 
center  occurs  during  the  breathing  pause,  while  the  respiratory  irritant 
persists.  The  laws  of  fatigue  in  the  central  nervous  system  are,  how- 
ever, so  imperfectly  understood  that  this  objection  to  Rosenbach's  ex- 
planation is  not  sufficient  to  make  us  reject  it  entirely.  At  all  events  it 
has  the  advantage  of  depending  upon  the  same  law  that  applies  to  the 
other  organs — that  periodic  activity  usually  arises  as  a  result  of  fatigue. 

Most  types  of  increased  respiratory  frequency  (polypnea)  necessitate 
an  increased  demand  upon  the  respiratory  activity,  and  will  therefore  be 
discussed  in  the  following  section  on  dyspnea.  We  should,  however, 
mention  the  fact  that  increased  frequency  of  breathing  may  arise  from 
purely  nervous  causes — e.  g.,  in  hysteric  people  and  in  certain  cases 
of  cerebral  disease. 

DYSPNEA, 

The  term  dyspnea  applies  to  a  large  group  of  variations  in  respira- 
tory activity,  which,  in  spite  of  considerable  diversity  in  detail,  have 
this  in  common,  that  they  serve  to  promote  the  object  of  breathing — 
i.  e.,  the  proper  oxidation  of  the  blood — despite  all  kinds  of  obstacles. 
On  this  account,  the  breathing  of  dyspnea  is  generally  increased  in 
frequency  or  in  depth.  The  obstructions  to  breathing  are,  however, 
sometimes  insurmountable,  so  that  neither  a  frequent  nor  a  deep  type 
of  breathing  is  possible — e.  g.,  in  marked  stenosis  of  the  air  passages. 
Therefore  quickened  breathing  must  not  be  considered  absolutely 
the  distinction  of  dyspnea.  The  only  definition  which  will  apply 
clinically  to  all  cases  is  that  dyspnea  is  an  increased  respiratory  exer- 
tion produced  by  obstruction  to  breathing  or  by  increased  demands  upon 
the  blood-oxidizing  process.  This  does  not  coincide  with  the  explana- 
tion frequently  given,  that  dyspnea  is  identical  witli  quickened  breath- 
ing, which  is  unquestionably  inaccurate  from  the  clinical  standpoint,  for 
not  every  case  of  quickened  respiration  is  dyspnea,  nor  is  the  breath- 
ing quickened  in  every  case  of  dyspnea.  As  we  shall  see,  there  are 
types  of  dyspnea  with  quickened  and  others  with  retarded  respiration. 


84  CHARACTER   OF  THE  RESPUiATION. 

To  conform  with  the  definition  cited  above  and  to  avoid  any  misunder- 
standing, it  is  advisible  to  apply  the  terms  polypnea  to  quickened  and 
oligopnea  to  retarded  breathing. 

The  word  dyspnea  is,  however,  employed  in  still  another  significa- 
tion to  express  the  subjective  sensation  of  oppressed  breathing  possessed 
by  patients  with  objective  dyspnea.  Ordinarily,  subjective  and  objec- 
tive dyspnea  go  hand  in  hand ;  but  exceptions  do  occur.  For  under 
certain  conditions,  despite  the  presence  of  some  obstruction  which  is 
responsible  for  an  objective  dyspnea,  breathing  may  continue  so  satis- 
factorily that  the  patient  does  not  experience  any  shortness  of  breath, 
because  the  aeration  of  the  blood  proceeds  as  completely  as  ever,  owing 
to  the  modification  of  the  respiratory  movement.  Again,  despite  a  very 
pronounced  objective  dyspnea  which  is  by  no  means  adequate  for  blood- 
aeration,  as  evidenced  by  the  accompanying  cyanosis,  a  patient  may  have 
become  so  accustomed  to  it  (see  93)  or  his  sensorium  may  be  so  be- 
numbed that  he  has  no  appreciation  of  subjective  dyspnea.  It  is  a  very 
benevolent  provision  of  nature  that  in  the  death  agony,  where  the  breath- 
ing is  difficult,  the  brain  becomes,  as  it  were,  so  narcotized  by  the  car- 
bon dioxid  intoxication  that  it  no  longer  appreciates  the  sensation  of  the 
struggle  for  breath.  Conversely,  the  objective  dyspnea  may  be  almost 
or  entirely  overshadowed  by  the  intense  ''air  hunger."  Examples  are 
the  so-called  "  precordial  terror "  of  melancholies,  which  (because  the 
individual  locates  the  sense  of  anxiety  in  the  chest)  we  prefer  to  con- 
sider as  a  purely  subjective  dyspnea.  Again,  some  nervously  organized 
individuals  will  complain  of  a  transitory  desire  to  draw  an  extra  deep 
breath  ;  they  have  the  sensation  of  dyspnea  without  any  evidence  of 
obstructed  l3reathing.  In  other  words,  it  is  a  purely  cerebral  phenom- 
enon, of  which  they  instinctively  try  to  rid  themselves  by  taking  a  long 
breath. 

Hence,  it  is  important  to  differentiate  sharply  betw^een  objective 
dvspnea — i.  e.,  difficult  and  hence  modified  breathing — on  the  one 
hand,  and  subjective  dyspnea,  or  the  sensation  of  lack  of  air,  on  the 
other.  Sometimes  breathing  modified  by  dyspnea  will  be  accompanied 
by  subjective  dyspnea,  but  at  other  times  this  is  not  the  case. 

Cyanosis,  like  subjective  dyspnea,  is  not  always  proportional  to  the 
degree  of  objective  dyspnea,  for  in  one  case  the  objective  dyspnea  may 
be  sufficient  to  regulate  the  proper  aeration  of  the  blood  and  to  bring 
conditions  back  more  or  less  to  a  normal  standpoint ;  whereas  in  other 
cases  this  is  not  possible  for  the  organism. 

The  occurrence  of  decided  objective  dyspnea  witliout  cyanosis  is  a  clinical  proof 
that  the  intensity  of  the  respiratory^  movement  does  not  depend  exclusively  upon 
the  grade  of  aeration  of  the  blood,  but  may  be  produced  directly  by  some  ob- 
struction to  breathing  without  the  appearance  of  cyanosis.  A  similar  proof  is  flir- 
nished  by  the  dyspnea  which  follows  physical  exertion.  This  in  no  way  depends 
upon  an  "excess  of  carbon  dioxid  nor  upon  a  deficiency  of  oxygen  in  the  blood  so  long 
as  the  breathing  and  the  circulation  remain  sufficient. 

To  aerate  the  blood  properly  under  adverse  circumstances  the  or- 
ganism avails  itself  of  an  increase  either  in  the   frequency  or  in  the 


DYSPNEA.  85 

depth  of  the  respiration.  With  an  increase  in  the  depth  of  the  indi- 
vidual breaths,  the  frequency  may  be  either  accelerated,  normal  or 
slowed.  There  are,  therefore,  various  types  of  dyspnea,  but  generally 
we  find  that  it  modifies  the  normal  breathing  in  that  way  which  seems 
best  adapted  to  meet  the  existing  deficiencies. 

In  the  following  we  shall  characterize  the  kinds  of  objective  dyspnea 
occurring  in  different  diseases. 

VARIOUS  TYPES  OF  DYSPNEA. 

1.  Dyspnea  Caused  by  Painful  Breathing-. — Patients  are  not 
infrequently  prevented  from  drawing  a  deep  breath  on  account  of  the 
pain  associated  with  each  respiratory  movement  in  certain  pulmonary, 
and  especially  pleural,  disorders,  in  affections  of  the  intercostal  muscles 
(rheumatism,  trichinosis)  and  of  the  diaphragm  and  its  vicinity  (perito- 
nitis). The  breathing  then  becomes  superficial  and,  to  satisfy  the  demand, 
more  frequent — in  other  words,  dyspnea  results.  In  this  instance  the 
obstruction  is  functional,  not  mechanical.^ 

2.  Dyspnea  Due  to  a  Diminution  in  the  Breathing  Surface 
of  the  I/Ung  or  to  a  Mechanical  I^imitation  of  the  Respira- 
tory Bxcursions  of  the  I/Ung. — The  two  factors  ordinarily  occur 
together.  Under  this  heading  are  included  all  affections  of  the  pul- 
monary parenchyma  which  lead  to  a  diminution  of  the  air  contents  of 
the  lung — i.  e.,  all  sorts  of  pulmonary  infiltration  ;  all  conditions  which 
limit  the  capacity  of  the  thorax,  such  as  pleuritic  effusions,  pneumo- 
tliorax,  intrathoracic  tumors,  lateral  curvature,  upward  displacement  of 
the  diaphragm  ;  further,  all  conditions  which  decrease  the  respiratory 
excursions,  such  as  brown  induration  and  emphysema  (with  regard  to 
emphysema,  see  p.  90  et  seq.),  as  well  as  paralyses  and  spasms  of  the 
respiratory  muscles. 

In  any  of  the  above  conditions  each  breath  aerates  the  lung  less 
efficiently  than  normally,  with  a  resulting  dyspnea  and  increased  fre- 
quency of  respiration.  Under  some  conditions  the  demand  for  air  will 
be  completely  satisfied,  so  that  in  spite  of  the  interference  with  respira- 
tion neither  cyanosis  nor  any  sense  of  dyspnea  (subjective)  ensues. 
Under  other  conditions  the  compensation  is  not  always  complete,  es])e- 
cially  when  any  increased  demand  for  air  arises,  so  that  physical  exer- 
tion will  occasion  cyanosis  and  a  subjective  sense  of  dyspnea. 

If  such. an  interference  with  breathing  is  unilateral — e.g.,  infiltration 
or  a  pleuritic  exudation — the  dyspnea  can  be  partially  overcome  by 
deeper  breathing  of  the  healthy  side  (vicarious  respiration),  as  well  as 
by  the  increased  frequency  of  respiration. 

(See  p.  80  et  se,q.  concerning  local  depressions  of  the  thorax  in  this 
variety  of  respiratory  interference.) 

3.  Dyspnea  Due  to  General  Circulatory  Disturbances. — 
Non-compensated  valvular  lesions  may  be  regarded  as  a  type.     Here 

'  In  this  connection  the  editors  wish  to  call  attention  to  a  type  of  dyspnea  associated 
with  a  remarkable  slowing  of  the  respiration  which  is  sometimes  observed  in  pneumonia 
when  the  accompanying  pleurisy  excites  intense  pain  with  each  respiration. 


86  CHARACTER   OF  THE  RESPIRATION. 

the  chief  factor  is  the  stasis  or  congestion — i.  e,,  the  circulation  is  slowed 
and  the  blood  accumulates  in  the  veins  whether  the  difficulty  affects  the 
left,  right,  or  both  sides  of  the  heart.  As  a  consequence  of  the  retarded 
current  the  different  organs  receive  less  arterial  blood  in  a  certain  time 
and  retain  more  venous  blood ;  and  since  the  respiratory  center  is  also 
affected  by  this  disturbance,  more  rapid  and  deeper  breathing  results. 

The  conditions  become  more  complicated  when  the  circulatory  trouble 
originates  in  the  left  heart,  because  the  congestion  then  includes  not  only 
the  general  systemic  veins,  but  also  the  pulmonary  veins,  thus  adding 
another  cause  for  dyspnea — namely,  a  marked  distention  of  the  pul- 
monary capillaries  with  blood.  It  was  formerly  assumed  that  this  dila- 
tation of  the  alveolar  vessels  impaired  respiration  by  diminishing  the 
amount  of  air  in  the  lung.  But  this  conception  was  shown  to  be  incor- 
rect by  V.  Basch's  experimental  investigations  upon  pulmonary  con- 
gestion, for  he  proved,  on  the  contrary,  that  the  lung  overdistended  with 
blood  contains  more  air  because  the  distention  of  the  alveolar  vessels 
also  increases  the  circumference  of  the  alveoli.  Nevertheless,  the  proc- 
ess in  question  does  impair  respiration,  because  the  lung,  stiffened  by  the 
distention  with  blood,  becomes  more  and  more  permanently  fixed  in  the 
position  of  inspiration  and  expands  but  little.  Pulmonary  rigidity  acts 
as  a  direct  impediment  to  breathing  (Category  2,  p.  85)  and  increases 
the  respiratory  rate.  If  it  is  persistent,  its  effect  is  intensified  by  the 
formation  of  the  so-called  "  brown  induration." 

In  opposition  to  this  mechanical  theoiy  of  pulmonary  rigidity  we  would  em- 
phasize the  work  of  Krause,  who  found  that,  in  spite  of  the  engorgement  of  the 
lung,  the  respiratoiy  excursion  may  even  be  increased.  In  this  case  the  dyspnea 
is  to  be  explained  by  the  fact  that  "the  respiratoiy  surface  of  the  dilated  pulmonary 
vessels  is  relati^-ely  decreased  in  comparison  with  their  contents. 

When  the  lung  is  affected  paroxysmally  by  pronounced  engorgement 
with  blood  and  rigidity,  in  disturbances  of  cardiac  activity,  the  result- 
ing attacks  are  named  "  cardiac  asthma."  This  term  is  often  wrongly 
applied  to  any  kind  of  dyspnea  which  appears  in  heart  disease.  These 
paroxysms  of  cardiac  asthma  are  brought  on  sometimes  by  exertion, 
sometimes  by  increased  flow  of  blood  to  the  lung  in  the  recumbent  pos- 
ture, sometimes  by  altered  innervation  at  the  moment  of  falling  asleep, 
and  sometimes  by  entirely  unknown  causes. 

Pulmonary  rigidity  and  brown  induration  arise  in  mitral  diseases, 
especially  when  compensation  is  good — i.  e.,  when  the  right  ventricle 
does  its  work  well.  For  this  reason  patients  with  a  mitral  lesion,  des- 
pite good  compensation,  experience  dyspnea,  even  with  very  moderate 
exertion. 

As  a  further  cause  of  dyspnea  may  be  added  the  bronchial  catarrh 
that  almost  always  accompanies  circulatory  disorders. 

4.  Dyspnea  Dependent  Upon  Obstruction  of  the  Upper  Air 
Passages. — Any  obstruction  in  the  large  upper  air  passages  makes 
breathing  difficult  because  it  furnishes  a  resistance  to  the  entrance  of  air 
and  to  the  inspiratory  pull  of  the  respiratory  musculature.  The  latter 
must  therefore  perform  more  work.     It  is  evident  that  under  these 


DYSPNEA.  87 

•circumstances  an  increase  in  the  rate  of  breathing  would  be  not  only  very 
difficult,  but  also  of  little  avail,  while  on  the  other  hand,  simple  reflection 
shows  that  slowed  breathing  would  more  readily  overcome  the  obstruc- 
tion. But  to  supply  the  requisite  amount  of  oxygen  the  breathing  must 
be  deeper  as  well.  And  this  is  sometimes  observed  to  be  the  method 
which  patients  adopt  to  overcome  obstruction  in  the  larger  air  passages, 
but  only  when  there  is  sufficient  inspiratory  power  to  entirely  overcome 
the  impediment  in  breathing.  Lacking  such  power,  the  economy  is 
obliged  to  depend  more  and  more  upon  the  less  efficient  means  of 
increasing  the  rapidity  of  the  breathing,  which,  of  course,  becomes 
superficial,  but  that  it  is  always  suited  to  the  particular  kind  of  mechan- 
ical obstruction  is  shown  by  the  fact  that  the  increased  frequency  is  slight 
in  comparison  with  the  extent  of  the  respiratory  obstruction,  since  too 
rapid  breathing  would  be  of  no  avail.  This  peculiar  type  may  be 
termed  dyspnea  with  a  tendency  to  slowed  breathing.  The  frequency  or 
the  depth  of  the  breathing  preponderates,  depending  upon  the  relation 
between  the  stenosis  and  the  respiratory  power.  It  is  observed  in 
stenosis  of  the  pharynx  from  swelling  of  the  tonsils  ;  in  retropharyngeal 
abscess ;  in  true  and  pseudocroup ;  in  edema  and  in  spasms  of  the 
glottis ;  in  paralysis  of  the  abductors  of  the  vocal  cords ;  in  stenosis  of 
the  larynx  or  trachea  from  tumors  or  foreign  bodies  ;  in  obstruction  of 
the  trachea  from  external  compression  (glands  of  the  neck,  aneurism, 
€tc).  If  the  stenosis  is  situated  in  one  of  the  main  bronchi,  it  will 
depend  again  upon  the  degree  of  obstruction  whether  the  dyspnea  is  com- 
bined with  slowed  or  accelerated  breathing.  If  the  lung  upon  the  affected 
side  can  still  be  made  use  of,  the  dyspnea  will  be  of  the  former  type ; 
but  if  the  healthy  lung  must  do  all  the  work,  the  breathing  will  be 
rapid.  In  either  case  the  economy  selects  the  more  advantageous 
method.  Thus,  in  all  the  conditions  in  question,  the  demand  for  air 
will  be  supplied,  and  the  subjective  dyspnea  and  cyanosis  avoided, 
unless,  of  course,  the  obstruction  is  too  great. 

When  the  obstruction  in  the  upper  air  passages  is  very  considerable, 
and  when,  despite  the  changes  in  respiration  resulting  from  the  dyspnea, 
the  lung  can  no  longer  completely  fill  itself  with  air  again,  the  chest 
"  pumps  empty,"  so  to  speak.  During  inspiration  an  abnormally  rare- 
fied space  is  found  in  the  lung,  and  the  lateral  flexible  portions  of  the 
chest-wall,  the  epigastrium,  the  supraclavicular  fossae,  and  the  supraster- 
nal notch  (jugulum)  sink  in  under  the  influence  of  the  external  atmo- 
spheric pressure. 

There  is  another  cause  for  depression  of  the  lower  lateral  chest 
regions  in  this  form  of  dyspnea.  As  a  result  of  the  empty  pumping, 
the  vault  of  the  diaphragm  is  not  depressed  with  inspiration,  but  may 
even  be  sucked  upward.  Besides,  as  a  result  of  the  stenosis,  the  ribs 
can  not  be  lifted  up  by  the  diaphragmatic  action  (described  by  Duch- 
enne,  p.  80),  and  so  the  contraction  of  the  diaphragm  practically  accom- 
plishes nothing  but  drawing  in  its  points  of  attachment  to  the  ribs. 
This  pathologic  retraction  of  the  lower  lateral  portion  of  the  entire 
chest-wall  must  not  be  confounded  with  the  purely  physiologic  retrac- 


88  CHARACTER   OF  TEE  RESPIRATION. 

tion  of  the  lower  intercostal  spaces  in  inspiration  (see  p.  79).  The 
differentiation  is  easy  enough.  In  the  latter  only  the  lower  intercostal 
spaces  along  the  line  of  the  diaphragm  are  affected,  and  there  is  never 
any  retraction  of  the  ribs  nor  of  the  epigastrium.  The  retraction  of 
stenosis  is  observed  most  distinctly  in  children  because  their  chests  are 
very  flexible.     It  is  very  common  in  croup. 

A  peculiar  stridor  or  a  sort  of  whistling,  due  to  the  passage  of  air 
through  a  narrowed  place,  is  a  most  characteristic  accompaniment  of 
dyspnea  caused  by  stenosis  of  the  upper  air  passages.  It  is  ordinarily 
heard  much  more  distinctly  with  inspiration  than  with  expiration.  In 
laryngeal  croup  the  stridor  is  due  to  the  membrane  covering  the  vocal 
cords.  The  inspiratory  accentuation  of  the  stridor  is  explained  by  assum- 
ing that,  in  spite  of  the  inspiratory  opening  of  the  glottis,  the  vocal  cords 
are  not  materially  separated,  and  that  as  a  result  of  their  slanting,  roof- 
like  position  they  are  approximated  still  more  closely,  valve  fashion,  by 
the  pneumatic  tug  of  inspiration.  Hence,  the  obstacle  to  inspiration  is 
greater  than  to  expiration.  This  explanation  is  probably  correct  for  cases 
of  laryngeal  croup.  Nevertheless,  the  same  inspiratory  increase  of  stridor 
is  observed  in  other  types  of  stenosis  of  the  upper  air  passages  where  we 
cannot  assume  the  result  of  any  such  valve-like  effect  in  the  larynx — 
e.  g.,  from  obstruction  either  above  or  below  the  larynx  (retropharyngeal 
abscess,  goiter,  etc.).  The  probable  explanation  of  such  cases  is  that 
the  obstruction  prevents  the  free  ingress  of  air  during  the  inspiratory 
effort  at  a  moment  when  suction  is  exerted  upon  the  surrounding  parts 
by  the  external  atmospheric  pressure,  so  that  the  trachea  is  constricted 
below  the  sternum  (iusjDiratory  retraction  of  the  jugulum,  suprasternal 
notch).  Therefore,  any  obstruction  in  the  upper  air  passages,  even  if 
not  actually  located  in  the  larynx,  acts  much  more  effectually  during 
inspiration  than  during  expiration.  In  other  words,  the  dyspnea  is 
essentially  inspirator^-.  Another  factor  may  influence  this  inspiratory 
accentuation  of  the  stridor.  The  velocity  of  the  air  current  in  inspira- 
tion is  much  greater  than  in  expiration,  which  is  passive,  depending 
upon  the  elasticity  of  the  lungs  and  the  thorax.  The  importance  of 
this  factor  is  sho^vn  by  the  fact  that  as  soon  as  patients  with  stenosis 
of  the  upper  air  passages  experience  a  sufficient  increase  in  the  respira- 
tory obstruction  to  necessitate  their  employing  the  help  of  abdominal 
pressure,  the  expiratory  stridor  will  become  more  marked,  and  may 
even  outweigh  the  inspiratory  stridor. 

5.  Dyspnea  in  Bronchitis. — The  types  of  bronchitis  which 
usually  lead  to  dyspnea  are  chiefly  those  affecting  the  smaller  bronchi. 
The  dyspnea  is  caused  by  the  stenosis  of  the  bronchial  lumen,  due  to 
swelling  of  the  mucous  membrane  and  to  secretion.  The  stenosis  affects 
so  many  places  that  ordinary  breathing  is  insufficient  and  dyspnea  arises. 

This  tv^pe  of  dyspnea  varies  with  the  conditions  which  prevail.  If 
the  stenosis  affects  only  a  small  number  of  bronchi,  simple  increase  of 
the  breathing  rate  will  usually  overcome  the  difficulty.  The  stenosed 
areas  are  not  benefited  much  by  this  method,  but  the  uninvolv^ed  por- 
tions receive  more  air,  and  so  the  effect  of  the  disturbance  is  equalized. 


DYSPNEA.  89 

This  type  of  dyspnea  then  comes  under  our  second  heading.  If  the  sten- 
osis affects  a  large  number  of  bronchi,  the  breathing  varies  according  to 
whether  the  bronchial  closure  is  quite  complete  and  insurmountable,  as 
in  capillary  bronchitis  proper,  or  whether  it  is  incomplete  and  still  con- 
querable by  the  respiratory  effort,  as  in  diffuse  dry  bronchitis  of  the 
medium-sized  tubes.  In  the  former  variety,  of  which  capillary  bronchitis 
is  a  type,  the  chief  effect  is  again  merely  a  diminution  of  the  breathing 
surface,  so  that,  as  before,  dyspnea  with  rapid  respiration  results.  This, 
of  course,  only  assists  bronchial  areas  which  still  remain  patent.  In 
the  second  type,  however,  where  we  suppose  that  most  if  not  all  of  the 
medium-sized  bronchi  are  stenosed,  although  only  moderately  so,  the 
respiratory  effort  must  attempt  to  get  a  sufficient  quantity  of  air  through 
the  constricted  areas  into  the  pulmonary  tissue  proper.  This  can  gen- 
erally be  best  accomplished  by  an  abnormally  deep  respiration,  very 
much  as  in  stenosis  of  the  upper  air  passages,  especially  of  the  larynx. 
And  just  as  in  these  cases,  the  respiratory  accommodation  and  the  fre- 
quency of  the  individual  efforts  will  vary  according  to  the  amount  of 
obstruction  as  compared  with  the  respiratory  force  available.  In  rare 
instances  even  a  slowing  of  respiration  may  result.  More  frequently, 
however,  we  merely  observe  a  certain  tendency  to  retardation  in  that 
the  increase  in  rate  does  not  correspond  to  the  degree  of  constriction, 
and  this  increase  is  comparatively  slight  as  contrasted  with  the  amount 
of  subjective  dyspnea  and  cyanosis.  The  passage  of  air  through  these 
constricted  areas  is  often  associated  here,  as  well,  with  a  stridor — 
i.  e.,  a  stenotic  noise  which  may  perhaps  be  heard  at  a  considerable  dis- 
tance from  the  patient.  This  type  of  dyspnea  in  bronchitis  presents, 
therefore,  a  prolongation  of  expiration  and  stridor,  chiefly  expiratory, 
and  so  can  be  distinguished  from  the  other  retarded  type  or  laryngeal 
dyspnea,  where  expiration  is  of  normal  length  and  the  stridor  is  chiefly 
inspiratory. 

These  two  points  of  distinction,  which  are  responsible  for  the  appli- 
cation of  the  name  expiratory  to  this  type  of  dyspnea,  require  some 
further  explanation.  The  prolongation  of  expiration  is  easily  under- 
stood, because  even  under  normal  conditions  expiration  is  longer  than 
inspiration,  and,  of  course,  the  increased  resistance  caused  by  the  bron- 
chial stenosis  must  be  felt  more  during  expiration,  since  the  excitation 
of  dyspnea  produces,  first  of  all,  marked  increase  of  the  inspiratory 
power.  To  be  sure,  if  the  dyspnea  is  pronounced,  the  expiratory  exer- 
tion must  be  also  increased  by  the  participation  of  abdominal  pressure 
in  the  expiratory  act,  so  that  the  lungs  will  then  be  emptied  somewhat 
more  quickly  by  the  active  expiratory  compression  of  the  thoracic  con- 
tents than  by  the  influence  solely  of  elasticity.  This  extra  abdominal 
pressure,  however,  will  also  compress  the  small  bronchi  still  more  ; 
hence  the  prolongation  of  expiration  as  compared  with  inspiration,  and 
the  increase  of  expiratory  stridor.  Increased  expiratory  stridor  may 
be  present  without  the  participation  of  abdominal  pressure.  For  if  the 
elastic  retraction  of  the  lung  is  interfered  with  by  stenoses  in  the  bronchi, 
the  latter  will  be  still  more  compressed  by  this  elastic  expiratory  move- 


90  CHARACTER   OF  THE  RESPIRATION. 

ment  just  as  by  abdominal  pressure.  Hence,  abdominal  pressure  is  not 
absolutely  necessary  for  the  increased  expiratory  stridor.  All  sorts  of 
intermediate  types  occur  between  this  type  of  retarded  breathing  with 
prolonged  expiration  and  expiratory  stridor  on  the  one  hand,  and  the 
type  in  which  the  breathing  is  simply  increased  in  frequency  on  the 
other.  These  types  will  vary  according  to  the  preponderance  of  bron- 
chial stenosis  or  of  the  available  respiratory  power. 

6.  Dyspnea  in  Bronchial  Asthma. — According  to  the  modern 
conception,  bronchial  asthma  depends  upon  a  stenosis  of  the  smaller 
bronchi,  due  to  spasm  of  the  bronchial  muscles.  Hence,  it  corresponds 
exactly  to  dyspnea  in  the  type  of  bronchitis  just  discussed,  that  with 
moderate  stenosis  of  the  bronchi.  The  breathing  is  retarded  and  expiration 
is  prolonged  and  combined  with  stridor  (so-called  expiratory  dyspnea). 
The  absolute  number  of  respirations  may  be  diminished  ;  or  an  increase 
in  rate  which  would  correspond  to  the  amount  of  subjective  dyspnea  may 
be  prevented.  This  depends  upon  the  degree  and  the  extent  of  the 
bronchial  muscles'  spasm.  Therefore,  in  bronchial  asthma  we  may 
observe  either  a  diminished,  normal,  or  increased  respiratory  frequency. 
The  conditions  are  analogous  to  those  in  emphysema  (see  next  section). 

7.  Dyspnea  in  i^mphysema. — Pulmonary  emj)hysema  causes 
dyspnea  because  the  lung  is  in  a  permanent  condition  approximating  the 
inspiratory  position,  and  because  with  inspiration  and  expiration  it  makes 
but  small  excursions  from  this  position.  Besides  this,  pronounced 
emphysema  destroys  numerous  alveolar  septa  and  their  capillaries,  thus 
diminishing  the  breathing  surface  very  extensively.  For  this  reason  the 
dyspnea  of  pure  uncomplicated  emphysema  is  evidenced  by  rapid  and 
superficial  respiration.  When  the  patient  is  quiet  the  disturbance  re- 
mains slight,  but  when  some  physical  exertion  makes  extra  demands 
upon  the  respiration  the  dyspnea  increases  very  decidedly.  As  a  rule, 
patients  with  emphysema  appear  for  the  treatment  of  marked  dyspnea 
only  when  this  affection  is  complicated  by  a  bronchitis  (usually  the  dry 
variety).  Consequently,  in  emphysema  the  same  influences  which  we 
have  just  discussed  in  bronchitis  tend  to  render  the  respiration  now 
quicker  and  now  slower.  The  tendency  to  retardation  is  very  pro- 
nounced, because  the  bronchitis  complicating  the  emphysema  is  usually 
diffuse  and  produces  a  stenosis  of  most  of  the  bronchi.  The  loss  of 
elasticity  in  the  emphysematous  lung  especially  promotes  a  retardation 
of  breathing  and  prolongation  of  expiration.  But  the  dyspnea  in  emphy- 
sematous bronchitis  is  not  always  associated  with  a  slowing  of  respira- 
tion, for  the  system  will  accommodate  itself  to  the  respiratory  obstruc- 
tion with  or  without  an  increase  of  respiration,  depending  entirely  upon 
the  proportion  between  the  loss  of  elasticity  in  the  lung,  the  degree  of 
bronchial  stenosis,  and  the  respiratory  power.  As  a  matter  of  fact,  in 
the  bronchitis  ot  emphysema  there  is  very  often  a  certain  amount  of  in- 
crease in  the  frequency  of  breathing.  Still,  the  subjective  oppression  out- 
weighs the  slight  increase  so  decidedly  that,  unless  we  count,  the  impres- 
sion is  made  that  the  respirations  are  slow,  although  actually  20  to  25 
a  minute.    In  some  cases  this  tendency  to  retardation  leads  to  an  actual 


DYSPNEA.  91 

diminution  in  the  number  of  respirations  ;  in  other  cases,  only  to  a  lack 
of  any  increase  ;  in  still  another  class  of  cases,  to  an  increase  in  respira- 
tions which  is  but  slight  in  proportion  to  the  subjective  dyspnea.  Thus, 
the  bronchial  dyspnea  of  the  emphysematous  may  be  characterized  as  a 
dyspnea  Avith  a  prolonged  expiration  and  expiratory  stridor  (so-called 
expiratory  dyspnea)  and  also  with  a  more  or  less  pronounced  tendency 
to  a  diminution  in  the  frequency  of  the  breathing.  These  conditions 
are  unchanged  if,  as  is  often  the  case,  the  emphysema  is  complicated  with 
bronchial  asthma. 

8.  So-called  Uremic  Dyspnea  of  Nephritis. — This  exhibits 
no  uniform  symptom-complex.  In  individual  cases,  and  particularly  if 
retarded  breathing  and  prolonged  expiration  occur,  we  are  justified  in 
assuming  the  existence  of  some  true  uremic  phenomenon — i.  e.,  an  actual 
bronchial  asthma  due  to  uremia.  Many  diagnostic  conditions  in  neph- 
ritis are,  however,  erroneously  considered  uremic.  They  depend  rather 
more  upon  some  cardiac  disorder,  upon  the  accompanying  bronchial 
catarrh,  or  upon  a  beginning  pulmonary  edema,  etc.  Corresponding  to 
the  diversity  in  causation,  these  types  of  dyspnea  vary  decidedly  in  their 
character. 

9.  Febrile  Dyspnea. — A  febrile  elevation  of  the  body  temperature 
is  nearly  always  combined  with  an  increase  in  respiratory  frequency. 
Even  the  artificial  application  of  heat  to  the  body  will,  increase  the  res- 
piratory rate,  so  that  it  seems  plausible  that  the  irritation  of  warmer 
blood  upon  the  respiratory  center  is  responsible  for  the  febrile  rise  of 
the  respiratory  rate. 

However,  the  frequency  of  respiration  in  febrile  diseases  with  exactly 
the  same  degree  of  temperature  may  differ  widely,  so  that  the  nature  of 
the  toxin  probably  exerts  some  direct  influence  upon  the  respiratory 
center.  The  increased  respiratory  frequency  in  fever  probably  corresponds 
to  an  increased  demand  upon  the  metabolism.  Therefore,  according  to 
our  definition  (p.  83),  we  are  correct  in  speaking  of  febrile  dyspnea  as 
well  as  of  febrile  polypnea. 

The  respiratory  frequency  found  with  a  certain  degree  of  fever  varies 
with  each  individual  case.  Experience  shows  that,  unless  some  respira- 
tory complication  exists,  only  the  severe  types  of  fever  increase  the 
respiratory  frequency  very  noticeably.  Fig.  24,  the  curve  of  an  uncom- 
plicated typhoid,  illustrates  the  usual  ratio  between  temperature  and 
respiration  rate. 

10.  Anemic  Dyspnea. — Exaggerated  Breathing  in  Diabetic 
Coma. — Dyspnea  occurs  in  anemia  (oligochromemia)  because  the  availa- 
ble amount  of  hemoglobin  is  so  small  that  only  the  most  complete  aeration 
will  be  sufficient  to  supply  the  demand  for  oxygen.  With  no  mechani- 
cal impediment  to  respiration,  the  organism  can  adapt  itself  very  com- 
pletely to  the  altered  conditions.  This  is  accomplished  by  a  simultaneous 
increase  in  the  frequency  and  in  the  depth  of  respiration.  The  resulting 
dyspnea  produces  a  peculiar  clinical  picture,  for  the  respirations  are  not 
only  very  rapid,  but  also  of  maximum  depth.  This  tyjie  is  observed 
especially  in  pernicious  anemia ;  rarely,  however,  in  other  disorders. 


92  CHARACTER   OF  THE  RESPIRATION. 

The  same  type  of  breathing  is  observed  in  diabetic  coma.^  We  do  not  know 
its  cause,  so  that  it  seems  doubtful  if  we  should  consider  it  as  actual  dyspnea  (in 
the  sense  of  p.  83,  et  seq.) — i.  e.,  analogous  to  anemic  dyspnea.  However,  the 
outn-ard  resemblance  of  the  two  phenomena  makes  such  a  supposition  possible 
(diminution  of  the  hemoglobin  oxidation  capacity  in  diabetic  coma). 

11.  <<  Mixed"  Dyspnea — Inspiratory  and  Expiratory. — 

Thus  far  we  have  been  discussing  the  various  factors  which  determine  the 
different  types  of  objective  dyspnea.  Two  main  types  occur  :  (1)  breath- 
ing with  increased  frequency  and  (2)  slowed  breathing  with  increased 
depth.  In  the  former  "  mixed  dyspnea "  inspiration  and  expiration 
seem  equally  accelerated.  In  the  latter,  inspiration  and  expiration 
are  affected  differently ;  in  some  cases  the  inspiration,  in  others  the  ex- 
piration appearing  prolonged.  One  type  is  termed  "  inspiratory  dysp- 
nea," the  other  "  expiratory  "  ;  because  in  the  one  it  is  principally  in- 
spiration, and  in  the  other  expiration,  which  is  rendered  more  difficult. 

In  this  connection  compare  the  paragraphs  on  the  types  of  dyspnea 
in  obstruction  of  the  upper  air  passages  in  bronchitis,  in  emphysema, 
and  in  asthma.  Inspiratory  dyspnea  can  usually  be  distinguished  im- 
mediately by  inspiratory,  expiratory  dyspnea,  by  expiratory  stridor, 
without  necessarily  estimating  the  length  of  the  two  phases  in  respira- 
tion. If  the  examiner  is  inclined  to  do  this  he  should  remember  that 
normally  expiration  lasts  longer  than  inspiration  (4:1). 

AUXILIARY    OR    ACCESSORY    BREATHING;    FORCED    ATTITUDES 

EST  DYSPNEA. 

In  all  types  of  dyspnea  the  economy  ordinarily  employs  all  the 
available  aid  to  lighten  the  burden  of  the  respiration.  In  this  way  a 
number  of  muscles  are  used  for  breathing  which,  under  normal  condi- 
tions, serve  other  purposes.  These  are  the  so-called  accessory  respira- 
tory muscles,  chiefly  the  scaleni,  trapezius,  levator  angulse  scapulae,  sterno- 
cleidomastoid, sternothyroid,  thyrohyoid,  serrati,  and  the  pectorals.  The 
last  five  mentioned  muscles  may  serve  as  inspiratory  muscles,  because 
their  usual  fixed  attachment  to  the  chest  is  made  the  mobile  point,  the 
other  end  becoming  stationary. 

We  have  already  considered  upon  page  24  how  the  erect  posture 
facilitates  the  task  of  these  accessory  muscles  (orthopnea),  and  the  im- 
portance of  constrained  lateral  positions  with  a  unilateral  obstruction 
to  breathing.  The  abdominal  muscles  are  the  only  ones  employed 
as  accessory  muscles  to  expiration.  Naturally  they  are  chiefly  active  in 
expiratory  dyspnea,  but  they  may  also  be  utilized  to  advantage  in  mixed 
and  in  inspiratory  dyspnea  to  accelerate  expiration  and  thus  to  facilitate 
a  new  inspiration. 

If  the  dyspnea  is  very  pronounced  various  other  accessory  muscles 
to  respiration  may  be  called  into  play.  Their  activity  is  of  certain 
diagnostic  importance,  although  it  must  be  acknowledged  that  they  do 
not  materially  assist  the  respiration.  The  facial  muscles  of  expression 
are  examples.  During  inspiration  they  distend  the  openings  of  the 
1  Kussmaul,  D.  Arch. J.  klin.  Med.,  vol.  iv.,  1874. 


SPIROMETRY  AND  PNEUMATOMETRY.  93 

mouth,  and  especially  of  the  nose,  to  a  maximum.  The  patient  thus 
presents  quite  a  characteristic  and  pitiful  appearance.  This  dilatation  of 
the  alae  nasse  is  especially  pronounced  in  small  children  with  pnelimonia. 
Such  a  maximal  distention  of  the  entrances  to  the  respiratory  tract  may 
sometimes  be  of  real  value  in  diagnosis  ;  but  it  ordinarily  means  that 
some  effect  of  the  vigorous  respiratory  stimulation  has  been  transferred 
to  related  muscle  groups. 

RELATION  OF  OBJECTIVE  DYSPNEA  TO  CYANOSIS  AND  TO 
SUBJECTIVE  DYSPNEA;  HABITUATION  TO  RESPIRATORY 
OBSTRUCTION   AND   TO   DYSPNEA. 

Objective  dyspnea  serves  to  diminish  both  cyanosis  and  the  sub- 
jective sense  of  dyspnea.  This  task  is  not  always  performed  equally 
well.  The  more  completely  the  dyspnea  aerates  the  blood,  the  less 
danger  to  the  individual ;  but  cyanosis  can  only  be  entirely  overcome  when 
the  obstruction  to  inspiration  is  slight.  Wherever  a  marked  obstruc- 
tion occurs,  some  little  (oftentimes  considerable)  cyanosis  must  persist. 
The  economy  then  performs  its  functions  with  blood  rich  in  carbonic 
acid  and  poor  in  oxygen,  and  the  dyspnea  only  succeeds  in  preventing  a 
progressive  deterioration  of  the  blood.  In  cases  of  chronic  dyspnea  the 
economy  may  become  more  or  less  accustomed  to  the  cyanosis.  This  is 
evidenced  not  only  by  the  relatively  good  maintenance  of  the  other  body 
functions,  but  also  'because  the  sense  of  subjective  dyspnea — "  air  hun- 
ger"— gradually  and  progressively  disappears.  Conversely,  with  the 
same  degree  of  respiratory  obstruction,  the  quicker  the  latter  develops, 
the  more  intense  the  subjective  dyspnea. 

Pneumothorax  furnishes  one  of  the  most  striking  examples  of  the 
economy's  power  of  adaptation  to  respiratory  obstruction.  After  the 
sudden  onset  of  the  respiratory  obstruction,  both  the  objective  and  sub- 
jective dyspnea  are  at  first  very  pronounced,  but  soon  diminish.  In 
pneumothorax  this  does  not  merely  depend  upon  a  simple  adjustment 
of  the  economy  to  cyanotic  blood  any  more  than  in  other  conditions. 
For  in  this  type,  as  in  many  others,  the  disturbance  itself  is  lessened  by 
a  number  of  complicated,  equalizing  factors  which  proceed  especially 
from  the  circulatory  system.  This  also  becomes  plain  from  the  dimi- 
nution of  objective  dyspnea. 

We  need  scarcely  add  that  dyspnea  with  a  slight  degree  of  cyanosis 
suggests  a  far  better  prognosis  than  dyspnea  with  pronounced  cyanosis. 

SPIROMETRY  AND  PNEUMATOMETRY. 

Spirometry  and  pneumatometry — i.  e. ,  the  mensuration  of  the  vital  capacity 
and  of  the  respiratory  pressure  variations  in  the  upper  air  passages — have  not  as  yet 
acquired  any  great  diagnostic  importance.  This  failure  is  due  to  the  great  difficulties 
in  technic  and  to  the  pronounced  influence  of  practice  in  those  examined.  Read- 
ers who  wish  to  study  thoroughly  this  method  of  examination  should  consult  text- 
books upon  physiology  and  several  of  the  original  works  upon  pneumatometiy. ' 

1  P.  Bonders,  Zeit.  f.  rat.  Med.,  N.  F.,  vol.  iii.,  1853,  p.  287  el  seg.  ;  Waldenberg,  "  Die 
Manometrie  der  Lunge,  oder  Pneumatometi'ie  als  diagnostische  Methode,"  Berlin,  klin. 
Woch.,  1871,  N.  45;  Eichhorst,  D.  Arch.  J.  klin.  Med.,  1873,  vol.  xi.,  p.  268;  Biedert,  ibid., 
1876,  vol.  xviii.,  p.  115;  Rollet,  ibid.,\o\,  xix.,  p.  284;  Neupaur,  ibid.,yo\.  xxiii.,  p.  481. 


94    CHARACTER   OF   VOICE   UNDER  PATHOLOGIC  CONDITIONS. 

The  pneumoscope  described  by  Blocb'  seems  to  be  the  most  useful  for  clinical 
purposes.  This  instrument  calculates  the  respiratory  power  without  determining 
the  respiratory  pressure  manometrically,  but  by  estimating  the  minimum  diameter 
of  a  breathing  cannula  held  in  the  mouth,  through  which  a  sufficient  quantity  of 
air  may  be  breathed.  More  accurate  information  of  the  respiratoiy  mechanism  can 
usually  be  obtained  by  directly  measuring  the  thoracic  excursions  with  a  tape 
measure  than  by  spirometry  or  pneumatometry  (see  p.  29,  et  seq.). 


CHARACTER   OF  THE  VOICE  UNDER   PATHOLOGIC 

CONDITIONS. 

Pathologic  alterations  in  the  voice  arise  partly  from  demonstrable 
disorders  of  the  vocal  organ  proper  (the  larynx)  and  partly  from  other 
influences,  either  direct  affections  of,  or  disorders  indirectly  connected 
with,  the  respiratory  apparatus.  We  shall  mention  here  only  such  altera- 
tions of  the  voice  as  are  of  some  diagnostic  importance. 

If  the  expiratory  current  of  air  does  not  make  the  vocal  cords  vibrate 
normally  the  voice  will  be  "hoarse'' — e.g.,  in  all  inflammations,  ulcer- 
ations, tumors,  or  paralyses  of  the  cords.  A  hoarse  voice  always  indi- 
cates some  affection  of  the  larynx  and  necessitates  a  laryngoscopic 
examination.  If  combined  with  inspiratory  dyspnea,  hoarseness  is 
very  suggestive  of  laryngeal  obstruction.  It  may,  however,  be 
due  to  some  general  condition — e.  g.,  the  loss  of  the  cords'  normal 
tone,  in  weak  cachectic  patients.  Again,  it  may  result  from  a  fit  of 
violent  coughing.  Here  a  paresis  of  the  tensors  of  the  cords  is  caused 
by  the  marked  stretching  of  the  cords  during  the  glottis  closure  which 
precedes  the  cough.  The  hoarseness  in  phthisis,  therefore,  does  not 
always  mean  an  ulceration  of  the  larynx  or  cords. 

The  voice  is  frequently  lost  in  hysteric  aphonia  without  preliminary  hoarse- 
ness; whereas  a  similar  loss  of  voice  is  always  preceded  or  introduced  by  hoarseness 
if  the  aphonia  is  due  to  anatomic  changes  in  the  larynx.  This  is  a  point  of  some 
diagnostic  importance. 

The  voice  may  acquire  a  nasal  twang  as  a  result  of  alterations  in 
the  conditions  of  resonance  in  the  mouth  or  nasal  cavity.  We  distin- 
guish a  closed  or  stopped  from  an  open  nasal  voice.  The  former  is 
observed  when  the  nasopharynx  or  the  nasal  cavity  itself  is  obstructed 
by  any  pathologic  products,  such  as  tumefactions  of  the  mucous  mem- 
brane, polypi,  adenoids.  The  latter,  the  "  open  nasal  voice,"  is  observed 
when  anything  prevents  the  normal  closure  between  the  nasal  cavity 
and  the  mouth — e.  g.,  palate  paralysis,  cleft  palate,  syphilitic  affections 
of  the  palate,  etc. 

Aphonia  (lack  of  voice)  results  either  from  an  inability  to  approx- 
imate the  vocal  cords  or  from  a  prevention  of  the  normal  vibration. 
It  may  be  preceded  by  hoarseness. 

The  voice  is,  moreover,  very  dependent  upon  the  general  condition 

and  upon  the  thoracic  organs.      Patients  who  are  very  ill  usually  have 

a  weak  voice,  corresponding  to  their  general  muscular  weakness.      In 

diseases  of  the  respiratory  and  circulatory  organs  the  voice  is  affected  by 

'  Arch,  de  Physiol.,lS97 ,  p.  1. 


COUGH.  95 

the  disturbed  respiratory  excursions  and  by  the  various  sorts  of  dyspnea. 
In  many  patients  with  heart  disease  the  voice — i.  e.,  the  cord  tonus — is 
a  very  delicate  indicator  of  the  condition  of  their  general  circulation — 
it  becomes  weak  and  feeble  when  they  fail,  and  full  and  sonorous  when 
they  improve.  In  painful  aifections  of  the  lungs  or  pleura  and  in  peri- 
tonitis the  voice  becomes  characteristically  feeble,  soft,  and  often  broken. 
Cholera  patients  speak  with  a  "  toneless  "  voice  (vox  cholerica),  and  the 
moribund  with  a  faint,  scarcely  audible  voice.  [Further  reference  will 
be  made  to  these  and  similar  points  in  the  section  on  Auscultation  (bron- 
chophony)] . 


COUGH. 


A  COUGH  consists  of  a  single  or  of  a  consecutive  series  of  explosive 
expiratory  movements  produced  by  abdominal  pressure,  which  result 
in  overcoming  the  preliminary  closure  of  the  glottis.  It  is  a  very  im- 
portant reflex  act,  serving  the  purpose,  on  the  one  hand,  of  expelling  any 
foreign  bodies  which  may  have  become  lodged  in  the  respiratory  passages, 
and,  on  the  other  hand,  of  expectorating  any  material  which  may  have 
accumulated  there  from  some  pathologic  process — e.  g.,  bronchial  or 
alveolar  secretions,  eifused  blood,  pus  which  has  perforated  into  the 
bronchi,  disintegrated  necrotic  or  tubercular  lung  material,  etc.  A 
cough  may  be  excited  from  various  places  in  the  body.  The  commonest 
type  of  cough  is  one  in  which  the  reflex  arises  from  the  region  supplied 
by  the  sensory  branches  of  the  vagus.  Experimental  investigations 
have  shown  (especially  Nothnagel's)  that  irritation  of  the  laryngeal 
mucous  membrane  above  the  vocal  cords  produces  spasmodic  closure  of 
the  larynx,  but  no  cough.  Coughing  will,  however,  be  induced  if  the 
irritation  aifects  the  parts  heloio  the  vocal  cords.  The  most  sensitive 
areas  are  the  interarytenoid  mucous  membrane  and  the  region  of  the 
bifurcation  of  the  trachea.  Coughing  may  also  be  excited  from  any 
other  part  of  the  tracheal,  as  well  as  from  all  parts  of  the  bronchial, 
mucous  membrane,  but  not  from  the  pulmonary  parenchyma  proper. 

Experimental  results  do  not  agree  as  to  whether  a  cough  can  be 
excited  directly  from  the  pleura ;  but  it  seems  probable,  judging  from 
experience  with  individuals  whose  pleura  has  been  opened. 

These  are  the  most  important  sources  of  coughing,  but  there  are 
other  less  common  ones.  In  some  individuals  coughing  may  be  pro- 
duced by  irritatipn  of  the  pharynx  or  of  the  base  of  the  tongue,  or 
occasionally  of  the  esophagus.  Coughing  has  been  observed  very  ex- 
ceptionally to  result  from  tickling  the  external  auditory  canal  (auricular 
branch  of  the  vagus)  or  from  manual  pressure  upon  the  spleen  or  liver. 
Some  people  cough  as  soon  as  their  feet  become  cold  or  whenever  their 
body  surface  is  exposed.  This  suggests  the  therapeutic  value  of  warm 
clothing  in  diseases  complicated  with  a  cough.      The  existence  of  a 


96  COUGH. 

stomach  cough  is  very  doubtful,  although  the  lay  public  believe  in  it  very 
thoroughly.  Cough  has  not  as  yet,  however,  been  experimentally  excited 
from  the  stomach,  and  the  so-called  stomach  cough  which  is  so  common 
in  drunkards  can  probably  be  most  satisfactorily  explained  by  assuming 
that  an  affection  of  the  pulmonary  passages  is  combined  with  the 
stomach  disorder. 

Nervous  Coilg"]i. — The  so-called  nervous  cough  merits  a  few 
words.  We  cannot  deny  the  possibility  of  a  nervous  cough  if  we  con- 
sider that  a  cough  can  be  produced  by  an  abnormal  excitability  any- 
where in  the  course  of  the  coughing  reflex  arc.  When  such  reflex 
excitability  is  accentuated  sufficiently,  even  physiologic  irritants  may 
cause  a  cough.  As  a  matter  of  fact,  a  purely  nervous  cough  is  a  very 
rare  occurrence,  and  should  only  be  diagnosed  as  such  when  it  is  observed 
in  an  exquisitely  nervous  or  hysteric  person,  and  when  at  the  same  time 
it  differs  decidedly  from  the  ordinary  type  of  cough.  Under  no  circum- 
stances is  such  a  diagnosis  justifiable  from  exclusion — i.  e.,  because  the 
cough  is  the  only  sign  of  disease  of  the  respiratory  tract  that  can  be 
made  out  from  physical  examination.  It  is  well  known  that  a  cough 
frequently  precedes  all  other  signs  of  tuberculosis  by  weeks,  often  by 
months.     (See  under  Barking  Cough). 

Much  more  frequent  than  a  purely  nervous  cough  is  one  which  is 
disproportionate  to  its  cause — i.  e.,  secretion  or  inflammatory  irritation 
of  the  air  passages — on  account  of  an  abnormal  excitability  of  the 
coughing  reflex.     In  such  cases  soothing  remedies  afford  great  relief. 

On  account  of  the  rarity  of  other  causes,  a  cough  is  usually  an 
important  symptom  for  the  recognition  of  some  state  of  pathologic  irri- 
tation in  the  region  of  the  respiratory  branches  of  the  sensory  vagus. 
This  irritation  is  in  many  cases  produced  by  the  accumulation  of  secretion 
in  the  air  passages.  Experience  teaches  us  that  a  cough  caused  by 
accumulation  of  secretion  differs  from  the  other  types  of  cough.  This 
difference  is  often  appreciated  by  the  laity.  Its  task,  which  is  gener- 
ally fulfilled,  is  to  remove  the  secretion.  It  thus  acquires  a  peculiar 
ring,  recognized  as  a  combination  of  the  noise  of  the  cough  explosion 
with  the  noise  of  the  moving  secretion,     (See  later  Rales,  Rattling.) 

Such  a  cough  is  called  a  moist  or  loose  COUgfh  as  contrasted  with 
a  dry  cough.,  in  which  either  the  secretion  is  too  tenacious  to  be  set 
in  motion  or  no  secretion  exists.  The  acoustic  distinction  between  a 
moist  and  a  dry  cough  is  of  considerable  diagnostic  importance,  because 
the  secretion  is  by  no  means  always  expelled  from  the  mouth  by  the 
cough,  and  so  appreciated  by  the  patient  and  the  examiner,  but  very 
frequently  after  leaving  the  larynx  is  unconsciously  sw^allowed. 

There  are  certain  other  important  peculiarities  in  a  cough  which  may 
point  to  the  cause  of  the  disease. 

The  peculiar  rough  barking  cough  observed  in  simple  laryn- 
gitis is  characteristic  of  swelling  without  marked  ulceration  of  the  vocal 
cords.  Here  the  voice  may  be  clear,  but  it  is  usually  very  hoarse  or 
aphonic.  The  barking  tone  is  probably  due  to  the  swelling  of  the  false 
cords  which  aid  in  closing  the  glottis.     A  similar  barking  is  sometimes 


COUGH.  97 

observed  in  the  cough  of  hysteric  individuals.  Here  the  laryngoscopic 
examination  proves  that  it  is  due  to  some  abnormal  innervation  with- 
out any  swelling.  With  a  certain  amount  of  practice  one  can  really 
cough  with  a  bark  by  adding  phonation  to  the  cough  impulse.  Like 
most  other  hysteric  phenomena  it  can  be  reproduced  voluntarily.  If 
not  associated  with  swelling  of  the  larynx,  a  barking  cough  suggests 
its  hysteric  nature. 

If  the  margin  of  the  vocal  cords  is  irregular  from  deposition  of 
secretion  or  from  ulceration,  the  cough  is  equally  rough  but  not  bark- 
ing, and  the  voice  is  hoarse.  If  the  closure  of  the  glottis  is  imperfect 
on  account  of  marked  ulceration  of  the  cords  or  on  account  of  paraly- 
sis of  the  approximating  muscles,  or,  if  there  is  paresis  of  the  expira- 
tory muscles  or  general  debility,  the  cough  is  noiseless.  This  peculi- 
arity is  observed  in  phthisis  of  the  larynx,  in  paralysis  (bulbar  paralysis, 
myelitis),  in  any  patient  who  is  severely  ill  or  weak.  If  a  patient  is 
unable  to  approximate  the  glottis  perfectly,  he  may  instead  be  compelled 
to  close  the  mouth  for  the  purpose  of  coughing,  and  then  the  resonation 
from  the  distended  buccal  cavity  will  furnish  a  very  hollow  ring  to 
the  cough.  Such  a  hollow  ringing  is  so  generally  observed  in  advanced 
phthisis  that  even  the  laity  appreciate  its  prognostic  significance. 

A  hacking"  cough  consists  of  a  series  of  very  weak,  frequently 
repeated  coughing  explosions.  It  is  to  be  attributed  to  the  mildness 
of  the  irritant,  which  in  these  cases  is  usually  continuous  and  is  not 
dependent  upon  any  great  amount  of  secretion.  A  hacking  cough  is 
most  commonly  observed  in  chronic  catarrh  of  the  upper  air  passages, 
in  pharyngitis  and  laryngitis,  and  especially  in  beginning  pulmonary 
tuberculosis  ;  hence  its  importance. 

Conversely,  violent  coughing  paroxysms  are  observed  in 
acute,  intensely  irritated  conditions  of  the  air  passages  from  acute 
inflammations  or  from  foreign  bodies  in  the  air  passages ;  in  "  swallow- 
ing the  wrong  way  ";  in  affections  of  the  air  passages  associated  with 
a  profuse  secretion,  especially  where  cavities  or  bronchiectatic  dilations 
empty  themselves  periodically  (see  p.  25),  and  finally  in  ivhooping-cough. 
In  the  last-mentioned  affection  we  may  attribute  the  cause  to  the  abun- 
dant production  of  glary  mucus  and  to  the  increased  irritability  of  the 
nervous  coughing  mechanism.  The  "  whoop,''  so  important  for  diag- 
nosing this  disease,  is  a  resounding  crowing  or  whistling  inspiration 
combined  with  a  spasm  of  the  glottis,  and  separates  individual  groups 
of  coughing  attacks.  The  glottis  spasm  is  evidently  due  to  some 
radiation  of  the  irritation  from  the  coughing  center  to  the  neigh- 
boring structures  of  the  central  organ,  and  depends  merely  upon  the 
intensity  of  the  irritation.  During  violent  coughing  paroxysms  of 
other  diseases  we  sometimes  observe  resonant  inspirations  very  much 
like  this  whoop,  but  so  rarely  that  the  "  crowing  inspiration  "  is  the 
most  important  diagnostic  sign  of  whooping-cough. 

Vomiting  sometimes  complicates  very  intense  coughing  paroxysms ; 
it  is  due  to  the  central  diffusion  of  the  irritation. 

Hemorrhage  into  the  skin  or  mucous  membranes,  unconsciousness, 
7 


98        ARTERIAL  PULSE  PALPATION,  SPHYGMOORAPHY,  ETC. 

or   even  epileptic  convulsions  may  be  produced  by  the  general  venous 
congestion  due  to  compression  of  the  intrathoracic  veins. 

A  physician  must  be  very  careful  in  taking  the  history  of  a  patient  in  regard 
to  coughing.  So  long  as  the  cough  or  the  hacking  causes  neither  inconvenience 
nor  discomfort,  patients,  especially  the  phthisical,  persistently  deny  that  they  cough 
even  when  the  physician  hears  the  hack  himself.  By  imitating  the  sound  and 
movements  of  such  a  "hack,"  a  physician  can  sometimes  get  the  patient  to 
acknowledge  that  he  does  ' '  hack, ' '  but  that  he  never  considered  it  a  cough. 

It  must,  however,  be  acknowledged  that  some  cases  of  phthisis  or  bronchitis 
with  very  intense  inflammation  of  the  lungs  occur  without  any  cough  or  even  a 
"hack."  Here  the  secretion  is  probably  brought  up  to  the  vocal  cords  by  the 
ciliary  motion  of  the  mucous  membrane;  and  is  then  removed  by  ' '  clearing  the 
throat."  If,  as  frequently  happens,  the  secretion  is  swallowed,  the  patients  neither 
cough  nor  even  expectorate. 

LOCALIZED  PROMINENCE  OF  THE  CHEST  IN  COUGHING. 

As  a  result  of  the  marked  positive  pressure  and  variations  in  the 
chest  interior  which  are  combined  with  the  act  of  coughing,  certain  pli- 
able portions  of  the  thorax  may  be  pushed  forward  at  the  commence- 
ment of  the  coughing  spell  in  quite  a  remarkable  way.  If  the  glottis 
is  closed,  expiratory  pressure  distends  the  upper  part  of  the  chest  chiefly, 
because  the  expiratory  power  attacks  the  lower  thoracic  aperture.  In 
coughing,  therefore,  we  generally  observe  a  bulging  forward  of  the 
upper  intercostal  spaces  and  apices  of  the  lungs.  Such  bulging  is 
especially  prominent  in  emphysema  because  the  pulmonary  resistance 
is  impaired.  The  portion  of  the  lung  situated  above  the  level  of  the 
clavicles  shows  an  increase  in  volume,  so  that  during  a  cough  in 
emphysema  we  frequently  notice  that  large  swellings  are  produced 
above  the  clavicles.  This  phenomenon  should  not  be  confounded  with 
the  distention  of  the  jugular  veins  during  a  cough,  which  is  also  often- 
times quite  pronounced  (p.  146  et  .seg.).  If  the  lung  tissue  is  infiltrated 
and  shrunken,  coughing  will  evidently  not  produce  such  an  inflation. 
Hence,  a  careful  inspection  of  the  supraclavicular  fossae  sometimes 
furnishes  important  conclusions  as  to  the  condition  of  the  apices  in 
beginning  tuberculosis. 

PALPATION,  SPHYGMOGRAPHY,  AND   SPHYGMOME- 
TRY  OF  THE  ARTERIAL  PULSE. 

Examination  of  the  arterial  pulse  is  of  great  diagnostic  importance 
because  it  informs  us  of  many  things,  such  as  the  cardiac  innervation 
the  force  of  the  heart,  the  blood -pressure,  and  the  condition  of  the 
peripheral  arteries,  and  sometimes  suggests  the  existence  of  valvular 
diseases  of  the  heart  or  of  fever.  Many  individual  peculiarities  must 
be  considered  and  various  methods  employed  to  recognize  them. 

The  commonest  method  and  the  one  employed  almost  exclusively  by 
practitioners  is  manual  palpation  of  the  arterial  pulse. 

Sphygmography  and  sphygmomanometry  are  less  used.  Auscultation 
of  the  arterial  pulse  is  much  less  important. 


PALPATION  OF  THE  PULSE.  99 

PALPATION  OF  THE  PULSE, 

Any  superficially  placed  artery  may  be  utilized  for  the  purpose  of 
palpation  ;  but  we  nearly  always  choose  the  same  vessel,  so  as  to  have 
a  certain  uniform  standard,  experience,  and  practice  in  judging  of  the 
pulse.  On  account  of  its  accessibility,  the  radial  artery  is  usually 
selected.  It  is  palpated  between  the  styloid  process  of  the  radius,  or 
the  tendon  of  the  supinator  longus  and  the  tendon  of  the  flexor  carpi 
radialis.  An  anomalous  position  of  the  artery  or  of  the  tendons  will, 
of  course,  necessitate  our  trying  another  place.  In  doubtful  or  difficult 
cases  the  two  radials  should  be  compared,  so  as  not  to  attribute  some 
abnormality  really  due  to  local  causes  to  an  alteration  in  the  entire  cir- 
culatory condition.  One  radial  not  infrequently  seems  smaller  than  the 
other,  while  in  reality  it  is  merely  a  small  branch  which  lies  in  the 
ordinary  place  of  the  radial,  and  the  main  trunk  takes  some  abnormal 
course. 

The  best  method  of  palpating  the  pulse  is  to  put  the  tips  of  three 
adjoining  fingers  of  the  more  adept  hand  along  the  artery  and  to  vary 
the  pressure.  With  every  heart  beat  the  artery  is  found  to  expand  and 
to  lift  the  fingers.  This  lifting  is  what  we  call  the  pulse.  Palpation 
with  one  or  two  fingers  is  sufficient  to  determine  the  frequency  and  the 
rhythm;  but  we  need  three  fingers  for  judging  the  form  of  the  pulse 
wave  and  the  height  of  the  blood-pressure. 

CHARACTER  OF  THE  ARTERIAL  WALL. 

Palpation  of  the  arterial  wall  permits  us  to  determine  whether 
arterial  sclerosis  is  present  or  not,  and  whether  the  pulse  wave  is  modi- 
fied by  any  factors  in  the  wall  itself. 

The  most  important  thing  to  determine  is  the  amount  of  elasticity 
— i.  e.,  the  rigidity  of  the  arterial  tube.  This  can  be  most  effectually 
determined  by  rolling  the  artery  back  and  forth  under  the  finger 
and  by  running  the  finger  along  the  length  of  the  artery,  at  the  same 
time  being  careful  to  prevent  the  influence  of  the  blood-current  by 
occluding  the  artery  with  another  of  the  fingers.  The  artery  is  soft 
and  elastic  in  young  and  healthy  individuals ;  but  in  arteriosclerosis  or 
where  the  blood-pressure  is  permanently  raised  by  an  increase  of  the 
vasomotor  tonus  (chronic  nephritis,  lead-poisoning)  we  can  often  distinctly 
appreciate  the  increased  resistance  of  the  walls.  The  tortuous  character 
of  the  artery  so  frequent  in  these  conditions  is  produced  by  a  fresh  de- 
posit of  histologic  elements  in  its  wall.  At  the  same  time  some  arteries 
may  be  tortuous  without  any  arteriosclerosis — e.  g.,  the  temporal  arteries. 
The  deposit  of  lime  in  the  wall,  which  is  observed  in  very  pronounced 
cases  of  arteriosclerosis,  can  be  felt  very  distinctly  as  rough,  hard 
irregularities.  Although  palpation  is  diagnostically  important  in  de- 
termining the  existence  of  arteriosclerosis  of  the  peripheral  arteries,  it 
does  not  necessarily  show  whether  the  aorta,  coronary  arteries,  or  other 
deep-seated  vessels  are  normal  or  not.     The  arteriosclerotic  changes  may 


100     ARTERIAL  PULSE  PALPATION,  SPHYGMOGBAPHY,  ETC 

be  very  unevenly  distributed,  and  the  radial  artery  is  one  which  shows 
no  marked  predilection  for  arteriosclerosis.  Therefore,  to  demonstrate 
arteriosclerosis  we  should  palpate  as  many  as  possible  of  the  superficial 
arteries.  Arteriosclerosis  must  not  be  absolutely  excluded,  even  when 
the  results  of  palpation  are  negative. 

A  persistently  high-tension  pulse  is  one  of  the  most  reliable  indications  of  dif- 
fuse arteriosclerosis  when  the  examination  shows  no  other  cause  for  it  (nephritis). 

CHARACTERS  OF  THE  PULSE. 
FREQUENCY  OF  THE    PULSE. 

The  pulse  frequency — i.  e.,  the  number  of  beats  in  a  minute — is 
estimated  by  counting  the  radial  pulse.  It  is  advisable  to  count  an 
irregular  pulse  for  at  least  one  minute  and  then  to  repeat,  for  otherwise 
the  count  may  not  be  accurate.  If  repeated  counts  furnish  different 
figures,  the  extremes  should  be  noted. 

A  great  many  influences  affect  pulse  frequency,  so  that  it  is  advisable 
to  estimate  the  rate  under  conditions  which  are  as  nearly  alike  as  pos- 
sible, or,  in  case  this  cannot  be  done,  to  make  allowance  for  the  action 
of  these  influences  in  forming  an  opinion.  In  sensitive  people  any 
mental  excitement  whatsoever  decidedly  influences  the  pulse  rate.  The 
physician's  entrance  is  enough  to  cause  a  marked  rise  in  the  pulse,  so 
that  at  the  bedside  it  is  advisable  to  delay  counting  the  pulse  until  after 
having  conversed  with  the  patient  for  awhile. 

Any  bodily  exertion  or  movement  increases  the  pulse  rate.  After 
running,  gymnastics,  fencing,  or  mountain-climbing  the  rate  may  be 
very  greatly  increased  and  still  be  within  physiologic  bounds.  Even 
the  quieter  motions  in  bed,  voiding  urine,  or  evacuating  the  bowels, 
materially  increases  the  pulse  rate  in  very  sensitive  or  very  ill  patients. 
After  moderate  activity  the  increase  in  rate  soon  subsides,  but  after 
prolonged,  fatiguing  exertion  it  may  persist  for  some  time.  The  pulse 
rate,  furthermore,  depends  upon  the  position  of  the  body.  After  lying 
down,  sitting  up  increases  the  frequency ;  so  does  standing  up  after 
sitting.  This  rise  may  be  only  transitory,  due  to  the  muscular  exertion 
attendant  upon  the  change  of  position,  or  to  some  extent  permanent  so 
long  as  the  position  is  maintained. 

Guy  found  that  in  fasting,  healthy  men  who  had  previously  rested, 
the  pulse  rate  was  66  to  the  minute  while  prone,  71  while  sitting,  and 
81  when  standing. 

Digestion  of  food  increases  the  pulse  rate  for  several  hours  during 
the  period  of  digestion,  the  amount  of  increase  varying  according  to  the 
quantity  of  food.  The  daily  variations  of  the  pulse  are  only  partly  due 
to  the  influence  of  the  meals  ;  for  daily  variations  approximately  parallel 
to  the  daily  variations  of  temperature  are  observed  even  in  fasting  indi- 
viduals.    They  usually  amount  to  only  a  few  beats. 

Generally  speaking,  a  high  blood-pressure  produces  a  slowing  of  the  pulse,  a 
low  blood-pressure  an  increase  in  its  rate.  There  are,  however,  many  exceptions  to 
this  rule,  although  it  undoubtedly  possesses  some  physiologic  importance.     Marey 


PALPATION  OF  THE  PULSE.  101 

attributes  the  increased  pulse  rate  in  standing  up  as  contrasted  with  lying  down 
to  the  difference  in  blood-pressure.  This,  he  believes,  is  much  higher  in  the  recum- 
bent posture. 

Respiration  usually  influences  the  pulse  rate ;  during  inspiration  it 
is  increased,  during  expiration  diminished. 

Coughing  or  Valsalva's  experiment  produces  a  marked  increase  in 
the  pulse  rate.  In  the  latter  the  increased  frequency  persists  longer 
than  the  increased  intrathoracic  pressure. 

The  time  of  life  has  a  very  distinct  influence  upon  pulse  frequency. 
Rollet  ^  quotes  the  following  figures,  collected  from  various  observers,  as 
averages  : 

Pulse  beats  Pulse  beats 

Age.  to  minute.  Age.  to  minute. 

End  of  fetal  life 144-133     10th  to  15th  year 91-76 

Newborn  and  1st  year  of  life  143-123     20th-60th         "       73-69 

Vierordt  ^  gives  the  following  detailed  table  for  childhood  : 

Pulse  beats  Pulse  beats 

Age.  per  minute.  Age.  per  minute. 

1  year 134  7-8  years 94.9 

1-2  years 110         8-  9     "  88.8 

2-3      "      108        9-10     "  91.8 

3-4      "      108       10-11     "  87.9 

4-5      "      103       11-12     "  89.7 

5-6      "      98.0     12-13     "  87.9 

6-7      "      92.1     13-14     "  86.8 

The  pulse  rate  practically  diminishes  with  the  advancing  years 
until  the  age  of  sixty,  after  which  time  it  begins  to  increase  again 
slightly.  Sex  also  has  some  influence.  According  to  Guy,  women 
average  7  to  8  beats  a  minute  more  than  men  of  the  same  age.  In 
individuals  of  the  same  age  and  sex  the  pulse  rate  varies  according  to 
the  height ;  it  is  slower  in  tall  than  in  short  persons. 

Sometimes  the  pulse  count  at  the  wrist  is  less  than  over  the  heart. 
In  such  an  event  the  latter  must  be  the  accurate  measure  of  the  heart's 
frequency,  and  we  naturally  conclude  that  the  cardiac  power  has  be- 
come afi^ected,  so  that  some  of  the  pulse  waves  are  not  transmitted  to 
the  peripheral  arteries.  Such  an  omission  of  individual  beats  makes 
the  pulse  sequence  irregular,  so  that  the  examiner  then  turns  to  the 
heart.  If  the  radial  pulse  is  perfectly  regular  we  should  not  think  of 
the  existence  of  any  difference  between  it  and  the  heart-beat  unless  only 
every  other  beat  was  strong  enough  to  be  transmitted  to  the  radial  ar- 
tery, such  as  in  the  rare  condition  called  pulsus  alternaus  and  bigem- 
inus,  heart  bigeminus,  hemisystole,  systolia  alternans  (see  later  section 
upon  Cardiac  Impulse). 

The  pulse  frequency,  like  the  body  temperature,  can  be  conveniently 
represented  upon  a  chart  in  the  form  of  a  curve.  The  variations  of 
both  can  thus  be  very  accurately  compared  at  a  glance. 

Increase  of  Pulse  Frequency  ;  Tachycardia. — Fever  is  one 
of  the  most  common  causes  of  an  accelerated  pulse  rate.     The  tempera- 

^  Hermann,  Handhuch  der  Physiologie,  vol.  iv.,  1. 

="11.  Vierordt,  "Daten  und  Tabellen,"  Jena,  G.  Fischer,  1888. 


102    ARTERIAL  PULSE,  PALPATION,  SPHYGMOGRAPHY,  ETC. 

ture  and  the  pulse  curve  in  fever  usually  run  parallel.  Liebermeister 
estimated  that  the  pulse  frequency  was  increased  by  about  eight  beats 
for  every  degree  of  temperature.  So  long  as  pulse  and  febrile  disturb- 
ance run  parallel  in  this  way,  such  a  harmonious  preservation  of  the 
functions  may  be  regarded  as  relatively  favorable.  On  the  other  hand, 
the  more  the  acceleration  of  the  pulse  exceeds  the  elevation  of  tempera- 
ture the  graver  the  prognosis,  because  too  rapid  a  pulse  rate  usually 
means  some  serious  damage  to  the  circulation,  either  to  the  heart  or  to 
the  vasomotor  system.  If  the  patient  is  resting  quietly  a  pulse  of  140 
to  160  in  fever  is  always  of  grave  significance.  Under  various  condi- 
tions of  fever  the  pulse  frequency  and   the  temperature  may  follow  an 


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Fig.  33. — Relation  of  temperature  aud  pulse  frequency  In  tuberculous  meningitis. 

entirely  different  course.  Such  a  divergence  of  the  curves  is  of  very 
great  diagnostic  importance.  A  high  temperature  with  a  slow  pulse  is 
observed  chiefly  in  febrile  brain  diseases,  in  which  the  pressure  upon  the 
brain  is  responsible  for  the  slowing  of  the  pulse  as  in  tubercular  menin- 
gitis (Fig.  33) ;  again  in  a  combination  of  a  febrile  disease  with  a  car- 
diac disturbance  which  causes  brachycardia  (adiposity,  sclerosis  of  the 
coronary  arteries,  myocarditis).  The  converse,  a  high  pulse  rate  with 
an  abnormally  low  temperature,  is  characteristic  of  the  symptom  complex 
of  acute  circulatory  weakness  included  in  the  name  collapse  (see  Fig.  32). 
There  are  numerous  other  exceptions  to  this  rule  of  parallelism  of 
the  two  curves,  although  most  of  them  are  less  pronounced  than  the 
example  just  cited — e.  g.,  in  typhoid  fever  the  pulse  frequency  is  noto- 


PALPATION  OF  THE  PULSE.  103 

riously  moderate  as  compared  with  the  height  of  the  temperature  (see 
Fig.  24).  This  pecuharity  is  often  serviceable  in  differentiating  typhoid 
fever  from  acute  miliary  tuberculosis  or  septicopyemia.  For  in  the 
last  two  mentioned  the  pulse  rate  is  almost  always  accelerated  as  much 
as,  if  not  out  of  proportion  to,  the  rise  of  temperature.  Conversely,  in 
pulmonary  tuberculosis  a  very  high  pulse  rate  is  frequently  observed 
with  only  a  moderate  rise  of  temperature  or  even  with  no  rise  at  all. 
Yet  the  rectal  is  often  unexpectedly  higher  than  the  mouth  temperature. 
Children  usually  exhibit  a  relatively  rapid  pulse  rate  with  fever. 

A  rapid  pulse  rate  is,  furthermore,  found  in  affections  of  the  heart  or  of 
the  nerves.  Valvular  diseases  in  the  stage  of  disturbed  compensation — 
endocarditis,  pericarditis,  exophthalmic  goiter,  nervous  palpitation,  ner- 
vous tachycardia,  dislocation  of  the  heart  by  processes  in  its  vicinity 
which  limit  the  space — all  of  these  diseases  are  or  may  be  associated  with 
a  more  or  less  considerable  increase  of  the  pulse  rate,  to  a  certain  extent 
proportional  to  the  severity  of  the  affection.  Very  imperfect  explana- 
tion has  been  found  for  the  cause  of  the  increased  pulse  rate  in  these  cases. 
The  author  considers  that  the  cause  of  the  increased  pulse  frequency 
in  the  clinical  picture  of  so-called  "  paroxysmal  tachycardia  "  is  due  to 
an  epileptoid  discharge  in  the  neighborhood  of  the  cardiac  accelerating 
nerves,  although  he  realizes  that  such  an  opinion  is  at  variance  with 
Martius. 

An  increased  pulse  rate  also  occurs  combined  with  all  sorts  of  pain. 
Under  some  conditions  not  yet  understood  the  reverse  sometimes  takes 
place — i.  e.,  a  slowing  of  the  pulse  (see  p.  104).  The  reflex  influence 
upon  the  cardiac  nerves  is  the  probable  cause  in  both  cases. 

Atropin  and  alcohol  are  the  two  most  important  of  the  numerous 
poisons  which  accelerate  the  rate  of  the  heart. 

Not  infrequently,  under  pathologic  conditions,  the  acceleration  of  the 
pulse  due  in  a  healthy  individual  to  physiologic  influences  (p.  100  et  seq.) 
may  reach  an  excessive  degree  so  far  as  duration  and  intensity  are  con- 
cerned. This  always  points  either  to  some  damage  to  the  heart  itself  or 
to  its  nervous  system.  Thus,  in  chlorotics  or  in  other  weakly  individuals 
even  very  slight  exertion  (stair  climbing)  will  greatly  increase  the  pulse 
rate ;  and  this  increase  usually  is  associated  with  the  subjective  sense  of 
palpitation  of  the  heart  or  of  dyspnea. 

Diminution  of  the  Pulse  Rate  (Bradycardia ;  Brachy- 
cardia). — A  noticeably  slow  pulse  does  occur,  although  rarely,  as  an 
individual,  non-pathologic  peculiarity  in  a  healthy  person.  A  very 
pronounced  slowing  of  the  rate,  to  as  low  as  20  or  less  beats  to  the 
minute,  is  observed  pathologically  in  certain  diseases  of  the  heart  muscle, 
especially  in  the  "fatty  "  infiltrated  heart  and  in  sclerosis  of  the  coronary 
arteries.  A  slight  degree  of  retardation  is  sometimes  observed  in  com- 
pensated aortic  stenosis.  Cachectic  individual  usually  exhibit  not  only 
a  low  temperature  but  also  a  slow  pulse  rate  (carcinoma  of  esophagus, 
etc.).     Similar  results  are  observed  in  convalescence. 

A  temporary  slowing  of  the  pulse  (to  a  little  below  normal)  is  often 
found  in  acute  febrile  diseases  after  the  crisis.     When,  despite  the  criti- 


104    ARTERIAL  PULSE,  PALPATION,  SPHYGMOGRAPHY,  ETC. 

cal  drop  of  temperature,  the  pulse  remains  high,  there  is  always  reason 
to  suspect  a  "  pseudocrisis  "  (see  Fig.  23).  In  certain  painful  aifections 
(e.  g.,  gall-stone  colic,  lead-colic)  a  slowing  of  the  pulse  is  more  fre- 
quently observed  than  an  increase.  Icterus  often  produces  retardation, 
due  to  the  toxic  action  of  the  biliary  salts.  This,  however,  usually 
disappears  when  the  jaundice  is  prolonged,  either  because  the  heart 
becomes  accustomed  to  the  intoxication,  because  the  production  of  the 
biliary  salts  is  diminished,  or  because  their  elimination  is  more  complete. 
The  slowing  of  the  pulse  in  acute  cerebral  pressure  is  of  particular 
diagnostic  importance  (meningitis  (Fig.  33),  fracture  of  the  skull). 
Chronic  cerebral  pressure  usually  does  not  cause  any  slowing  of  the 
pulse  unless  acute  exacerbations  occur.  Shock  sometimes  causes  an 
excessive  slowing  of  the  pidse.  Rapid  emptying  of  peritoneal  or  pleu- 
ritic effusions  sometimes  diminishes  the  pulse  rate.^  Some  drugs  (digi- 
talis, etc.)  produce  a  slowing  of  the  pulse. 

PULSE  RHYTHM. 

Under  normal  conditions  the  pulse  is  regular  or  rhythmic — i.  e.,  the 
individual  pulse  waves  follow  each  other  at  equal  intervals  of  time. 
Only  slight  transitory  deviations  from  such  regularity  come  within 
physiologic  limits,  and  then  principally  under  conditions  which  modify 
the  pulse  frequency  as  well.  More  pronounced  irregularities  of  the 
sequence  of  beats,  or  arrhythmia,  are  probably  all  pathologic,  and  indi- 
cate either  some  distinct  lesion  of  the  heart  or  some  purely  functional 
disturbance  of  its  activity,  such  as  occurs  in  all  sorts  of  conditions  with 
or  without  cardiac  weakness. 

We  may  differentiate  between  an  absolutely  irregular  pulse  (pulsus 
irregularis),  which  is  usually  at  the  same  time  much  increased  in  rate 
(delirium  cordis),  and  a  partially  irregular  pulse.  In  one  type  of  the 
latter  the  irregularities  are  uneven — i.  e.,  the  intervals  between  the  beats 
are  sometimes  shortened  and  sometimes  lengthened  without  any  sign  of 
regularity.  In  the  other  type  of  the  partially  irregular  pulse  the  irreg- 
ularities are  periodic — i.  e.,  they  follow  each  other  at  regular  and  definite 
intervals. 

Irregularities  of  rhythm  are  nearly  always  associated  wnth  inequality 
of  the  individual  pulse  waves—/,  e.,  a  pulsus  irregularis  is  at  the  same 
time  a  pulsus  inequalis.  It  is  therefore  advisable  to  defer  the  consider- 
ation of  the  various  types  of  irregular  pulse  until  after  we  have  studied 
and  understood  the  differences  in  quality  of  the  individual  beat.  (See 
Sphygmography,  p.  122  et  seq.,  and  p.  130  et  seq.). 

CHARACTERS  OF  THE  INDIVIDUAL  PULSE  BEAT. 

The  proficiency  which  different  observers  attain  in  the  determination 
of  the  quality  of  the  individual  beat  by  palpation  varies  decidedly  with 
their  practice  and  skill.     He  who  is  less  adept  may  obtain  more  accurate 

1  Much  more  frequently  a  lupid  weak  pulse  is  the  immediate  result  of  tapping  the 
chest  or  abdomen  ;  the  retardation  follows  later. — Ed. 


PALPATION  OF  THE  PULSE.  105 

information  by  employing  sphygmography  or  sphygmomanometry.  In 
addition  to  the  regularity,  the  qualities  which  every  physician  should 
recognize  by  palpation  without  any  especial  instrument  are  :  the  size, 
the  celerity,  the  tension,  and  dicrotism. 

Si^e  of  the  Pulse ;  Pulse  Volume. — By  size  we  mean  the 
extent  of  the  excursion  which  the  arterial  wall  makes  under  the  influ- 
ence of  the  pulse  wave.  With  a  large,  full  pulse  (pulsus  magnus)  this 
excursion  is  considerable ;  in  a  small,  weak  pulse  (pulsus  parvus)  the 
excursion  is  small.  (As  to  the  significance  of  and  the  alterations  in  the 
volume  of  the  pulse  and  the  variations  in  the  size  of  the  individual 
waves,  see  Sphygmography,  p.  124  et  seq.) 

What  we  designate  as  the  pulse  volume  Marey  calls  its  strength,  and  with  a 
certain  amount  of  justice;  because,  of  course,  the  vital  power  of  the  rise  corre- 
sponds to  the  size  of  the  pulse  wave — i.  e.,  to  the  amount  of  matter  set  in  motion. 
This  corresponds  to  the  terminology  employed  in  describing  wave  motion,  where  the 
strength  of  a  vibration  is  measured  by  its  amplitude.  For  clinical  purposes,  how- 
ever, the  author  prefers  the  term  "volume,"  because  the  word  "strength"  would 
often  suggest  that  we  were  expressing  a  certain  opinion  about  the  heart's  activity 
or  power,  and  this  is  by  no  means  always  the  case,  as  we  shall  see  later  (see  Sj)hyg- 
mography). 

Celerity  of  the  Pulse. — By  celerity  is  meant  the  rapidity  of  the 
rise  and  subsidence  of  the  individual  pulse  wave.  A  quick  pulse  (pulsus 
celer)  is  one  whose  wave  rises  quickly  and  descends  quickly  ;  a  sluggish 
pulse  (pulsus  tardus)  is  one  whose  wave  rises  slowly  and  descends  slowly. 
Upon  the  fingers  a  pulsus  celer  produces  the  impression  of  a  quick,  sharp 
rap.  This  peculiarity  is  appreciated  most  distinctly  when  the  pulse  wave 
is  at  the  same  time  of  considerable  volume.  Therefore,  what  is  often 
called  a  pulsus  celer  is  generally  a  full  pulse  as  well.  The  pulse  of 
aortic  insufficiency  is  the  most  striking  as  well  as  the  commonest  ex- 
ample of  a  pulsus  celer.  It  very  frequently  can  be  appreciated  even 
by  the  eye  as  a  very  striking  pulsation  of  the  artery,  and  the  diagnosis 
of  aortic  insufficiency  made  correctly  at  a  distance.  The  rapidity  of  the 
ascent  and  that  of  descent  of  the  pulse  wave  do  not  take  an  equal  part 
in  producing  this  "rapping"  sensation.  For  although  the  rapidity  of 
the  rise  may  be  recognized  without  any  particular  training,  it  requires 
considerable  practice  to  recognize  the  quickness  of  the  drop.  Von 
Frey  claims  that  the  rapidity  of  the  descent  of  the  pulse  wave  can  be 
estimated  only  by  means  of  the  sphygmograph  and  not  by  palpation. 
But  the  author  believes  that  an  expert  physician  can  perfectly  well  dif- 
ferentiate between  a  pulse  whose  sharp,  bounding  quality  is  due  only  to 
a  rapid  onset  of  the  wave  and  a  pulse  with  a  rapid  descent  as  well  as 
ascent.  The  terms  "  pulsus  celer  "  and  "  pulsus  tardus  "  are  especially 
well  adapted  to  the  cases  in  which  both  limbs  of  the  pulse  wave  are 
either  steep  or  blUnt.  Where  either  the  ascent  or  the  descent  alone 
is  rapid  or  slow  this  peculiarity  should  be  specified.  Thus,  a  pulse 
may  be  celer  in.  its  ascent  and  twdus  in  its  descent.  Such  an  applica- 
tion of  the  terms  "  celer  "  and  "  tardus  "  to  the  same  pulse  is  no  con- 
tradiction. These  conditions  are  explained  more  fully  upon  p.  124  by 
Sphygmography.      (Figs.  47-51.) 


106     ARTERIAL   PULSE,   PALPATIOX,   SPHYGMOGRAPHY,   ETC. 

Pulse  Tension. — Consideration  of  Blood-pressure. — We 

consider  under  the  term  '•  pulse  teusion  "  the  qualities  of  the  indi- 
vidual pulse  wave  which  show  the  amount  of  pressure  in  the  arteries. 
The  difficulty  is,  however,  that  the  term  blood-pressure  may  be  under- 
stood in  quite  different  ways.  The  physiologist  ordinarily  uses  the  word 
to  mean  the  average  or  mean  blood-pressure  as  estimated  by  the  usual 
manometers.  But  the  maximum  or  systolic  and  the  minimum  or  dias- 
tolic blood  pressure  must  also  be  considered.  In  a  healthy  man  or 
animal  the  variations  of  blood-pressure  from  the  average  are  very  slight, 
and  so  we  ordinarily  speak  of  ''  blood-pressure  "  without  further  remark 
when  we  strictly  mean  average  blood-pressure.  AVe  do  not  know,  how- 
ever, whether  the  systolic  variations  in  pressure  under  pathologic  conditions 
are  so  very  slight.  Sphygmographic  and  sphygmomanometric  obser- 
vations (see  later)  seem  to  show  that  they  are  considerable.  Therefore, 
under  pathologic  conditions,  the  systolic  or  maximum,  the  average  or 
mean,  and  finally  the  diastolic  or  minimum  pressure  should  be  considered 
separately.  The  writer  believes  that  many  apparent  contradictions  in 
palpatory,  sphygmographic,  and  mauometric  estimations  of  pressure 
(see  p.  135)  can  be  explained  by  a  disregard  of  such  conditions.  A 
more  distinct  and  uniform  conception  of  the  terms  expressing  the  pulse 
tension  is  therefore  essential,  and  these  terms  should  be  clinically  correl- 
ative to  blood-pressure.  Just  as  we  distinguish  between  a  maximum, 
middle,  and  minimum  blood-pressure,  so  should  we  differentiate  between 
a  maximum  or  systolic,  an  average  or  mean,  and  a  minimum  or  diastolic 
tension  of  the  arteries.  The  ordinary  definition  that  tension  is  the 
measure  of  the  amount  of  finger  pressure  which  is  necessary  to  compress 
the  artery  is  not  accurate,  and  is,  therefore,  inadequate  to  teach  us  how  to 
palpate  pulses  correctly.  It  is  better  to  define  the  maximum  tension 
of  an  artery  as  the  amount  of  force  which  is  necessary  to  prevent  the 
transmission  of  the  pulse  wave  to  the  peripheiy,^  the  minimum  tension 
as  the  power  necessary  to  compress  an  artery  during  cardiac  diastole, 
and  the  average  or  mean  tension  as  a  certain  average  amount  of  power 
which  will  suffice  to  close  the  artery  between  systole  and  diastole.  A 
disregard  of  the  various  meanings  of  the  term  arterial  tension  thus  ex- 
plains the  variations  in  the  description  of  one  and  the  same  pulse,  one 
observer  calling  the  tension  high,  another  calling  it  low. 

As  the  manner  of  palpating  an  artery  varies,  so  do  conclusions  as  to 
the  pressure  conditions  in  the  artery  differ.  Usually  (although  only  partly 
justifiably)  most  importance  is  attached  to  the  maximum  or  systolic  ten- 
sion of  the  artery.  This  is  determined  ("  dynamic  "  procedure  of  taking 
the  pulse)  by  palpating  the  arteiy  with  three  adjoining  fingers  along  the 
long  axis  of  the  vessel.  The  distal  finger  compresses  the  artery  so  that 
no  recurrent  pulse  wave  can  reach  the  vessel  from  the  periphery.  The 
proximal  finger  exerts  a  gradually  increasing  pressure  upon  the  artery 
until  the  middle  finger,  which  should  rest  quite  gently  upon  the  vessel,  can 
no  longer  feel  the  wave.      The  power  used  is  the  measure  of  the  (heart) 

'  See  the  following  pages  for  the  doubts  alx)ut  identifying  this  exercise  of  power 
with  the  systolic  pressure. 


PALPATION  OF  THE  PULSE.  107 

systolic  or  maximum  tension  of  the  artery.  This  procedure  is  imitated 
by  von  Basch's  method  of  sphygmography  (p.  134  est  eq.).  The  physical 
accuracy  of  his  method  of  determining  the  systolic  pressure — i.  e.,  the 
correctness  of  identifying  the  amount  of  pressure  employed  with  the  sys- 
tolic pressure — is  questionable  (p.  135).  The  same  doubt  applies  to  this 
dynamic  method  of  palpation,  for  the  reason  that,  besides  the  systolic 
increase  of  pressure,  the  vital  energy  of  the  pulse  wave  has  an  impor- 
tant influence  upon  the  result  obtained  (p.  1 35  et  seq.).  This  vital  energy 
is  closely  dependent  upon  the  size  of  the  pulse  wave  (p.  135  et  seq.),  and 
the  size  in  turn  by  no  means  runs  parallel  with  the  blood-pressure ;  in 
fact,  it  is  often  inversely  proportional  to  the  latter.  We  have  not  only 
the  systolic  blood-pressure  to  overcome  in  the  procedure,  but,  generally 
speaking,  a  much  greater  pressure,  because  the  recoil  of  the  pulse  wave 
at  the  compressed  point  of  the  artery  acts  very  much  as  a  water-ram. 
On  account  of  the  size  of  the  pulse  wave,  the  excess  of  energy 
employed  above  the  systolic  pressure  is  oftentimes  greatest  with  a  low 
blood-pressure.  Consequently  this  dynamic  method  is  frequently  re- 
sponsible for  questionable  results,  for  it  is  often  hard  to  compress  an 
artery  if  the  pulse  is  full  (large),  even  though  the  tension  is  low,  while 
conversely,  a  small  (weak)  pulse  may  frequently  be  easily  compressed 
even  if  the  blood-pressure  is  high. 

The  following  "  static  "  method  for  determining  the  minimum  or 
diastolic  arterial  tension  is  probably  more  reliable.  If  the  fingers  exert 
but  slight  pressure  in  palpating  the  artery  we  notice  that  the  appreciable 
pulsatory  excursions  of  the  artery  are  usually  small,  and  that  they  in- 
crease as  soon  as  the  pressure  is  increased  until  a  maximum  excursion 
is  reached.  After  this  point  still  greater  pressure  again  diminishes  the 
size  of  the  pulse.  The  amount  of  pressure  necessary  to  produce  a 
maximum  excursion  corresponds,  in  all  probability,  to  the  minimum  or 
diastolic  pressure  in  the  artery.  This  may  be  explained  as  follows  :  The 
reason  why  the  excursion  of  the  artery  increases  as  we  increase  the 
pressure  upon  its  wall  is  evidently  because  a  part  of  the  pulsatory  in- 
crease in  pressure  is  absorbed  by  the  tense  arterial  wall  when  the  artery 
is  not  compressed ;  whereas,  if  we  remove  the  tension  from  the  arterial 
wall,  by  contrapressure,  the  pulse  wave  will  be  transmitted  to  the  palpa- 
ting finger  with  a  minimum  amount  of  loss.  The  greatest  excursion 
will  evidently  coincide  with  the  comjjlete  relaxation  of  the  arterial  wall 
at  the  onset  of  the  pulse  wave — i.  e.,  when  the  pressure  exerted  cor- 
responds to  the  minimum  pressure  of  the  artery.  Besides  this,  when 
pressure  is  brought  to  bear  upon  the  artery  from  without  which  exactly 
corresponds  to  the  minimum  arterial  pressure,  or,  more  strictly  speaking, 
is  the  slightest  ajnount  in  excess  of  it,  the  artery  will  then  be  occluded 
at  the  instant  of  the  arrival  of  the  pulse  wave,  and,  of  course,  the  latter 
will  back  up  considerably  from  reflections,  so  that  the  excursion  of 
the  wall  will  be  increased  in  this  way  too.  Any  compression  above 
this  point  will,  of  course,  diminish  the  excursion  again,  since  the  pulse 
wave  will  no  longer  be  capable  of  overcoming  the  resistance  of  the 
pressure  fingers.     The  digital  pressure  exerted  to  produce  the  greatest 


108     ARTERIAL  PULSE,   PALPATION,  SPHYGMOGRAPHY,  ETC. 

pulse  excursion  possible  by  this  method  is  considered  as  the  measure 
of  the  minimum  arterial  pressure.  It  is  important  to  estimate  the  size 
of  the  arterial  excursion,  and  not  its  strength  or  force. 

Beside  these  unavoidable  inaccuracies  we  can  readily  appreciate 
the  fact  that  an  especial  skill  in  appreciating  the  relations  of  pressure 
accrues  to  the  careful  clinician  only  after  years  of  practice  and  a  long 
experience  in  contrasting  and  remembering  diiferences  in  pressure. 
Another  difficulty  is  that,  according  to  Pascal's  law  (law  of  hydraulic 
pressure),  the  amount  of  pressure  necessary  to  compress  an  artery  is 
proportional  not  only  to  the  arterial  pressure,  but  also  to  the  diameter 
of  the  artery.  On  account  of  such  varied  and  manifold  difficulties  in 
judging  arterial  tension,  it  is  advisable  to  supplement  palpation  by 
sphygmography  (p.  129  et  seq.). 

Custom  has  come  to  employ  the  expression  "  hard "  or  "  tense " 
pulse  (pulsus  durus)  as  synonymous  with  increased  arterial  tension,  and 
"  soft "  or  "  relaxed "  pulse  (pulsus  mollis)  with  diminished  tension. 
Of  course,  we  must  not  confuse  these  with  the  same  terms  applied  to 
qualities  of  the  arterial  wall  (softness  versus  rigidity  of  the  artery) 
(p.  99).  Again,  these  terms  may  at  one  time  be  applied  to  the  systolic, 
at  another  to  the  diastolic,  pressure.  In  nephritis  and  arteriosclerosis 
the  diastolic  as  well  as  the  systolic  pressure  is  ordinarily  increased ;  iu 
fever  usually  the  diastolic  is  low  while  the  systolic  is  more  frequently 
high ;  in  disturbances  of  compensation  systolic  and  diastolic  pressure  are 
both  low. 

Dicrotic  Pulse. — We  speak  of  a  pulse  as  being  dicrotic  when  a 
second  wave  follows  immediately  after  the  principal  rise.  (The  nature  of 
this  will  be  discussed  under  Sphygmography,  p.  113  et  seq.  and  p.  129  et 
seq.)  A  dicrotic  pulse  furnishes  a  certain  sense  of  after  beating  to  the  pal- 
pating finger.  It  is  usually  associated  with  diminution  of  the  minimum 
pressure.  Both  the  primary  and  the  secondary  wave  are  felt  to  be 
greatest  when  the  palpating  finger  presses  only  slightly ;  therefore  a 
dicrotic  pulse  is  best  appreciated  with  gentle  pressure.  This  can  be 
readily  understood  from  the  explanation  given  of  the  excursion  of  the 
arteries  (p.  106  et  seq.).  The  beginner  is  apt  to  employ  too  great  press- 
ure to  recognize  readily  such  a  condition. 

Combined  Qualities  of  the  Pulse. — We  have  a  number  of 
terms  which  refer  to  a  pulse  which  comprises  two  or  more  of  the  qualities 
already  described.  Of  these  we  shall  mention  only  those  in  most  common 
use  :  pulsus  fortis,  strong  pulse  =  large  +  tense  (see  also  p.  105) ;  pulsus 
plenus,  full  pulse  ^  large  and  medium  hard  ;  pulsus  debilis  s.  inanis, 
weak  or  feeble  pulse  =  small  +  weak  ;  pulsus  undosus  =  large  +  soft ; 
pulsus  serratus  ==  large  +  tense  +  rapid ;  pulsus  vibrans  =  very  large  + 
very  tense.  This  name  is  applied  because  the  so-called  elasticity  eleva- 
tions (see  p.  116)  may  be  distinctly  appreciated  by  palpation.  These  terms 
are  fitting  enough,  but  I'ather  unnecessary.  Instead  of  employing  them, 
it  is  better  for  a  beginner  to  mention  the  individual  qualities  one  after 
another.  The  Latin  terms  are  sometimes  combined.  For  instance,  we 
speak  of  a  pulsus  tardodicrotus  or  a  pulsus  magnodurus,  etc.     Such 


8PHYGM0GRAPHY. 


109 


combination  terms  are  practical  enough  in  themselves,  but  some  of  them 
are  not  sufficiently  clear,  considering  the  double  meaning  of  the  terms 
"  celerity  "  and  "  tension  "  (see  above).  In  general  a  detailed  descrip- 
tion is  better  than  an  attempt  to  describe  the  pulse  by  one  word.  There 
are  some  terms  employed  to  characterize  peculiarities  of  a  sequence  of 
beats  and  not  of  individual  beats.  These  terms  as  well  as  further 
details  about  pulse  peculiarities  will  be  described  in  connection  with  the 
Sphygmographic  Curves  (p.  122  et  seq.). 

SPHYGMOGRAPHY, 

Sphygmography  is  the  method  of  registering  the  pulse  wave  of  some 
peripheral  vessel,  generally  the  radial  artery,  upon  a  moving  surface 
(usually  smoked  paper)  by  means  of  a  special  instrument,  the  sphygmo- 
graph. 

Vierordt  constructed  the  first  sphygmograph,  and  since  then  a  great 
many  impi'oved  instruments  have  appeared.  Most  of  them,  however, 
have  retained  Vierordt' s  principle  of  transmission  by  means  of  a  lever. 
The  best  known  and  most  frequently  employed  sphygmographs  are  : 
Marey's,  for  a  long  time  the  only  one  used  clinically ;  Landois', 
Sommerbrodt's,  Riegel's,  Dudgeon's,  Jaquet's,  and  v.  Frey's.     Dud- 


FiG.  34.— V.  Frey's  sphygmograph. 

geon's  apparatus  has  been  a  favorite  in  recent  years,  because  with  it 
curves  of  considerable  excursion  are  easily  traced.  Jaquet's  is  an  im- 
provement upon  this  pattern,  including  a  really  excellent  mechanism  for 
marking  intervals  of  time.  v.  Frey's  sphygmograph,^  also  a  very 
excellent  instrument,  is  depicted  in  Fig.  34. 

It  possesses  this  advantage  over  other  instruments  :  the  motions  of 
the  pulse  are  transmitted  to  the  writing-lever  as   simply  as   possible. 
^  V.  Frey,  Die  Untersuchung  des  Pulses,  Berlin,  1892,  J.  Springer. 


110     ARTERIAL  PULSE,   PALPATION,   SPHYGMOGRAPHY,   ETC. 

The  method  of  employing  this  instrument  is  as  follows  :  The  most 
superficial  part  of  the  radial  artery  is  marked  upon  the  wrist  with  a 
skin-pencil;  and  the  apparatus  is  adjusted  so  that  the  "pelotte"  im- 
pinges exactly  over  the  indicated  artery,  and  wnth  the  drum  toward  the 
elbow.  It  is  then  fastened  to  the  forearm  by  means  of  the  carrier  or 
slide,  S,  with  a  strap.  The  carrier  (Fig.  35)  is  fastened  separately 
with  the  hooks  that  are  attached  for  this  purpose.  The  screw  Sch  serves 
to  fix  the  strap.  Loosening  screw  2  makes  it  possible  to  move  the 
entire  apparatus  upon  the  "  carrier  "  This  is  very  convenient  for  the 
purpose  of  adjusting  the  "pelotte"  more  accurately.  By  means  of 
screw  3  we  attempt  to  regulate  the  amount  of  pressure  upon  the  pad 
until  the  lever  needle  begins  to  make  excursions.  The  apparatus  is  then 
firmly  fixed  in  place  by  tightening  screw  2. 

The  drum  has,  of  course,  been  removed  from  the  apparatus  before 
this,  covered  with  wax  paper,  smoked  ^  by  revolving  over  a  flame,  and 
then  replaced  upon  the  clock  mechanism,  U.      By  turning  key  1  the 


Fig.  35. — The  carrier  or  slide  of  v.  Frey's  sphygmograph. 

drum  can  be  moved  so  that  the  bent  point  of  the  registering-needle  rests 
lightly  upon  the  smoked  paper.  The  height  of  its  excursion  and,  hence, 
of  the  curve  can  be  regulated  by  turning  screw  3,  w^hich  controls  the 
tension  of  the  "  pelotte."  The  clockwork  is  then  started  by  means  of 
the  lever  which  is  visible  behind  the  writing-lever  H,  to  the  right 
of  the  drum.  The  drum  revolves  and  the  bent  point  of  the  needle 
registers  the  sphygmographic  curve  upon  the  smoked  drum.  The  drum 
is  then  taken  off  again,  the  paper  carefully  cut  off,  separated  from  the 
drum,  and  fixed  in  shellac  or  in  a  10  per  cent,  solution  of  dammar  bal- 
sam in  benzin.  The  part  E,  which  has  not  yet  been  described,  is  a 
small  electromagnet  with  a  registering-needle  attached  to  the  anchor,  so 
that  it  registers  upon  the  drum.  AVhen  connected  with  an  electric  cur- 
rent, intervals  of  time  or  signals  may  be  indicated  in  the  same  way  as 
is  customary  in  physiologic  experiments.  When  it  is  not  being  used  it 
may  be  disconnected. 

V.   Frey  has  recently  modified  his  sphygmograph  ;  and,  it  would  seem,  very 
advantageously.     The  chief  improvement  is  the  substitution  of  a  delicate  metal 

^  A  pointed  gas  flame  is  perhaps  the  best  source  for  smoking,  or  a  kerosene  lamp, 
or  a  piece  of  burning  camphor.  "We  must  be  careful  not  to  smoke  too  thickly,  because 
the  friction  between  the  registering-needle  and  the  drum  would  be  so  great  that  the  curve 
would  be  disturbed. 


SPHYGMOGRA  PHY.  Ill 

spring  for  the  joint  connections,  so  that  the  motions  of  the  registering-needle  are 
less  angular.  Besides  this,  the  drum  is  connected  with  a  Jaquet's  chronometer 
works,  so  that  the  time  intervals  are  pictured.  The  curve  may,  of  course,  be  regis- 
tered by  means  of  air  transmissions  ujjon  a  kymographion  placed  at  some  distance. 

Jaquet's  sphygmograph^  (Fig-  36)  consists  of  a  metal  frame,  Dp,  to 
which  is  sewed  a  cuff,  B,B,  for  attaching  to  the  wrist.  The  sphvgmo- 
graph  proper,  Ar,  is  attached  to  the  frame.  The  window  cut  out  of  the 
frame  is  to  be  applied  accurately  along  the  radial  artery  (previously 
marked  out  with  a  pencil),  and  the  cuff  then  strapped  around  the  wrist 
(|uite  tightly.  The  sphygraograph  proper  is  set  into  the  frame  by  hook- 
ing into  the  hinge,  p;  and  then  the  connection  of  the  two  parts  is 
effected  by  pressing  down  at  r  and  tightening  the  screw  m.  The  pulse- 
registering  apparatus  consists  of  a  short,  broad  spring,  which  presses 
upon  the  artery  and  transmits  its  movements  to  the  registering-needle 
by  means  of  the  lever  system  ef.  The  screw  m  also  serves  to  adjust 
the  registering-needle  at  the  desired  height  upon  the  smoked  strip  of 
paper.  By  screwing  it  down  the  spring  d  is  pressed  against  the  artery. 
The  screw  c  is  connected  with  an  "  eccentric  "  contrived  to  increase  or 
diminish  the  pressure  upon  the  spring.  The  amount  of  pressure  can  be 
determined  by  noting  the  position  of  the  figures  upon  the  screw.  With 
this  mechanism  the  instrument  can  be  adjusted  with  practically  equal 
pressure  in  each  case,  and  taken  away  from  the  frame  and  reapplied  in 
the  same  case  without  alteration  of  the  pressure.  Jaquet's  instrument, 
like  Dudgeon's,  writes  upon  a  flat  and  not  upon  a  curved  surface,  as  most 
other  sphygmographs  do.  Another  advantage  consists  in  the  very  slight 
and  constant  amount  of  friction  between  the  writing  needle  and  the  paper, 
so  that  there  is  very  little  trouble  in  adjusting  the  registering  part  of  the 
apparatus.  The  paper  is  horizontal ;  it  need  not  be  especially  strong ; 
and  it  may  easily  be  40  or  50  cm.  long.  The  little  box  a  contains 
the  clockwork  which  moves  the  strip  of  paper,  p.  This  is  started 
by  pressing  down  on  lever  6.  The  rate  that  the  paper  moves  may  be 
increased  from  1  to  4  cm.  in  a  second  by  altering  the  position  of  lever  a. 
The  slower  motion  produces  a  curve  which  presents  a  better  general  idea  ; 
the  more  rapid  motion,  one  which  may  be  more  accurately  analyzed. 
This  rate  of  motion  may  be  altered  while  the  sphygmograph  is  in  action. 
The  box  a  also  contains  a  stop-watch  connected  with  the  time-registering 
mechanism,  8.  The  latter  consists  of  a  small  pen  which  registers  a  mark 
upon  the  margin  of  the  smoked  ribbon  every  fifth  of  a  second  (Fig.  39). 

The  old'style  of  the  Jaquet  sphygmograph,  illustrated  in  Fig.  36,  has 
the  disadvantage  that  the  individual  parts  of  the  pulse-registering  mech- 
anism are  not  connected  firmly  enough  to  insure  their  constant  contact 
with  every  change  in  the  rate  of  motion.  At  e  and  d  the  movements 
of  the  lever  system  are  transmitted  by  loose  joints.  This  is  not  a  dis- 
advantage when  the  excursions  are  slow,  since  the  parts  are  held  in 
contact  by  the  metallic  ball  which  is  visible  at  the  top  of  the  apparatus. 
When  the  excursions  are  rapid  (increased  frequency  of  the  pulse,  great 

^  Described  in  Zeit.f.  Biol,  vol.  xxviii.,  N.  F.  x.  Manufactured  by  Scbiile,  Mechanic 
to  Physiologic  Institute  of  Basel. 


112     ARTERIAL  PULSE,  PALPATION,  SPHYGMOGRAPHY,   ETC. 

elevation  of  the  pulse),  however,  the  oscillations  of  this  mechanism  may 
give  rise  to  errors.  These  consist  particularly  of  the  appearance  of 
artificial  elevations  in  the  pulse  curve,  dependent  entirely  upon  the 
apparatus.  One  part  of  the  lever  system  may  advance  independently 
until  it  meets  with  resistance ;  then,  at  the  moment  of  the  occurrence  of 
this  resistance,  there  is  a  jolt  of  the  writing-lever,  which  appears  as  an 
artificial  elevation  in  the  curve,  with  no  existence  whatever  in  the 
pulse  wave.     In  addition  to  the  occurrence  of  these  artificial  elevations, 


Fig.  36.— Jaquet's  sphygmochronograph  (old  style). 

the  oscillation  dependent  upon  the  defective  connections  of  the  parts  of 
the  lever  system  also  causes  an  increase  in  the  height  of  the  curve.  As 
we  shall  subsequently  learn  (p.  125),  it  is  difficult  under  any  circum- 
stances to  gain  an  idea  of  the  volume  of  the  pulse  from  the  height  of 
the  curve,  and  this  error  of  oscillation  renders  the  employment  of  the 
sphygmograph  for  this  purpose  still  more  questionable.  A  further  source 
of  error  is  the  fact  that  the  rate  of  motion  of  the  needle  at  the  moment 
.when  the  individual  parts  of  the  lever  system  are  not  in  contact  is 


SPHYGMOGRA  PHY.  113 

dependent  upon  the  weight  of  the  small  metallic  ball.  Jaquet  himself 
has  criticised  these  faults  of  his  apparatus,  the  lever  system  of  which 
he  copied  from  the  Dudgeon  sphygmograph,  and  has  recently  attempted 
to  overcome  them  by  a  rearrangement  of  the  recording  mechanism,  of 
which  he  gives  the  following  description,^  aided  by  the  accompanying 
diagrammatic  drawing  (Fig.  37) :  "  The  movements  of  the  needle  a  are 
transmitted  to  the  bent  lever  c  c  by  means  of  a  wedge-shaped  blade,  6. 
The  upper  portion  of  the  bent  lever  is  marked  at  s  by  a  carefully  made 
screw-thread  which  works  in  a  corresponding  cog-wheel,  bearing  the 
writing-lever.  The  contact  between  the  screw-thread  and  the  cog-wheel 
is  insured  by  a  spring  (e),  which  constantly  presses  the  lever  c  c  against 
the  cog-wheel.  In  addition  to  this  the  bent  lever  c  c  does  not  turn  upon 
an  axis  passing  through  its  angle,  as  in  the  old  instrument,  but  about 
the  point  /,  and  the  axis  of  rotation  is  replaced  by  a  short,  flat  watch 
spring,  which  insures  the  contact  between  the  lever  c  and  the  edge  b. 
This  spring  is  so  short  that  individual  oscillations  are  not  to  be  feared, 
since  the  length  of  such  an  oscillation  is  less  than  -^^  of  a  second, 
and  is  consequently  trivial  in  comparison  to  the  velocity  of  the  pulse- 
registering  mechanism.  This  spring  also  renders  unnecessary  the 
eccentric  of  the  old  instrument,  since  its  tension  is 
sufficient  to  overcome  the  resistance  which  the 
stretched  skin  offers  to  contact  with  the  pulsating 
artery.  The  ratio  of  transmission  in  the  short  arm 
•of  the  lever  cc  is  1:2,  and  that  between  the  cog- 
wheel and  the  writing-lever  1  :  50,  so  that  the  total 
enlargement  amounts  to   1  :  100." 

An  artificial  pulse  has  been  constructed  by  Lan- 
gendorflP,  upon  a  principle  first  employed  by  Donders, 
in  which  a  revolving  eccentric  transmits  to  the  pin 
of  the  sphygmograph  excursions  similar  to  those  of        Fig.  37.— Diagram  to 

j_*i*iT  ji        ,1  r>   .^  •  1  explain  the  improved 

an  arterial  pulse.  Jaquet,  by  the  use  of  this  mech-  mechanism  in  the  reg- 
anism,  found  that  his  modified  sphygmograph  records  quIt'T^hVlmochro- 
the  movements  of  the  pulse  accurately  and  without  os-  °ograph. 
cillation  for  all  of  the  velocities  usually  encountered  in  sphygmography. 
In  spite  of  the  marked  improvements  obtained  by  these  changes,  it 
seems  to  the  writer  that  the  construction  of  the  modified  Jaquet  sphyg- 
mograph is  still  open  to  some  objections,  and  particularly  because  there 
is  not  a  firm  connection  between  the  blade  b  and  the  lever  arm  c  (Fig. 
37) ;  if  the  velocity  is  very  great  or  the  pulse  rate  very  rapid,  the 
parts  c  and  b  may  become  separated,  and  thus  still  produce  artificial 
elevations  in  the  curve.  The  oscillating  pad  is  a  further  disadvantage 
of  the  old  instrument  which  has  not  been  overcome  in  the  new  modifi- 
cation. In  both  the  old  and  the  recent  models  this  pad  is  connected  to 
the  spring  a  6  by  a  loose  joint.  This  naturally  simplifies  the  applica- 
tion of  the  spring  to  the  artery,  but  from  the  lack  of  a  firm  connection 
it  may  also  produce  distortions  of  the  curve.  In  order  to  obviate  these 
faults  the  author  had  mechanic  Schiile,  who  executed  the  improvements 
1  Miinch.  med.  WocL,  1902,  No.  2. 
8 


114    ARTERIAL  PULSE,  PALPATION,  SPHYGMOQRAPHY,  ETC. 

in  Jaquet's  modified  sphygmograph,  attach  the  pad  firmly  to  the  spring, 
as  in  Marey's  and  v.  Frey's  sphygmographs,  and  also  connect  the  arm 
/  c  of  the  bent  lever  with  the  blade  6  by  a  small  wire  stirrup,  which 
passes  over  the  lever  from  the  profile  of  the  blade,  so  that  any  separa- 
tion of  the  blade  and  the  lever  is  rendered  impossible.  This  mechan- 
ism was  recommended  to  the  author  by  mechanic  Schtile ;  it  acts  like  a 
hinge  joint,  but  possesses  none  of  its  disadvantages.  By  these  modifi- 
cations the  entire  lever  system  has  been  united  into  a  firm  whole,  in 
which  no  displacement  is  possible  without  implicating  the  entire  system, 
and  which  must  consequently  accurately  represent  the  movements  of  the 
arterial  wall,  disregarding  the  possibility  of  the  oscillation  of  the  entire 
system,  a  condition  that  the  author  has  been  able  to  exclude,  for 
the  velocities  ordinarily  encountered  in  sphygmography,  by  tests  with 
Bonder's  artificial  pulse.  The  jointed  connection  of  the  edge  with  the 
bent  lever  has  the  additional  advantage  that  we  may  employ  the  eccen- 
tric of  the  original  apparatus,  which  the  author  sorely  missed  in  the 
improved  Jaquet  sphygmograph,  since  it  not  only  greatly  facilitated  the 
application  of  the  sphygmograph  and  rendered  possible  the  necessary 
variations  in  the  tension  of  the  spring,  but  also  permitted  us  to  ob- 
tain in  every  pulse-tracing  exactly  the  same  amount  of  tension  of  the 
spring  with  the  same  position  of  the  pencil.  The  writer  believes  that 
Jaquet's  sphygmograph,  with  these  different  improvements,  now  an- 
swers all  reasonable  requirements.  It,  of  course,  produces  lower  curves 
than  the  old  model,  on  account  of  the  suppression  of  oscillation.  Me- 
chanic Schiile,  of  the  Physiologic  Institute  at  Basel,  adds  the  described 
improvements  to  the  old  Jaquet  sphygmograph  for  28  to  35  francs,  ac- 
cording to  the  condition  of  the  instrument,  and  also  furnishes  the  modi- 
fied sphygmograph  at  the  original  price  of  165  francs. 

Compare  p.  123  et  seq.  in  regard  to  the  degree  of  tension  which  is  de- 
sirable upon  the  spring. 

EXPLANATION  OF  A  NORMAL  PULSE  CURVE;  FACTORS  WHICH 
INFLUENCE  ITS  FORM. 

The  curves  obtained  with  the  good  modern  sphygmographs  usually 
correspond  quite  uniformly.  Fig.  38  represents  a  normal  pulse  curve 
of  the  radial,  the  artery  which  is  commonly  selected.  This  illustrates 
what  we  have  already  learned  from  palpation,  that  the  pulse  wave  is 
composed  of  a  steep  ascending  and  a  rather  slanting  descending  limb. 
Palpation  alone  might  lead  us  to  believe  that  the  ascending  and  descend- 
ing limbs  of  the  wave  present  smooth  lines,  but  sphygmographic  tracings 
show  a  number  of  small  elevations  in  the  descending  limb  (so-called 
catacrotic  elevations).  Similar  irregularities  which  may  appear  under 
pathologic  conditions  in  the  ascending  limb  are  termed  anacrotic  eleva- 
tions. A  pulse  with  catacrotic  elevations  is  termed  catacrotic;  one 
with  anacrotic  elevations,  anacrotic. 

The  normal  pulse  has  usually  three  distinct  catacrotic  elevations, 
and  is  therefore  catatri erotic.  The  significance  of  the  individual  parts 
of  the  pulse  curve,  especially  of  these  elevations,  has  created  much 


SPHYGMOGRAPHY.  115 

discussion.  Marey  and  Landois,  and  recently  Hiirthle,  v.  Frey,  and 
Krehl,  have  taken  the  most  active  part  in  the  dispute. 

To  understand  the  pulse  curve  we  must,  first  of  all,  avoid  confusing 
the  progressive  motion  of  the  blood  with  the  wave  motion.  This  dif- 
ference is  very  clearly  illustrated  by  E.  H.  Weber's  well-known  expres- 
sion, "  Unda  non  est  materia  progrediens  sed  forma  materiae  progrediens." 

In  palpating  a  pulse  or  in  employing  a  sphygmograph  we  study  exclu- 
sively the  wave  motion  of  the  blood.  Of  course,  the  wave  motion  has  some 
connection  with  the  conditions  of  the  blood-current,  but  only  indirectly. 
The  pulse  of  a  peripheral  artery  is  a  wave  motion  which  has  reached 
this  vessel  by  transmission  to  the  periphery  of  the  primary  wave  arising 
in  the  aorta,  long  before  the  blood  whose  impulse  produced  the  pri- 
mary aortic  wave  has  reached  the  artery.  The  rate  of  transmission  of 
the  wave  motion  of  the  blood  is  quite  rapid,  according  to  E.  H.  Weber 
about  9  m.  a  second.  As  we  should  expect  from  what  has  just  been 
said,  an  aortic  curve  (from  an  animal)  corresponds  very  closely  to  the 
human  radial  curve.  It  rises  quickly,  and  falls  oif  gradually  with 
secondary  waves  and  depressions.  To  understand  the  radial  curve 
thoroughly,  it  is  well  to  begin  by  analyzing  the  aortic  curve.     The  wave 


Fig.  38.— The  normal  radial  pulse  curve  (Riegel). 

motion  in  the  aorta  is  evidently  due  to  the  fact  that  during  the  "  expul- 
sion period  "  of  systole  the  blood-content  of  the  aorta  is  increased.  After- 
ward, when  the  aortic  valves  have  closed,  this  increase  is  carried  toward 
the  periphery  by  the  increased  tension  of  the  aortic  wall.  Thus  the 
ascending  limb  of  the  aortic  curve  evidently  corresponds  in  general  to 
the  so-called  "expulsion  time" — i.  e.,  the  period  during  which  blood 
flows  from  the  heart  into  the  aorta.  The  summit  of  the  pulse  curve, 
however,  does  not  correspond  exactly  to  the  end  of  the  "expulsion 
time  " — i.  e.,  to  the  closure  of  the  semilunar  valves.  On  the  contrary, 
the  "  expulsion  time "  is  probably  extended  over  into  a  part  of  the 
descending  arm  of  the  curve,  because  the  flow  of  blood  into  the  aorta  is 
being  diminished,  so  that  the  aorta  is  being  partially  emptied  toward  the 
periphery  all  the  time.  The  end  of  systole  is,  then,  not  marked  in  a  pulse 
curve,  but  lies  in  the  descending  limb  of  the  curve,  somewhere  near  the 
summit.  The  descending  limb  of  the  curve  thus  includes  this  remnant 
of  the  "expulsion  time"  plus  the  whole  period  during  which  the  semi- 
lunar valves  of  the  aorta  are  closed — /.  e.,  that  part  of  systole  which 
lasts  after  the  close  of  the  semilunar  valves  (Martins  "  persisting  in- 
terval ")  ;  the  whole  of  diastole  ;  and  the  so-called  "  closure  time  "  of 


116     ARTERIAL  PULSE,  PALPATION,  SPHYGMOGRAPHY,  ETC. 

systole.  Hence,  the  descending  limb  is  more  than  diastolic ;  but  for 
the  sake  of  brevity  it  may  be  called  diastolic. 

The  secondary  elevation  of  the  descending  limb,  which  is  designated 
a  in  Fig.  38,  is  usually  distinguished  from  the  others  by  being  very 
distinctly  marked.  If  it  is  still  further  developed  the  pulse  becomes 
dicrotic.  It  is  therefore  called  the  "  dicrotic  elevation  or  wave,"  and 
is  pretty  generally  considered  to  be  a  "  recoil  elevation,"  coiuciding 
with  Laudois'  theory  of  its  origin.  His  theory  is  as  follows  :  At  the 
moment  when  the  primary  positive  wave  leaves  the  aorta — i.  e.,  when 
the  stretched  aortic  wall,  in  virtue  of  its  elasticity,  retracts  again — this 
elastic  contraction  exerts  an  impulse  upon  the  column  of  blood.  This 
impulse  strikes  the  closed  semilunar  valves,  is  reflected  back,  and  passes 
through  the  aorta  centrifugally  to  all  the  peripheral  vessels  in  the  form 
of  a  second  positive  pressure  wave. 

In  cases  where  the  duration  of  each  pulse  wave  is  sufficiently  long 
for  a  complete  formation  of  the  pulse  curve,  the  recoil  wave  may,  in  its 
turn,  produce  another  second  recoil  wave.  This  second  recoil  elevation 
may  be  recognized  by  the  fact  that  it  follows  about  as  quickly  after  the 
recoil  elevation  as  the  latter  did  after  the  primary  wave. 

Landois  considers  that  b  and  c  (Fig.  38),  which  are  smaller  eleva- 
tions, are  elasticity  elevations — i.  e.,  due  to  individual  vibrations  of  the 
arterial  wall  which  are  not  transmitted  from  the  blood-column  to  the 
arterial  wall,  but,  conversely,  from  the  arterial  wall  to  the  blood-column. 
(See  p.  118  et  seq.  for  a  criticism  of  this  conception  of  the  secondary 
elevations.) 

From  experiments  witli  rubber  tubes  Landois  ^  states  the  following  laws  about 
botb  kinds  of  secondary"  elevations  : 

1.  The  further  the  artery-  is  from  the  heart,  the  later  the  recoil  elevation  appears 
in  the  diastolic  portion  of  the  cur\-e. 

2.  In  the  same  artery,  the  further  from  the  heart  we  apply  the  sphygmograph, 
the  less  pronounced  is  the  recoil  elevation. 

3.  The  recoil  elevation  is  so  much  the  more  pronounced  at  the  heart  the  shorter 
(sharper)  the  primary  wave,  and  vice  versa.  The  duration  of  the  primary  wave 
being  equal,  one  of  large  volume  produces  a  stronger  recoil  wave  than  one  of  small 
volume.  If,  however,  such  a  large  voluminous  wave  persists  for  some  time,  while 
a  small  wave  lasts  only  a  short  time,  the  latter  will  produce  the  larger  recoil  eleva- 
tion. The  deciding  factor  is  thus  always  the  bre^-ity — i.  e. ,  the  celerity  of  the 
primary  wave. 

4.  Other  things  being  equal,  the  recoil  elevation  is  larger  the  lower  the  mean 
arterial  pressure. 

5.  The  further  fi-om  the  heart  the  examined  artery  is,  the  more  marked  are  the 
elasticity'  elevations  in  the  descending  limb  of  the  curve. 

6.  An  accentuation  of  the  mean  pressure  in  the  arterj'  will  increase  the  number 
of  the  elasticity  elevations  upon  the  descending  limb  and  at  the  same  time  bring 
them  nearer  the  summit  of  the  curve. 

7.  When  the  mean  blood-pressure  is  very  low,  the  elasticity  elevations  disap- 
pear entii-ely. 

8.  In  diseases  of  the  vessels  which  affect  or  destroy  the  elasticity  of  the  artery, 
the  elasticity  elevations  are  either  much  diminished  or  else  disappear  entirely. 

The  following  assertions  may  be  ventured  in  regard  to  the  varying  shapes  of 

^  Die  Lehre  vom  Arterienpuls,  1872. 


SPHYGMOGRAPHY.  117 

the  entire  curve.      They  are  based  partly  upon  experimental  investigations  by 
Marey,  Landois,  and  others  with  tubes,  and  partly  upon  clinical  observations  : 

1.  Other  things  being  equal,  the  curve  is  lower  the  higher  the  mean  blood- 
pressure,  and  vice  versa.  This  can  easily  be  understood,  because  under  a  high  blood- 
pressure  the  arterial  wall  is  already  so  tense  even  during  diastole  that  the  increase 
in  pressure  during  systole  can  produce  but  a  very  small  excursion.  When,  on  the 
contrary,  the  pressure  is  low,  the  artery  easily  yields  to  the  wave.  Of  course,  this 
does  not  apply  to  those  cases  where  the  high  pressure  is  produced  by  a  large  systole 
(left-sided  cardiac  dilatation  and  hypertrophy  in  compensated  heart  affections),  nor 
where  a  low  pressure  is  due  to  a  small  systole  (disturbances  of  compensation ) . 

2.  Other  things  being  equal  (the  same  blood-pressure),  the  pulse  cui-ve  is  higher 
the  larger  the  systole,  and  vice  versa. 

3.  Other  things  being  equal  (equal  systole  and  equal  blood-pressure),  the  ascend- 
ing limb  of  the  curve  is  steeper  the  quicker  systole  takes  place. 

4.  Other  things  being  equal,  a  low  mean  blood-pressure  produces  both  a  steep 
ascent  and  a  steep  descent — i.  e.,  a  pointed  curve  (celerity  of  curve  in  toto).  Con- 
versely, a  high  blood-pressure  produces  a  slanting  rise  and  gradual  descent  (tardi- 
ness of  curve). 

5.  Other  things  being  equal, rigid  arterial  walls  (like  high  blood-pressure)  pro- 
duce low  curves  with  slanting  ascent  and  gradual  descent  (tardiness).  On  the 
contrary,  delicate  elastic  arteries  (like  low  blood-pressure)  produce  curves  with 
steep  ascents  and  descents  (celerity).^ 


Fig.  39.— Reduction  of  a  sphygmogram  to  Its  simplest  form.  The  above  curve  was  taken 
with  a  Jaquet's  instrument,  the  four  waves  at  the  left  while  the  paper  was  moving  slowly;  the 
three  at  the  right  while  moving  rapidly.  The  time  intervals  are  shown  in  the  notched  line 
above  (0.2  seconds). 

As  a  matter  of  clinical  experience,  however,  it  must  be  acknowledged  that  only 
the  descending  limb  of  the  curve  is  affected  by  either  arterial  rigidity  or  blood- 
pressure,  for  the  great  working  capacity  of  the  heart  is  sufficient  to  make  the  rise 
of  the  curve  steep  even  with  rigid  arteries  and  with  a  high  blood-pressure.  All 
these  statements  possess  more  theoretic  than  diagnostic  interest. 

Anacrotic  elevations  occur  only  under  pathologic  conditions.  Landois  has 
come  to  the  following  conclusions  concerning  them  : 

Anacrotic  elevations — i.  e.,  secondary  elevations  in  the  ascending  limb  of  the 
curve  (Fig.  49) — are  elasticity  elevations.  They  depend  upon  similar  influences  to 
those  which  cause  the  ordinary  elasticity  elevations  of  the  descending  limb.  The 
reason  that  anacrotic  elasticity  elevations  are  so  rarely  obser\'ed  is  because,  as  a  rule, 
the  ascending  limb  is  so  steep  that  elasticity  elevations  could  not  be  reproduced  in 
it.  Hence,  all  the  factors  which  tend  to  retard  the  rise  of  the  curve  are  capable 
of  producing  anacrotic  elevations,  especially  when  these  factors  referred  to  also  favor 
the  formation  of  elasticity  rises  (compare  above  and  p.  131). 

The  shape  of  the  curve  is  decidedly  influenced  by  the  frequency  of  the  cardiac 
action,  because  a  quick  sequence  of  the  chief  wave  makes  a  complete  formation  of 
secondary  waves  in  the  descending  limb  impossible.  At  the  moment  that  the  sys- 
tolic rise  of  a  new  wave  begins,  all  secondary  elevations  disappear  in  the  great  rise 
of  the  new  wave;  although  otherwise  they  would  have  developed  in  the  descending 

^  A  very  good  way  of  judging  the  real  shape  of  a  curve  with  many  elevations  is  to 
divide  each  elevation  in  half  and  then  join  the  points  by  a  dotted  line,  as  in  Fig.  39. 


118     ARTERIAL  PULSE,  PALPATION,  SPHYGMOGRAPHY,  ETC. 

limb  of  the  preceding  wave.  Curves  with  a  slow  sequence  of  beats  are  therefore 
generally  richer  in  secondary  elevations.  An  illustration  of  the  action  of  the  fre- 
quency of  beats  uj^on  the  pulse  wave  is  the  change  of  a  febrile  dicrotism  of  the 
pulse  to  hyperdicrotism  (compare  Fig.  51). 

The  facts  mentioned  above  may  be  considered  correct.  At  the  same 
time  Landois'  explanation  of  the  origin  of  secondary  elevations  is  not 
generally  accepted.  Both  v.  Frey  and  Krehl  have  recently  attacked 
it.  These  investigators  studied  the  pressure  curve  by  an  artificially 
produced  current  impulse  upon  an  animal's  fresh  aorta  (left  in  situ). 
They  registered  simultaneously  the  manometric  pressure  curve  from  the 
beginning  of  the  aorta  and  from  the  celiac  axis.  They  found  by  a 
detailed  examination  that  each  individual  secondary  elevation  may  be 
explained  by  the  fact  that  the  primarily  produced  variations  in  pressure 
are  reflected,  as  it  were,  from  the  periphery  to  the  center  and  then  back 
again  to  the  periphery.  Under  certain  conditions  they  may  traverse 
this  path  repeatedly  in  the  curve.  According  to  this  there  would  be 
neither  recoil  nor  elasticity  elevations  ;  the  so-called  waves  (even  the 
anacrotic  elevations)  would  be  nothing  more  than  centrifugal  or  centrip- 
etal reflections  of  the  principal  wave,  which  interferes  with  it  in  vari- 
ous ways  as  well  as  with  each  other,  v.  Frey  and  Krehl  claim  that 
these  elevations,  and  especially  the  dicrotic  rise  in  every  vascular  area, 
are  due  to  centrifugal  and  centripetal  impulses,  but  in  diiferent  and 
complicated  ways.  They  characterize  the  dicrotic  rise  practically  as  a 
reflected  wave  which  arises  late,  and  which  is  therefore  very  distinctly 
marked  from  the  main  wave ;  whereas  they  characterize  the  so-called 
elasticity  waves  which  precede  the  dicrotic  rise  merely  as  waves  derived 
by  reflection  of  the  main  wave  from  points  closer  together,  so  that  they 
are  partly  confluent  with  the  main  wave.  Further,  they  characterize 
the  elasticity  elevations  which  come  after  the  dicrotic  rise  as  waves  of 
reflection,  like  the  latter,  but  arriving  late  and  becoming  less  and  less 
distinct  toward  the  end  of  the  curve,  because  the  distance  they  traverse 
progressively  increases. 

It  is  questionable  whether  these  theories  will  explain  the  relationship  between 
the  height  of  the  blood-pressure  and  the  so-called  elasticity  elevations  and  the 
dicrotic  waves.  But  v.  Frey  and  Krehl  found  that  an  increase  of  the  blood- 
pressure  pushed  the  reflected  waves  nearer  to  the  main  summit  of  the  curve  {i.  e. , 
in  the  sense  of  time),  because  the  rate  of  transmission  of  the  waves  increases  with  the 
blood-pressure.  This  explains  the  fact  that  those  reflection  waves  which  are  situated 
nearest  to  the  main  summit  (which  are  ordinarily  described  as  elasticity  elevations  i, 
and  which  include  the  anacrotic  elevations,  occur  chiefly  when  the  blood-pressure 
is  high.  It  also  explains  the  fact  that  with  a  low  blood-isressure  a  reflection  wave  as 
a  so-called  dicrotic  wave  arrives  veiy  late  and  that  it  is  characterized  by  being  very 
distinctly  formed,  because  at  this  moment  tlie  tension  of  the  arterial  wall  is  low 
enough  for  the  wall  to  make  quite  a  marked  excursion.  So  we  see  that  as  a  matter 
of  fact  these  relations  between  blood-pressure  and  the  form  of  the  curve  may  be 
explained  by  the  theory  of  the  reflection  of  the  secondary  elevation. 

INFLUENCE   OF  BREATHING  UPON  THE  PULSE  CURVE. 
It  has  long  been   known   that  deep  breathing  may  have  some  influence  upon 
the  pulse  curve.     This  influence  is  chiefly  due  to  the  changes  of  arterial  pressure 
which  occur  in  the  two  phases  of  respiration.     The  respiratory  increase  in  pressure 


SPHYGMOGRAPHY.  119 

manifests  itself  in  a  sphygmographic  tracing  by  an  elevation  of  the  whole  cun-e ' 
and  by  an  alteration  in  the  shape  of  the  individual  beat  (the  latter  corresponds  to 
what  was  said  in  4,  5,  and  6,  p.  116  et  seq. ) — viz.,  a  diminution  of  the  dicrotic  rise, 
an  increase  of  the  elasticity  elevations. 

Authors  difier  very  materially,  however,  as  to  whether  the  variations  in  press- 
ure which  are  evident  in  a  sphygmographic  tracing  belong  to  inspiration  or  to  ex- 
piration. The  reason  for  such  a  difference  of  opinion  is  that  the  factors  which 
alter  the  blood  during  respiration  are  manifold  ;  they  frequently  produce  opposing 
results,  and  the  final  effect  varies  according  to  the  way  that  the  breathing  progresses. 
The  most  important  influence  of  breathing  upon  the  blood-pressure  is  probably  to 
be  found  in  the  change  of  diameter  of  the  pulmonary  vessels.  They  become  wider 
during  active  inspiration  and  narrower  during  expiration.'-* 

Consequently,  so  long  as  the  dilating  pulmonary  vessels  receive  an  excess  of 
blood  at  the  beginning  of  inspiration,  the  greater  circulation  must  receive  less 
blood  (because  the  size  of  the  diastole,  and  with  it  that  of  the  systole,  is  dimin- 
ished), and  so  the  blood-pressure  will  fall.  However,  in  the  second  pai't  of  in- 
spiration the  pulmonary  circulation  through  the  dilated  pulmonary  vessels  improves  ; 
this  in  turn  favors  both  diastole  and  systole,  and  eventually  the  greater  circulation, 
and  so  increases  the  blood-pressure.  During  expiration  the  reverse  occurs.  The 
pulmonary  vessels  become  narrower  ;  they  therefore  empty  a  part  of  their  blood 
into  the  greater  circulation  ;  the  diastole  and  the  systole  of  the  left  heart  becomes 
fuller  and  the  pressure  increases.  As  soon,  however,  as  the  pulmonary  vessels 
have  become  empty,  the  increased  resistance  in  the  lung  will  be  felt  as  a  factor  in 
diminishing  the  diastole  of  the  left  side  and  the  pressure  in  the  general  circulation 
will  be  reduced. 

Therefore,  under  these  conditions  blood-pressure  falls  during  the  first  half  and 
increases  during  the  second  half  of  insijiration  ;  whereas,  conversely,  pressure  in- 
creases during  the  first  half  and  diminishes  during  the  second  half  of  expiration. 
Hence,  a  maximum  of  pressure  occurs  at  the  beginning  of  expiration  ;  a  minimum, 
at  the  beginning  of  inspiration.  These  rules,  however,  apply  only  to  very  slow 
and  deep  breathing.  Only  the  initial  effect  of  the  change  of  diameter  of  the  pul- 
monary vessels  is  felt  during  rapid  breathing — viz. ,  expiration  increases  the  press- 
ure, inspiration  diminishes  it.  Hence,  I'espiration  influences  blood-pressure  in 
two  opposite  ways,  according  to  its  rapidity.  And  especially  in  pathologic  cases, 
where  the  breathing  is  abnormal,  it  is  evident  that  the  two  types  may  be  merged 
beyond  recognition,  so  that  we  are  unable  to  formulate  any  fixed  rule  for  the 
relation  of  the  sphygmogram  to  the  respiratory  phases.  This  is  one  of  the  causes 
for  the  diversity  of  opinions  found  in  literature.  As  a  matter  of  fact,  we  have 
considered  only  the  most  important  factor  by  which  respiration  affects  the  arterial 
pressure — namely,  the  varying  diameter  of  the  pulmonary  vessels,  whereas  in 
reality  the  conditions  are  much  more  complicated  ;  for  example,  we  might  consider 
the  influence  of  the  varying  intrathoracic  pressure  upon  the  heart  and  upon  the 
great  intrathoracic  vessels,  the  effect  of  varying  intra-abdominal  jjressure  upon  the 
vessels  of  the  abdominal  cavity,  which  changes  with  respiration,  and  ftirther  the 
changes  of  the  vasomotor  tonus  synchronous  with  respiration,  etc.  Nevertheless, 
it  may  be  stated,  as  a  rule,  that  in  the  sphygmographic  tracing  (Fig.  40)  deep  and 
slow  breathing  increases  the  pressure  during  inspiration  and  diminishes  it  during 
expiration  ;  whereas  deep  and  rapid  breathing  produces  the  reverse  effect.  The 
pulse  frequency  is  often  accelerated  during  inspiration.  Corresponding  to  the 
mode  of  origin  of  the  variations  in  pressure,  the  individual  beats  which  coincide 
with  the  increase  in  pressure  are  greater  than  those  which  correspond  to  its  de- 
crease.^ 

'  This  sign  is,  however,  ambiguous,  because  the  pelotte  of  the  sphygmograph  rests 
not  only  upon  tlie  artery,  but  also  upon  the  vense  comites,  and,  of  coui-se,  any  increased 
dilatation  of  the  latter  will  also  lift  the  registering-lever. 

''  The  conditions  differ  in  the  case  of  the  artificial  respiration  employed  in  animal 
experiments. 

*  For  further  information  see  Tigerstedt,  Lehrhuch  der  Physiologie  c/e.s  Krieslaufes, 
1893,  p.  453  et  mj. 


120     ARTERIAL  PULSE,  PALPATION,  SPHYGMOGRAPIIY,  ETC. 

It  should  also  be  noted  that  the  lower  the  arterial  pressure,  the  more  decided 
are  the  effects  of  respiratory  influence  upon  the  pulse  curve,  since  thoracic 
aspiration  naturally  causes  a  greater  increase  of  arterial  pressure  when  the  arteries 
are  comparatively  empty  than  when  they  are  full.  Such  imperfect  filling  of 
the  arteries  generally,  but  not  always,  coincides  with  low  pressure.  Upon  the 
other  hand,  with  a  low  arterial  pressure  the  arteries  may  be  even  abnormally 
distended — e.  g.,  when  the  low  pressure  depends  upon  dilatation  of  the  arteries 
with  a  good  volume  of  circulating  blood.  Arterial  pressure  in  itself  is  consequently 
not  responsible  for  the  occurrence  of  pronounced  respiratory  variations  in  the  pulse 
curve,  but  for  the  volume  of  blood  contained  in  the  arteries.  To  this  extent  the 
occurrence  of  max'ked  inspiratory  variations  in  the  pulse  curve  possesses  a  certain 
interest  in  our  consideration  of  circulatory  conditions. 

The  influence  of  respiration  upon  the  pulse  curve  is  naturally  more  pronounced 
if  the  respiration  produces  great  variations  in  intrathoracic  pressure.     As  a  result 


Fig.  40. — The  influence  of  deep  and  slow  breathing  upon  a  normal  pulse  curve :  R,  Respiration 
curve,  inspiration  above ;  P,  pulse  curve  ;  T,  time  curve  (intervals  =  0.5  seconds)  (Rollet). 

of  this  we  observe  particularly  pronounced  variations  of  the  pulse  curve  in  stenoses 
of  the  air  passages  and  in  all  conditions,  like  pneumonia  and  pleurisy,  in  which 
the  equalization  of  the  intrathoracic  and  extrathoracic  air  pressures  is  disturbed. 

Respiration  exerts  a  particularly  pathologic  influence  upon  the  pulse  curve 
when,  as  the  result  of  intrathoracic  adhesions  (particularly  in  the  mediastinum), 
inspiration  or  expiration  exerts  an  abnormal  traction  or  pressure  upon  the  veins 
leading  to  the  heart,  by  which  the  blood  is  more  or  less  withheld  from  the  vessels 
during  one  of  the  respiratory  phases  (pulsus  paradoxicus,  cicatricial  mediastinitis, 
see  p.  126  etseq.). 

Under  normal  conditions  the  influence  of  respiration  upon  the  pulse  curve  is 
slight  and  scarcely  perceptible  even  in  the  sphygmogram,  so  that  when  marked 
inspiratory  variations  are  present  in  the  pulse  curve  we  should  look  for  one  of  the 
above-mentioned  pathologic  factors. 

Superficial  breathing  has  no  especial  influence  upon  the  sphygmogram. 

OTHER  FACTORS  WHICH  INFLUENCE  THE   PULSE  CURVE. 

1.  Diminution  of  the  amount  of  blood.  This  produces  a  diminution  and  a 
delay  in  the  elasticity  elevations  and  a  decided  prominence  of  the  recoil  elevation. 
Venesection  for  therapeutic  purposes  may  sometimes  be  sufficient  to  accomplish 
this  effect. 

2.  An  intermitting  cardiac  activity  diminishes  the  arterial  pressure  during  the 
intermission  of  the  pulse.  Consequently  the  pulse  wave  following  upon  the  pause 
presents  signs  of  diminished  pressure — i.  e.,  the  elasticity  elevations  are  weaker  and 
delayed  and  there  is  dicrotism. 

3.  Elevating  an  extremity   diminishes,   depressing  it   increases,   the  arterial 


SPHYGMOGBAPHY.  121 

pressure  in  the  part.  Consequently  the  sphygmogram  of  an  elevated  area  shows 
more  distinct  dicrotism  and  slighter  elasticity  elevations  than  that  of  a  horizontal 
or  dependent  area. 

4.  Compressing  the  larger  vascular  trunks  produces  an  increase  of  pressure  in 
the  other  pulsating  vessels.  This  is  shown  in  a  well-known  way  by  the  sphyg- 
mogram. 

5.  An  interference  with  the  venous  flow  from  an  extremity  acts  in  an  opposite 
way.  The  arterial  pressure  in  the  supplying  artery  increases,  and  its  sphygmo- 
gram is  correspondingly  altered.  The  rise  of  the  curve  as  a  whole  is,  however, 
partly  due  to  the  distention  of  the  congested  veins  (see  p.  118). 

We  are  indebted  to  Landois  and  Marey  for  most  of  these  statements. 

DIAGNOSTIC  SIGNIFICANCE  OF  THE  PULSE  CURVE. 

At  first  observers  were  naturally  inclined  to  overestimate  the  value 
of  sphygraographic  tracings  for  the  diagnosis  of  pathologic  conditions, 
but  to-day  most  clinicians  have  gone  to  the  opposite  extreme.  As  a 
matter  of  fact,  sphygmography  is  more  than  an  interesting  amusement ; 
it  is  really  a  valuable  help  in  the  interpretation  of  circulatory  changes. 
But  the  factors  which  influence  its  shape  are  so  numerous  that  many 
different  circulatory  conditions  may  be  responsible  for  an  identical 
sphygmogram ;  so  that  even  in  a  cardiac  case  we  are  not  justified  in 
making  a  diagnosis  merely  from  the  type  of  the  curve.  Even  the 
curve  of  aortic  insufficiency,  one  of  the  most  characteristic  of  all  curves, 
cannot  be  considered  as  pathognomonic  of  this  affection  ;  exactly  the 
same  type  may  occur  without  any  valvular  mischief.  Still,  the  sphyg- 
mogram is  valuable  in  the  diagnosis  of  many  conditions,  provided  that 
other  symptoms  are  given  their  proper  value,  and  provided  that  the 
clinician  possesses  considerable  technical  skill  in  making  the  tracings 
and  a  very  accurate  knowledge  of  the  significance  of  the  sphygmographic 
curve  and  of  the  way  it  may  be  modified  by  various  factors.  Such  a 
knowledge  can  only  be  obtained  by  studying  physiologic  works. ^ 

One  of  the  main  objections  to  making  use  of  the  sphygmogram  for 
diagnostic  purposes  has  been  that  all  the  variations  in  the  curve  attrib- 
uted upon  p.  116  et  seq.  to  the  arterial  tension — i.  e.,  to  the  general  blood- 
pressure — can  be  produced  by  local  changes  in  the  vasomotor  tone 
of  the  artery  examined  with  a  uniform  blood-pressure.  Of  course,  if  this 
objection  were  correct,  sphygmography  would  practically  be  relegated 
to  a  useless  place.  Mosso  is  chiefly  responsible  for  this  objection.  He 
found  that  the  pulse  curve  could  be  changed  by  local  thermic  applica- 
tion— e.  g.,  the  local  application  of  heat  to  the  arm  dilates  the  vessels 
and  produces  a  pulse  curve  characteristic  of  low  tension,  while  local 
cold  produces  a  curve  characteristic  of  high  tension.  But  a  closer  ex- 
amination of  Mosso's  curves  shows  that  such  changes  are  quantitatively 
quite  insignificant,  and  apply  much  more  to  the  height  of  the  curve 
than  to  its  shape.     Variations  in  the  pressure  acting  upon  the  vessels 

^  We  mention  especially  Landois,  Die  Lehre  vom  Arterieupuls,  1872 ;  Marey,  La 
Circulation  du  Sane/,  1881 ;  Grashey,  Die  Wellenbewef/ung  elastischer  Rbhren  und  der 
A  rterienpuls  des  Menschen,  Leipzig,  F.  C.  W.  Vogel,  1881;  v.  Frey,  Die  Untersuehung 
des  Pulses,  Berlin,  J.  Springer,  1892 ;  Mosso,  Die  Diac/nostilc  des  Pidses  in  Bezug  avf  die 
localen  Verdnderungen  dessetben,  Leipzig,  Veit  &  Co.,  1879. 


122     ARTERIAL  PULSE,   PALPATION,  SPHYGMOQRAPHY,   ETC. 

from  without  produce  but  an  insignificant  effect  upon  the  shape  of  the 
23ulse  curve.  This  Mosso  easily  determined  in  his  investigations,  which 
were  made  with  a  water  sphygmograph.  The  writer  has  become  con- 
vinced that  it  is  extremely  difficult  to  alter  very  materially  the  shape 
of  the  individual  beats  by  such  local  thermic  influences,  either  in  the 
sphygmogram  or  in  the  tachogram.^  Besides,  where  the  changes  are 
pronounced,  it  is  not  possible  to  exclude  the  effect  upon  the  general 
blood-pressure  which  can  be  produced  reflexly  by  the  local  application 
of  heat  or  cold.  In  fact,  where  the  greatest  alterations  were  observed 
the  patients  reacted  to  the  thermic  changes  with  sensations  of  heat  and 
cold.  The  author  has  never  been  able  to  change  a  high  tension  to  a 
dicrotic  pulse,  or  the  reverse,  by  purely  local  influences  of  so  moderate 
a  degree  that  a  general  influence  could  at  the  same  time  be  excluded. 
The  general  character  of  the  pulse  curve  remains  the  same  even  after  a 
more  extensive  application  of  heat  or  cold  to  the  arm.  The  difficulty  in 
influencing  the  character  of  the  curve  is  well  illustrated  by  making  tracings 
with  a  different  amount  of  pressure  upon  the  spring.  Although  the 
height  of  the  curve  as  a  whole,  and  that  of  the  secondary  curves,  will  be 
influenced,  neither  the  general  shape  of  the  curve  nor  the  number  and 
position  of  the  secondary  elevations  will  be  effected  in  the  least.  This 
remains  true  even  if  the  artery  is  almost  compressed  at  the  periphery, 
and  such  a  compression  would  apparently  be  quite  similar  to  the  effect 
of  a  sharp  vasomotor  contraction  there.  This  fact  convinced  v.  Frey 
that  the  best  way  to  employ  the  sphygmograph  was  with  a  very  strong 
pressure  of  the  spring,  thus  avoiding  any  excessive  swinging  of  the 
registering  lever.  The  more  frequently  and  carefully  one  employs  the 
sphygmograph,  the  more  one  is  convinced  that  it  registers  the  condition 
of  the  general — i.  e.,  the  aortic — circulation,  and  that  it  is  but  slightly 
influenced  by  local  vasomotor  influences.  The  sphygmogram  is,  first 
of  all — and  herein  lies  its  clinical  value — the  expression  of  the  form 
which  the  pulse  wave  assumes  under  the  circulatory  conditions  of  press- 
ure and  resistance  in  the  aorta  and  its  large  branches.  Another  thing 
worth  remembering  is  this,  that  excessive  vasomotor  conditions,  such  as 
Mosso  employed  (local  baths,  violent  muscular  motions,  etc.),  rarely 
affect  the  ordinary  radial  heat.  If  they  did  we  should  notice  other  evi- 
dences of  vasomotor  action,  such  as  an  increased  temperature  or  red- 
ness of  the  skin.  The  radial  vasomotor  tonus  of  an  individual  ordi- 
narily clothed  and  reasonably  quiet  in  all  probability  varies  but  little 
from  the  average  value,  which  depends  upon  the  condition  of  the  general 
circulation. 

One  practical  difficulty  with  the  sphygmograph  is  that  in  one  case,  even 
under  physiologic  conditions,  the  pulse  curve  may  present  several  pecu- 
liarities which  in  another  case  would  signify  some  pathologic  variations. 
Hence,  a  sphygmogram  is  more  practically  useful  in  following  the  circu- 
latory conditions  in  the  same  patient — i.  e.,  for  what  might  be  termed 
functional  diagnosis  of  circulatory  disturbances — than  for  ordinary  diag- 

'  E.  Balli,  Ihber  den  Einduss  von  Erwdmumj  unci  Abfciihlmig  der  Haul  ciitf  das  Flam- 
mentachogramm,  J.  A.  D.,  Bern,  1896. 


SPHYGMOGRAPHY.  123 

nostic  purposes.  It  is  of  decided  assistance  in  studying  more  closely 
the  therapeutic  action  of  certain  measures  upon  the  circulation  and 
of  determining  the  more  rational  plan  of  treatment  in  a  given  case. 
Jaquet's  sphygmograph  is  especially  suitable  for  this  purpose,  not  only 
because  an  accurate  time-measuring  apparatus  is  attached,  but  also  be- 
cause the  amount  of  pressure  upon  the  spring  can  be  reproduced  each 
time  exactly  the  same.  Another  advantage  is  that  the  examiner  can 
make  at  each  trial  five  different  curves  (corresponding  to  the  five  degrees 
of  tension  in  the  spring,  and  so  compare  them  with  five  others).  This 
will  prevent  misjudging  rather  insignificant  local  variations  of  vasomotor 
tension.  The  increased  pressure  on  the  spring  evidently  has  the  same 
effect  on  the  circulation  of  the  hand  as  a  marked  increase  of  tonus  of 
the  radial  artery.  After  a  little  practice  one  can  take  five  such  tracings 
very  rapidly.  There  is  still  quite  a  diiference  of  opinion  whether  high 
or  low  curves  present  the  more  correct  picture.  Since  the  modern  instru- 
ments do  not  permit  much  swinging,  the  high  curves  seem  rather  more 
suitable,  because  they  show  that  the  sphygmograph  was  very  perfectly 
applied,  and  because  their  results  are  perhaps  better  for  comparison  in 
dilferent  patients  as  well  as  in  the  same  patient.  It  is  evident  that  the 
excursions  of  the  registering-needle  will  be  the  highest  when  the  ten- 
sion upon  the  spring  either  just  balances  or  is  but  very  slightly  in  ex- 
cess of  the  minimum  (cardiac  diastolic)  pressure  in  the  artery  (see  p. 
107).  On  the  one  hand,  this  is  because  the  transmission  of  the  sys- 
tolic increase  of  pressure  to  the  sphygmograph  is  not  interfered  with  by 
the  relaxed  arterial  wall ;  and,  on  the  other  hand,  because  with  such  an 
amount  of  pressure  the  artery  will  be  closed  during  the  passage  of  the 
trough  of  the  pulse  wave,  so  that  the  next  wave  will  back  up  consid- 
erably, and  consequently  the  rise  will  be  magnified,  just  as  with  a  hy- 
draulic press.  Comparing  the  various  pulse  curves  with  each  other, 
especially  under  those  well-definable  conditions,  is  really  very  valuable. 

FREQUENCY    OF   THE    PULSE    IN    THE    SPHYGMOGRAM. 

With  Jaquet's  and  with  v.  Frey's  latest  sphygmograph,  both  of 
which  are  furnished  with  a  time-marking  apparatus,  we  can  estimate  the 
frequency  of  the  pulse  very  accurately  merely  by  the  sphygmographic 
tracing. 

RHYTHM    OF   THE    PULSE. 

A  pulse-tracing  shows  the  pulse  rhythm  at  a  glance,  and  much  more 
accurately  than  it  can  be  described.  A  regular  pulse  is  one  in  which 
the  individual  waves  follow  each  other  at  exactly  equal  intervals  of  time. 
Where  this  is  not  the  case  the  pulse  is  termed  irregular.  If  the  ir- 
regularity is  complete  we  call  it  a  pulsus  irregularis,  without  further 
comment.  A  pulsus  intermittens  is  one  in  which,  after  a  regular  number 
of  waves,  one  beat  from  time  to  time  is  omitted.  A  pukus  intereidens 
is  one  in  which  a  small  beat  is  inserted  into  a  regular  sequence  of  beats. 
The  so-called  bigeminus  (Fig.  41)  and  trigeminus  (Fig.  42)  represent 
periodically  irregular  pulses.  In  the  former  2  beats,  and  in  the  latter 
3   beats,  are  grouped  together  and  separated  from  the  preceding  and 


124    ARTERIAL  PULSE,  PALPATION,  SPHYGMOGRAPHY,  ETC. 

following  beats  by  a  somewhat  longer  interval.  Their  curves  usually 
do  not  reach  the  base  line  between  the  groups  of  2  or  3  beats,  so  that 
the  sphygmogram  looks  like  a  two-  or  three-peaked  curve. 

The  clinical  significance  of  the  periodically  irregular  pulse  (see  p.  104) 
is  that  of  a  slight  degree  of  irregularity.  We  have  no  accurate  informa- 
tion as  to  the  mode  of  origin  of  the  various  irregular  rhythms. 


Fig.  41.— Pulsus  bigeminus  sequalis  (Riegel). 

[In  an  exhaustive  recent  work  by  Wenckebach  ^  a  masterful  demon- 
strative explanation  is  given  of  many  of  the  most  puzzling  of  heart 
symptoms.  The  various  types  of  arrhythmia  are  considered.  It  may 
only  be  said  in  this  place  that  he  accepts  without  reservation  the  myo- 
genic theory  of  the  heart's  action  as  opposed  to  tlie  neurogenic — /.  e.,  that 
the  ordinary  rhythm  of  the  heart  is  independent  of  its  nervous  con- 
nections, the  muscle  fibers  possessing  all  the  attributes  necessary  for  the 
rhythmic  production  of  the  heart's  work. 


Fig.  42.— Pulsus  trigeminus  sequalis  (Riegel). 

The  editors  earnestly  recommend  a  study  of  the  work  to  all  interested 
in  heart  studies.  A  slight  criticism  may  be  made  that  Wenckebach  does 
not  give  the  credit  due  to  English  observers  in  the  same  field  of  work 
(see  the  Appendix). — Ed.] 

(Compare  "the  practical  examples"  (p.  133)  with  regard  to  the 
possibility  of  differentiating  a  "  sufficient "  from  an  "  insufficient "  heart 
by  the  irregularity  in  the  sphygmogram.) 

VOLUME    OF   THE   PULSE   IN   THE   SPHYGMOGRAM. 

According  to  our  definition  on  p.  105,  the  volume  of  the  pulse  is 
represented  by  the  height  of  the  primary  curve  summit  above  the  base 
of  the  curve.     Other  things  being  equal,  it  is  evident  that  the  volume 

1  Die  Arhythmie  als  Ausdruck  besiimmter  Funktionsstorungen  des  Herzens,  by  K.  F. 
Wenckebach,  Groningen,  Leipzig,  1903. 


SPHYGMOGRAPHY.  125 

of  the  pulse  depends  upon  the  amount  of  blood  M^hich  is  thrown  into 
the  artery  during  systole.  If  this  systolic  amount  of  blood  is  equal,  the 
volume  of  the  pulse  then  depends  upon  the  facility  with  which  the 
arterial  wall  gives  way  to  the  wave  motion  of  the  blood — i.  e.,  on  the 
one  hand,  upon  the  passive  tension  of  the  artery  as  determined  by  the 
blood-pressure,  and,  on  the  other  hand,  upon  the  active  tension  of  the 
muscularis  of  the  artery.  The  volume  of  the  pulse — /.  e.,  the  height 
of  the  sphygmographic  curve — also  depends  very  decidedly  upon  the  size 
of  the  surface  of  the  artery  (according  to  Pascal's  law  of  the  hydraulic 
press).  Provided  the  systole  of  the  left  heart  is  equal  and  the  blood- 
pressure  is  equal,  the  larger  the  diameter  of  the  radial  artery  the  higher 
the  spring  of  the  sphygmograph  will  be  raised,  and  hence  the  larger  the 
pulse.  The  frequency  of  the  pulse  also  influences  the  height  of  the 
sphygmograra.  If  the  pulse  is  rapid  a  part  of  the  descending  limb  of 
the  curve  will  be  cut  off  by  the  following  wave.  So  many  factors  in- 
fluence the  volume  of  the  pulse  in  ways  which  we  cannot  perfectly 
determine  from  the  appearance  of  the  curve  itself,  that  the  mere  volume 
of  the  pulse  is  of  very  uncertain  diagnostic  significance.  In  the  follow- 
ing cases,  provided  the  tracings  compared  are  all  of  a  maximum  height, 
the  volume  of  the  pulse  is  of  some  significance  : 

1.  When  the  size  of  the  individual  beat  varies  in  any  one  pulse 
curve  we  may  be  sure  that  the  larger  beat  corresponds  to  a  larger  expul- 
sion— i.  e.,  is  preceded  by  a  more  complete  diastole  of  the  heart — and 
that  the  smaller  beat  corresponds  to  a  smaller  expulsion. 

2.  If  the  same  patient's  pulse  becomes  fuller  and  of  higher  tension 
when  examined  with  the  same  sphygmograph  (secondary  rises  nearer  the 
chief  elevation,  p.  116,  6,  128  et  seq.),  then  we  are  justified  in  assum- 
ing that  a  greater  systolic  expulsion  is  the  cause. 


Fig.  43.— Pulsus  alternans  (Eichhorst). 

On  the  other  hand,  if  the  full  pulse  is  at  the  same  time  of  diminished 
tension,  then  its  increased  size  may  depend  upon  the  flaccidity  of  the 
arterial  tube-i-i.  e.,  upon  diminished  blood-pressure. 

The  following  terms  refer  to  the  size  of  the  pulse  :  Pulsus  equalis 
and  inequalis  (the  latter  is  usually  a  pulsus  irregularis  as  well) ;  )>M/x?t.s 
inequalis  periodicus.  The  most  interesting  types  of  the  latter  are  the 
pulsus  alternans  (Fig.  43),  pulsus  bigeminus  alternans  (Fig.  44),  and 
pulsus  paradoxus  (Fig.  45). 

Inequality  of  the  pulse  is  of  similar  clinical  importance  as  irregu- 
larity  (see  p.   104),  and  is  usually  found  combined  with  it.      Periodic 


126     ARTERIAL  PULSE,  PALPATION,  SPHYGMOGRAPHY,  ETC. 

inequality  means  the  same  thing  as  a  slight  degree  of  inequality.  The 
pulsus  paradoxus,  a  poorly  chosen  name,  was  first  described  by  Griesin- 
ger/  and  later  by  Kussmaul,  as  a  constant  symptom  of  indurative 
mediastinitis.  Its  peculiarity  is  that  during  inspiration  the  pulse  becomes 
feeble  or  else  cannot  be  felt  at  all.  Kussmaul  explains  it  as  due  to  an 
inspiratory  pull  upon  the  veins  leading  to  the  heart  by  the  intrathoracic 
adhesions.  From  the  explanation  given  at  p.  118  et  seq.  it  follows 
that  this  symptom  can  have  no  pathognomonic  importance  in  the  diag- 
nosis of  indurative  mediastinitis.     From  the  physiologic  significance  of 


Fig.  44. — Pulsus  bigeminus  alternans  (Eichhorst). 

the  phenomenon  as  there  explained,  it  is  not  surprising  that  it  has  been 
observed  also  in  pericarditis,  in  valvular  disease,  in  weak  heart,  in 
pneumonia,  in  pleurisy,  and  in  stenoses  of  the  air  passages  (laryngeal 
and  tracheal  stenoses,  obliterative  bronchitis).  Even  when  the  heart 
and  lungs  are  absolutely  normal,  it  is  possible  that  respiration  may  pro- 
duce some  evident  eifect  upon  the  pulse,  although  this  is  not  usually  the 
case,  as  we  have  previously  pointed  out  on  p.  120. 

It  seems  to  the  writer  that  the  pulsus  paradoxus  is  of  value  in  the 
diagnosis  of  indurative  pericarditis  only  when  there  is  a  concomitant 
inspiratory  engorgement  of  the  jugular  veins,  a  symptom  which  indi- 
cates a  stenosis  of  the  jugular  veins  during  inspiration. 


Fig.  45.— Pulsus  paradoxus  :  E,  Beginning  of  expiration  ;  /,  beginningof  inspiration  (Kussmaul). 

The  typical  pulsus  paradoxus  (Fig.  45)  is  copied  from  Kussmaul's 
original  communication.  It  especially  seems  to  the  writer  to  possess  no 
diagnostic  importance  whatsoever.  As  is  easily  seen  from  the  figure, 
the  pulsus  paradoxus  is  just  twice  as  frequent  as  the  respirations,  so  that 
expiration  always  coincides  with  one  beat  and  inspiration  with  the  other. 
If  the  breathing  is  energetic  this  relation  will  naturally  emphasize  the 
physiologic  factors  described  on  p.  118.  As  a  matter  of  fact  the 
breathing  is  rapid,  so  that  under  the  circumstances,  according  to  p.  119, 
even  if  the  circulation  is  normal,  the  pulse  shows  more  or  less  distinctly 
an  inspiratory  decrease  or  even  a  disappearance.  Besides,  from  what 
'  Widenmann,  Beitrag  zur  Diagnose  der  Mediastinilis,  Tubingen,  1856. 


SPHYGMOGRAPHY. 


127 


has  been  mentioned  on  p.  119,  it  is  evident  that  under  certain  circum- 
stances, and  practically  independent  of  the  frequency  of  the  respiration, 
a  noticeable  diminution  or  even  an  omission  of  the  pulse  may  be  observed 
even  during  expiration.  Such  a  phenomenon  could  just  as  well  be  called 
a  "  pulsus  paradoxus,"  and  it  certainly  has  just  as  little  significance  in 
the  diagnosis  of  any  definite  disease. 

Although  all  these  phenomena  of  an  alteration  in  the  pulse  from 
respiratory  influences  coincide  with  the  occurrence  of  a  low  arterial 
pressure  (p.  120),  we  are  not  justified  in  diagnosing  any  one  definite 
disease,  such  as  pericarditis  or  mediastinitis,  but  merely  a  deficient 
general  peripheral  circulation. 

CELERITY    OF   THE    PULSE    IN   THE    SPHYGMOGRAM. 

The  celerity  of  a  pulse  is  a  quality  which  we  can  appreciate  by  pal- 
pation (p.  105).  It  is  also  plainly  represented  in  the  sphygmographic 
curve.  Both  ascending  and  descending  limbs  of  a  pulsus  celer  are  steep 
and  the  summit  is  sharp.  On  the  contrary,  both  limbs  of  a  true  j^uisus 
tardus  are  sloping ;  the  curve  is  flat  and  the  summit  blunt  (Fig.  47). 


Fig.  46.— Pulsus  celer  in  aortic  insufficiency  (Paegel). 

Either  limb  of  the  curve  may  exhibit  the  signs  of  celerity  or  tardiness, 
while  the  other  limb  either  is  not  affected  or  may  exhibit  the  opposite 
condition.  In  this  case  our  description  must  include  the  character  of 
each  limb.  For  the  method  of  determining  by  construction  the  sliape 
of  the  general  curve,  or  of  the  main  summit  in  the  case  of  polycrotic 


Fig.  47.— Pulsus  tardus  in  aortic  stenosis  (Striimpell). 

curves,  see  Fig.  39.  The  ascending  limb  of  aortic  insufficiency  (Fig. 
46)  is  steep  because  a  large  mass  of  blood  is  suddenly  expelled  from  the 
dilated  left  ventricle  into  the  aorta  ;  and  the  descending  limb  is  also 
steep  because,  on  account  of  regurgitation  of  the  blood  into  the  left 
ventricle,  the   negative  stage  of  the  wave   is    introduced   abnormally 


128     ARTERIAL  PULSE,   PALPATION,  SPH TOMOGRAPHY,   ETC. 

rapidly.  Conversely,  the  ascending  and  descending  limbs  of  aortic 
stenosis  are  oblique ;  it  is  a  typical  pulsus  tardus  (Fig.  47).  Here  the 
rise  as  well  as  the  drop  of  the  curve  takes  place  slowly  because  the  sys- 
tolic impulse  is  deadened  and  prolonged  at  the  seat  of  stenosis.  In 
relaxed  vessels — /.  e.,  in  fever — the  rise  as  well  as  the  drop  is  usually 
quick  (see  p.  116).  The  dicrotic  febrile  pulse  is  therefore  usually  a 
pulsus  cder  (Fig.  51).  With  high  arterial  tension  the  descending  limb 
of  the  curve  is  usually  quite  gradual  and  oblique  (p.  116).  The  rise  is 
generally  rapid  and   steep  on  account  of  the  energetic  cardiac  action. 


Fig.  48.— Senile  pulse  in  arteriosclerosis  (Riegel). 


This  is  the  type  of  pulse  which  is  usually  observed  in  old  people  with 

arteriosclerosis  (Fig.  48).     Nevertheless  a  very  decided  degree  of  arterio- 


FiG.  49.— Pulse  in  advanced  arteriosclerosis :  Slow  ascent  and  descent  of  the  wave  ;  anacrotism— 
only  32  beats  to  the  minute  (taken  with  Jaquet's  instrument). 

sclerosis   (Fig.   49)  is  generally  accompanied  by   a   gradual   rise.      In 
nephritis  (Fig.  50)  the  rise  is  steep  and  the  descent  slow,  but  the  pulse 


Fig.  50.— Pulse  in  chronic  nephritis. 

differs  from  that  of  arteriosclerosis  by  the  great  number  of  secondary 
elevations. 

Although  the  general  shape  of  the  sphygmogram  gives  some  idea  of 
the  arterial  pressure  and  the  way  the  blood  flows  into  the  arteries,  and 
from  them  to  the  periphery,  yet  neither  the  descent  nor  the  ascent  of  the 
curve  is  absolutely  diagnostic.  In  the  first  place,  the  height  of  the 
curve  influences  the  slant  of  the  descending  limb;  and,  as  a  rule,  we 
are  unable  to  interpret  the  significance  of  variations  in  the  height  (p. 
125).     Again,  the  frequency  of  the  pulse  decidedly  modifies  the  slant 


SPHYGMOGRAPHY.  129 

of  the  descending  limb,  because  if  a  pulse  is  rapid  a  portion  of  its 
descending  limb  is  simply  cut  off  by  the  following  wave,  so  that  the 
height  of  the  curve  seems  lessened.  Even  in  aortic  insufficiency  the 
value  of  the  slant  of  the  descending  limb  is  rather  more  for  demonstra- 
tion than  for  diagnosis.  The  slant  of  the  ascending  limb  is  almost  as 
variable.  The  steepness  of  its  ascent  does  not,  in  itself  alone,  give  us 
accurate  information  concerning  the  quickness  of  the  rise  of  the  pulse 
wave.  The  only  really  accurate  way  of  determining  the  celerity  of  the 
rise  of  the  ascending  limb,  and  this  is  of  decided  importance  in  pro- 
nounced arteriosclerosis  or  in  aortic  stenosis,  is  to  measure  the  length 
of  the  time-registering  line  between  the  base  of  the  rise  and  its  summit. 
We  must,  of  course,  remember  that  this  time  interval  should  not  be 
confounded  with  the  duration  of  the  cardiac  systole,  for  systole  (p.  115) 
extends  beyond  the  main  elevation.  It  should  be  observed  that  as  a 
result  of  the  fact  that  the  duration  of  the  ascent  of  the  pulse  curve  does 
not  correspond  with  the  duration  of  the  delivery  of  the  blood  into  the 
aorta,  the  demonstration  of  the  characteristic  pulse  of  aortic  stenosis  is 
frequently  unsuccessful,  since  the  duration  of  the  ascending  limb  of  the 
curve  is  shortened  by  the  rapid  flowing  of  the  blood  toward  the  periph- 
ery. The  pulse  simply  seems  small,  but  does  not  present  the  typical 
characteristics  of  the  pulsus  tardus.  To  the  best  of  the  writer's  knowl- 
edge, attention  has  not  been  previously  directed  to  this  evident  explana- 
tion of  the  frequent  absence  of  the  pulsus  tardus  in  aortic  stenosis. 

TENSION  OF  THE   PULSE    IN    THE    SPHYGMOGRAM  (POLYCROTISM ;    DICRO- 

TISM;  ANACROTISM). 

The  secondary  elevations  of  the  descending  limb  (p.  116  ef  seq.)  are 
most  significant  in  attempting  to  estimate  from  the  pulse-tracing  the 
tension  of  the  pulse — i.  e.,  the  mean  blood-pressure.  Elasticity  eleva- 
tions which  are  pronounced  or  which  arise  early  in  the  curve  [according 
to  V.  Frey's  and  Krehl's  conception  (p.  118)  the  early  reflex  waxes — 
i.  e.,  secondary  elevations  near  the  summit]  or  anacrotic  elevations  (p. 
117)  generally  indicate  a  high  mean  blood-pressure.  The  converse — 
i.  e.,  the  so-called  dicrotic  wave  (p.  116) — is  usually  more  pronounced 
with  a  loio  mean  blood-pressure  (p.  116).  Where  none  of  the  secondary 
elevations,  either  from  their  size  or  their  position,  can  be  considered  as 
a  dicrotic  wave,  we  are  justified  in  assuming  that  numerous  and  pro- 
nounced secondary  elevations  are  more  in  favor  of  a  high  pressure ; 
because,  according  to  Landois,  these  numerous  elevations  should  be 
regarded  as  elasticity  elevations,  and  according  to  v.  Frey's  and  Krehl's 
idea,  powerful  and,  at  least  in  part,  early  reflex  waves. 

Compare  IIQ  et  seq.  and  122  in  regard  to  the  general  form  and  size 
of  the  pulse  under  variable  mean  pressure. 

The  type  of  the  pulse  curve  with  varying  arterial  pressure  may  be 
represented  as  follows  : 

1.  Normal  Pressure.- — Both  the  elasticity  elevations  and  the  dicrotic 
wave,  moderately  develo])ed  ;  the  latter,  however,  only  slightly  different 
from  the  elasticity  elevations  (see  Fig.  38). 
9 


130    ARTERIAL  PULSE,  PALPATION,  SPHYGMOGRAPEY,  ETC. 


2.  Low  Pressure. — Elasticity  elevations  disappear,  dicrotism  in- 
creases, and  eventually  becomes  transformed  into  monocrotism ;  the 
height  of  the  pulse  is  increased — i.  e.,  it  becomes  a  pulsus  celer,  except 
when  the  low  pressure  is  due  to  a  weak,  slight  systole  (Fig.  51,  6,  c, 
d,  e).        ^ 

3.  High  Pressure. — Elasticity  elevations  increase  in  size  and  num- 
ber ;  they  are  situated  nearer  the  summit  (Figs.  45  and  52)  or  even  on 
the  ascending  limb  of  the  curve  (anacrotic)  ;  the  descending  limb,  and 
in  rare  cases  the  ascending  limb,  are  oblique  (tardus)  ;  the  height  of  the 
curve  is  generally  low  except  when  the  high  pressure  is  due  not  to  in- 
creased resistance  alone,  but  to  a  strong,  full  systole  as  well.     If  the 


a.  Normal  with  beginning  dicrotism. 


6.  Hypodicrotism. 


c.  Dicrotism. 


d.  Hyperdicrotism.  e.  Monocrotism. 

Fig.  51.— Increasing  dicrotism  finally  transformed  into  monocrotism  (Riegel). 

blood-pressure  is  very  high,  and  especially  if  it  is  due  to  arteriosclerotic 
resistance,  not  only  the  dicrotic  rise  disappears,  but  even  the  elasticity 
elevations  fade  away  more  or  less  completely,  because  the  arterial  wall 
has  become  stiffened,  either  on  account  of  the  firm  contractions  of  its 
muscularis  or  on  account  of  the  anteriosclerotic  changes.  A  mono- 
crotic pulse  finally  results.  Fig.  49  represents  such  a  slow,  low,  and 
almost  monocrotic  sphygmogram  ;  but  there  still  remain  some  indica- 
tions of  elasticity  elevations  visible  especially  in  the  ascending  limb 
(anacrotism). 

In  this  schematic  grouping  the  relation  of  the  size  and  the  celerity 
of  the  pulse  curve  to  the  blood-pressure  has  only  a  theoretic  significance, 


SPHY'GMOGRA  PHY.  1 31 

because  the  qualities  of  size  and  celerity  in  the  sphygmogram  (pp.  124 
and  127)  possess  only  slight  diagnostic  value. 

Furthermore,  merely  counting  the  elasticity  elevations  is  not  always 
sufficient  to  determine  the  height  of  the  blood-pressure,  because  the 
pulse  frequency  always  plays  a  part.  With  a  frequent  pulse  the  curve 
is  not  completely  developed  ;  so  that  a  part  of  the  descending  limb  and 
the  elasticity  elevations  contained  in  it  will  not  show. 

The  development  of  a  dicrotic  wave  is  best  studied  in  a  febrile  pulse,  because 
dicrotism  usually  goes  hand  in  hand  with  a  diminution  of  the  vascular  tension.  The 
higher  the  fever,  the  more  hilly  the  dicrotic  wave  is  developed,  and  the  further  dis- 
tant is  it  from  the  main  summit  of  the  curve  (Fig.  51,  a,  b,  c,  d).  The  individual 
steps  of  this  change  have  received  separate  names.  If  the  dicrotic  elevation  begins 
before  the  descending  limb  reaches  the  base  of  the  curve,  the  pulse  is  called  Ay^jo- 
dicrotic  (Fig.  51,  6).  It  is  strictly  dicrotic  when  the  dicrotic  wave  starts  only  after 
the  descending  limb  reaches  the  base  line.  If  the  dicrotic  wave  occurs  still  later 
— i.  e.,  in  the  ascending  limb  of  the  following  wave — ^the  pulse  is  then  termed 
"  hyperdicrotic  "  (Fig.  51,  d).  This  peculiarity  may  arise  either  because  the  dicro- 
tic wave  is  retarded  or  because  the  following  wave,  coming  so  rapidly,  cuts  off  the 
descending  limb  of  the  dicrotic  wave.  If  in  Fig.  51,  c,  the  ordinary  dicrotic  pulse, 
we  imagine  that  the  individual  beats  follow  more  closely  one  after  the  other,  then 
"  hyperdicrotism "  results  (Fig.  51,  d).  If  the  dicrotic  wave  is  still  further  re- 
tarded or,  what  amounts  to  the  same  thing,  if  the  rate  of  the  pulse  is  still  further 
increased,  a  monocrotic  wave  results  (Fig.  51,  e).  This  monocrotism  with  relaxed 
vessels  and  low  pressure  differs  from  the  monocrotism  of  high  pressure  (Fig.  49). 
In  the  latter  the  tense  or  rigid  arterial  wall  cannot  produce  any  considerable  sec- 
ondary elevations.  The  j^ulse  wave  is  here  usually  low  and  the  pulse  very  slow. 
Typical  examples  of  high-tension  pulse  curves  are  the  arteriosclerotic  pulse  (Fig. 
49),  the  nephritic  pulse  (Fig.  45),  and  the  tense  pulse  in  lead  colic  (Fig.  52). 

Anacrotic  elevations  (p.  118)   probably  occur  only  with  high  blood-pressure. 


Fig.  52.— Tense  pulse  in  lead  colic :  Some  of  the  waves  anacrotic  (Riegel). 

Fig.  52  shows  anacrotism  in  some  of  the  summits,  and  it  is  also  suggested  in  the 
curve  of  Fig.  49.  Eounded  summits  (Fig.  48)  probably  signify  anacrotism  (con- 
sisting of  several  anacrotic  elevations).  The  rigidity  of  the  artery  prevents  it  from 
being  distinctly  indicated.  Similarly,  rounded  tops  which  slant  off  toward  the 
descending  limb  should  probably  be  imagined  as  confluent  catacrotic  elasticity  ele- 
vations. Sometimes  the  rounded  top  is  flattened  like  a  plateau.  But  the  signifi- 
cance is  probably  not  changed. 

SPECIFIC  SPHYGMOGRAMS. 

When  the  sphygmograph  was  first  employed,  it  was  believed  that  pathogno- 
monic pulse  curves  would  be  found  to  characterize  certain  affections,  especially  car- 
diac cases.  But  such  a  belief  has  not  been  justified.  Not  even  the  curve  of  aortic 
insufficiency  can  be  considered  specific  of  this  disease,  for  in  fever  and  in  exoph- 
thalmic goiter,  without  any  leak  at  the  aortic  valve,  a  very  pronounced  pulsus  celer 
is  often  observed.  The  pulse  curve  of  mitral  lesions  is  less  suggestive  or  certain, 
although  in  some  instances  it  is  of  decided  assistance  in  the  diagnosis.     A  serious 


132     ARTERIAL  PULSE,   PALPATION,   SPH TOMOGRAPH Y,   ETC. 

error  was  formerly  made  in  the  attempt  to  find  characteristic  signs  in  the  curve 
during  the  time  of  disturbed  compensation.  This  is  evidently  the  least  favorable 
time,  because  if  comjjensation  is  affected  to  any  extent  the  pulse  will  always  be  a 
small  pulse  and  of  low  tension  ;  and  such  a  condition  might  be  due  to  the  valve 
lesion  alone,  without  any  disturbance  of  compensation,  v.  Noorden^  has  par- 
ticularly emphasized  the  necessity  of  utilizing  well-compensated  cases  in  order  to 
obtain  characteristic  curves,  and  believes  that  compensated  mitral  stenosis  exhibits 


Fig.  53. — Tense  pulse  in  compensated  mitral  stenosis  (v.  Noorden). 

a   high-tension  pulse,  whereas    compensated  mitral  insufficiency  exhibits  a  low- 
tension  pulse  (Figs.  53  and  54). 

V.  Noorden  accounts  for  this  phenomenon  by  assuming  that  in  mitral  steno- 
sis an  increased  arterial  tone  aids  in  maintaining  the  compensation.     The  arterial 


Fig.  54.— Lack  of  tension  of  the  pulse  in  compensated  mitral  insuificiency  (v.  Noorden). 

system  is  thus  sufficiently  filled  and  the  pressure  preserved  despite  the  small  sys- 
tole. On  the  contrary,  in  mitral  insufficiency  the  compensation  is  favored  by  vaso- 
motor relaxation  of  the  vessels,  which  diminishes  the  resistance  in  the  arterial 
system.  In  this  way  a  much  larger  proportion  of  the  left  ventricular  contents  can 
be  utilized  by  the  circulation,  and  a  correspondingly  smaller  portion  returns  into 
the  left  auricle.  These  peculiarities  are,  the  writer  believes,  more  simply  explained 
as  follows  :  In  mitral  stenosis  there  is  no  reason  for  any  diminution  of  the  arterial 
pressure  ;  whereas  in  pronounced  mitral  insufficiency  a  high  arterial  pressure  can- 
not i^ossibly  occur  because  of  the  regurgitation  of  the  blood  into  the  left  auricle. 
If  the  circulation  should  be  appi'oximately  normal  in  such  a  marked  degree  of 
mitral  insufficiency,  in  spite  of  the  low  arterial  pressure,  it  is  an  indication  that  the 
vasomotor  tone  of  the  general  circulation  is  lowered,  a  fact  which  has  a  compensa- 
tory significance,  and  to  this  extent  v.  Noorden  is  correct. 

A  FEW  PRACTICAL  EXAMPLES  TO  ILLUSTRATE  THE  APPLICATION  OF  THE 

SPHYGMOGRAPH. 

The  deductions  which  may  be  made  from  the  sphygmogram  as  to  the  condition 
of  the  circulation  are  well  illustrated  in  Fig.  55,  a  and  b,  and  Fig.  56  a,  and  b. 
They  represent  tracings  taken  (a)  from  a  case  of  distur]:)ed  compen.sation  and  {b) 
from  the  same  case  after  compensation  has  been  re-established  by  the  employment 
of  digitalis. 

The  comparison  of  curves  in  Fig.  55,  a,  and  Fig.  57  is  very  interesting  from  a 

^  C'harite-Annalen,  15  Jahrgang. 


SPHYGMOGRA  PHY. 


133 


diagnostic  standiDoint.  Both  curves  show  an  irregular  pulse,  but  with  these  differences : 
The  curve  in  Fig.  57  in  general,  and  the  small  interposed  beats,  represent  a  pulse  of 
high  tension,  whereas  the  pointed  single  elevations  of  the  curve  in  Fig.  55,  a,  point 
in  general  to  a  low  degree  of  tension.  The  arterial  pressure  sinks  quickly,  especially 
in  the  little  beats  ;  this  is  evident  from  the  dicrotism  and  from  the  depression  of  the 


Fig.  55.— Sphygmogram  from  a  patient  with  mitral  insufficiency,  to  demonstrate  the  action 
of  digitalis  :  a,  Before  the  administration  of  digitalis— circulation  decidedly  affected,  radial  pulse 
128,  cardiac  beats  172;  6,  after  the  employment  of  digitalis— circulation  practically  normal. 

base  of  the  curve.     The  latter  fact  alone  points  to  an  insufficient  systole  as  compared 
with  the  curve  in  Fig.  57,  where  the  cardiac  apparatus  is  evidently  sufficient. 

The  type  of  irregularity  illustrates  another  difference  between  the  two  curves. 
In  Fig.  55,  a,  the  size  of  the  individual  pulse  wave  certainly  in  some  places  seems 
to  be  independent  of  the  size  of  the  preceding  interval,  whereas  in  Fig.  57  the  size 


Fig.  56.— Sphygmogram  from  a  patient  with  emphysema  and  cardiac  dilatation,  to  demonstrate 
the  action  of  digitalis:  a.  Before  the  administration  "of  digitalis— circulation  decidedly  affected, 
pulse  about  100;  b,  after  2  gra.  of  digitalis — circulation  normal,  pulse  70. 

of  the  individual  beat  is  directly  proportional  to  the  duration  of  the  preceding  in- 
terval. The  first  type  of  irregularity,  according  to  my  experience,  always  points 
to  cardiac  insufficiency  of  a  kind  that  can  be  helped  by  employing  digitalis.  This 
drug  will  improve  the  flow  of  blood  through  the  cardiac  muscle  itself,  and  so  help 
the  disturbed  innervation  which  is  the  cause  of  the  arrhythmic  condition. 

The  irregularity  represented  in  Fig.  57  is  quite  different.     Here  the  difference 


134     ARTERIAL  PULSE,  PALPATION,  SPHYGMOGRAPHY,  ETC. 

in  volume  of  the  beats  is  a  direct  sequence  of  the  irregularity.  Because  the  left 
ventricular  diastolic  filling  is  brief,  the  succeeding  pulse  must  be  smaller,  even  if 
the  cardiac  power  is  entirely  sufficient.     This  type  of  irregularity,  therefore,  does 


Fig.  57.— Arrhythmic  sphygmogram  in  cardiac  sufficiency. 

not  point  to  cardiac  insufficiency,  and  so  in  itself  presents  no  indication  for  the 
use  of  digitalis.  The  size  and  the  high  tension  of  the  individual  pulse  wave  evident 
in  Fig.  57  would  be  another  reason  for  the  uselessness  of  digitalis  in  this  case. 

SPHYGMOMANOMETRY  (TONOMETRY). 

The  sphygmograph  furnishes  only  relative  information  of  the  height  of  the 
arterial  pressure  ;  hence  v.  Basch  ^  attempted  to  construct  an  instrument  to  meas- 
ure the  arterial  pressure  upon  the  intact  human  body.  He  had  succeeded,  approxi- 
mately, with  the  sphygmomanometer.  Potain  has  since  modified  v.  Basch' s  more 
modern  instrument. 

V.  Basch  attempted  to  copy  the  method  of  estimating  pulse  ' '  tension ' '  with 
the  finger  (p.  106)  by  measuring  instrumentally  the  amount  of  pressure  required 
to  suppress  the  jjulse  wave.  Waldenburg  and  Talma  had  attempted  to  obliterate 
the  pulse  in  the  artery  by  compressing  the  artery  by  weights  or  springs.  The  size 
of  the  surface  pressed  upon  Avas  neglected  in  these  experiments,  so  that  their  re- 
sults are  of  no  particular  value.  To  obviate  this  difficulty,  v.  Basch  employed  a 
so-called  air  pelotte — i.  e. ,  a  thin  rubber  membrane  tied  like  a  bladder  over  a  metal 
cylinder,  filled  Avith  air  and  connected  with  a  manometer.  With  this  mechanism 
the  size  of  the  surface  pressed  upon  makes  no  difference;  the  manometer  reading 
will  always  be  the  same.  For,  according  to  hydrostatic  laws,  the  amount  of  press- 
ure indicated  by  the  manometer  is  that  exerted  upon  each  point  of  the  surface 
of  the  pelotte. 

V.  Basch  has  recently  made  a  practical  improvement  in  the  shape  of  the 
pelotte.     Fig.  58  represents  the  instrument  in  its  new  form:  A,  the  manometer; 


Fig.  58.— v.  Basch's  sphygmomanometer. 

B,  the  pelotte;  C,  the  connecting  tube.  By  means  of  the  cock,  D,  the  entire  system 
is  filled  with  air  under  a  low  pressure,  ^  so  that  the  pelotte  is  but  slightly  tense  and 
the  two  closing  membranes  bulge  a  trifle. 

1  Berlin,  klin.  Woch.,  1887;  Arch,  de  phydohcjie,  1889,  Ser.  5,  vol.  i.,  p.  556,  and  vol.  ii., 
p.  300.  ,        ,    , 

^  v.  Basch  formerly  filled  the  cylinder  with  water.  Air  was  first  employed  by 
Potain,  and  has  the  advantage  of  doing  away  with  hydrostatic  pressure,  and  so  enablmg 
us  to  disregard  the  level  of  the  manometer  in  reference  to  the  pelotte. 


SPHYGMOMANOMETRY  [TONOMETRY).  135 

The  employment  of  this  instrument  is  very  simple.  The  course  of  the  artery 
to  be  examined  is  first  marked  upon  the  skin ;  one  of  the  bulging  membranes  of 
the  jDelotte  is  placed  upon  the  artery,  and  the  manometer  is  laid  upon  the  bed  at 
the  side  of  the  patient.  The  examiner  then  attempts  to  estimate  the  amount  of 
pressure  (read  upon  the  manometer  scale)  necessary  to  obliterate  the  pulse  periph- 
eral to  the  pelotte.  This  he  does  by  palpating  with  one  finger,  while  with  another 
he  prevents  any  anastomotic  pulse  from  entering  the  artery.  This  method  will 
determine  the  arterial  pressure  at  least  approximately ;  perhaps  more  accurately 
if  the  manometer  is  read  at  the  moment  when  the  jjulse  reappears  after  the  press- 
ure has  been  gradually  diminished.  The  method  is,  of  course,  entirely  subjective, 
as  its  accuracy  must  depend  upon  the  examiner's  sense  of  touch.  To  obviate  this 
difficulty,  V.  Basch  has  attemj^ted  to  substitute  the  sense  of  sight.  A  rubber  band 
is  rather  loosely  2:)laced  over  the  radial  artery  and  a  small  pin  stuck  in  it,  so  that 
the  excursions  of  the  pin  are  plainly  visible.  If  the  pin  stops  moving  the  pulse  is 
considered  absent.  According  to  the  writer's  experience,  this  device  is  not  always 
successful. 

Two  factors  combine  to  prevent  this  method  from  accurately  measuring  the 
true  arterial  pressure.  In  the  first  place,  the  wall  of  even  an  empty  artery  remains 
open,  so  that  a  certain,  though  small,  amount  of  the  pressure  exerted  represents 
that  employed  to  com23ress  the  arterial  tube ;  and,  in  the  second  place,  the  tissues 
covering  the  artery  must  interfere  to  a  slight  extent  with  the  accurate  application 
of  the  pelotte,  so  that  the  instrument  must  register  a  somewhat  higher  pressure 
than  actually  exists. 

V.  Basch's  experiments,  however,  show  that  both  these  factors'  combined  can- 
not cause  a  deviation  of  the  real  values  from  those  recorded  of  more  than  about 
10  to  15  mm.  Tigerstedt^  gave  a  very  unfavorable  opinion  of  the  value  of  this 
method,  because  he  found  a  much  greater  deviation.  In  the  j^revious  editions  of 
this  book  the  author  shared  this  view,  but  feels  obliged  to  withdraw  his  criticism 
since  he  has  used  the  improved  air  pelotte  as  illustrated  in  Fig.  58.  As  a  matter 
of  fact,  the  results  given  by  the  old  pelotte  wei-e  not  very  reliable,  for  reasons 
which  cannot  be  here  given  in  detail.  The  temporal  artery  is  the  most  conve- 
niently situated  for  this  measurement ;  the  radial  next,  provided  that  it  is  com- 
pressible against  the  lower  end  of  the  radius.  In  the  former  v.  Basch  found 
that  the  pressure  varied  from  90  to  120  mm.  Hg.  ;  in  the  latter,  from  110  to  160. 
The  author's  own  estimations  at  the  radial  have  usually  been  from  160  mm.  ujsward. 
Potain's  investigations  {loc.  cit.)  show  that  these  figures  correspond  to  the  max- 
imum pressure  variations  during  a  pulse  wave — i.  e.,  to  the  systolic  pressure. 

Another  reason  to  doubt  the  accuracy  of  this  method  is  the  following  :  Since 
dynamic  processes — that  is,  moving  masses — are  chiefly  concerned,  we  must  con- 
sider the  vital  power  of  the  pulse  wave  according  to  the  laws  of  the  hydraulic 
press.  Now,  it  is  well  known  that  when  a  current  is  compressed  by  some  obstruc- 
tion, a  far  greater  force  is  developed  above  the  point  of  resistance  at  the  moment 
of  compression  than  the  corresponding  amount  of  lateral  pressure  of  an  unresisted 
flowing  fluid.  This  arises  from  the  transformation  of  the  pressure  of  velocity  into 
lateral  pressure.  The  hydraulic  press  or  ram  depends  upon  this  ])rinciple.  Con- 
sequently a  large  j^ulse  wave,  even  with  low  arterial  pressure,  will  force  its  way 
through  under  the  compressing  pelotte,  owing  to  the  greater  amount  of  "  energy," 
while  a  smaller  pulse  wave,  even  with  higher  arterial  tension,  will  be  completely 
obstructed,  because  the  latter  possesses  less  energy.  Again,  the  portion  of  the 
wave  which  passes  through  under  the  pelotte  will  be  felt  longer  if  the  pulse  is 
large  than  if  it  is  small  and  hard  to  feel,  even  though  of  high  tension.  This  objec- 
tion agrees  with  Potain's  results  {loc.  cit.),  according  to  which  the  values  found 
with  the  V.  Basch  instrument  correspond  to  the  maximum  (systolic)  pressure,  l)nt 
do  not  furnish  any  information  of  the  mean  or  of  the  minimum  pressure.  This 
only  means  that  the  manometric  values  depend  upon  the  potential  energy  of  the 
individual  jiulse  wave.  With  this  proviso  the  method  may  be  of  some  clinical  use, 
but  we  must  not  imagine  thattlie  values  tluis  determined  correspond  with  the  read- 

^  Lehibach  der  Pliysiohijie  des  Kreialaufef,  Leipzig,  1893. 


136     ARTERIAL  PULSE,  PALPATION,  SPHYGMOGRAPHY,  ETC. 


ings  of  a  mercury  manometer  connected  directly  with  an  artery.  It  is  commonly 
supposed  that  these  systolic  values,  to  be  sure,  are  not  so  very  different  from  the 
mean  arterial  pressure.  But  although  the  well-known  kymographion  curves  with 
the  mercury  manometer  seem  to  show  that  the  systolic  pressure  varies  but  little 
from  the  mean  pressure,  at  the  same  time  these  curves  are  not  at  all  applicable  for 
estimating  the  extent  of  pressure  variations,  because  the  inertia  of  the  mercury 
column  prevents  its  registering  the  variations  correctly.  As  a  matter  of  fact,  we 
know  very  little  about  normal  variations  of  blood-pressure  in  man  and  animals, 
and  still  less  about  the  size  they  may  attain  in  pathologic  conditions.  In  fever,  for 
example,  on  account  of  the  large,  bounding  jsulse  waves, 
V.  Basch's  sphygmomanometer  may  indicate  high  figures, 
although  the  sphygmographic  curve  shows  relaxation  of 
the  vessels  and  a  low  (mean)  arterial  pressure.  Such 
peculiar  contradictions,  which  have  thus  far  been  at- 
tributed entirely  to  the  fault  in  the  sphygmogram  and 
never  to  the  really  much  less  reliable  sphygmomanometer, 
can  only  be  explained  by  assuming  that  under  these  con- 
ditions there  exists  a  very  much  greater  difference  between 
minimum  and  maximum  or  between  mean  and  maximum 
pressure  in  the  arteries  than  is  generally  accepted.  The 
writer  believes  that  the  mean  arterial  pressure  in  fever  is 
probably  low,  corresponding  to  the  shape  of  the  sphygmo- 
gram, in  spite  of  the  fact  that  v.  Basch's  instrument  in- 
dicates high  values,  on  account  of  the  large  and  powerful 
systole  in  consequence  of  free  flow  of  blood  through  the 
relaxed  vessels.  Should  these  views  be  confirmed,  the 
clinical  value  of  sphygmography  will  be  increased  at  the 
expense  of  sphygmomanometry.  At  all  events,  the  writer 
recommends  the  greatest  caution  in  the  clinical  use  of  v. 
Basch's  instrument.  (See  p.  106  for  the  real  significance 
of  the  term  arterial  tension  or  blood-pressure. ) 

The  author  has  recently  made  what  he  believes  to  be 
an  improvement  in  v.  Basch's  instrument  by  increasing 
the  diameter  of  the  air  pelotte  from  scarcely  2  cm.  to  3- 
4  cm.  This  greatly  aids  us  in  securing  pneumatic  pressure 
upon  the  artery  ;  while  with  the  small  pelotte  of  v.  Basch 
there  is  danger  of  compressing  the  vessel  by  the  resistant 
portion  of  the  caoutchouc  near  the  rim  of  the  pelotte  or 
by  the  rim  itself. 

As  it  has  been  my  experience  that  the  metal  manom- 
eter of  the  shops  is  not  very  accurately  graduated,  and 
that,  although  it  may  be  correct  originally,  the  values- 
of  the  scale  gradually  change,  I  have  constructed  a 
pocket  mercury  manometer,  which  may  be  easily  trans- 
ported, is  absolutely  correct,  and  has  the  additional  ad- 
vantage of  being  cheap.  ^  This  manometer  may  also 
be  employed  for  any  other  manometric  method,  in 
the  Riva-Rocci  sphygmomanometer,  for  example  (see 
p.  137,  et  seq.),  for  the  measurement  of  the  pressure  of  pleural  exudates,  and, 
in  virtue  of  its  fine  caliber,  for  the  measurement  of  the  pressure  of  the  cerebro- 
spinal fluid  in  lumbar  puncture.  (See  section  upon  Exploratory  Puncture. )  The 
instrument  is  illustrated  in  Fig.  59,  and  consists  simply  of  a  U-shaped  manometer 
in  which  one  branch  can  be  elongated  by  inserting  a  glass  tube,  the  -connection 
being  accurately  ground.  The  caliber  is  sufficiently  large  to  exclude  the  disturbing 
element  of  capillarity,  and  yet  not  large  enough  to  require  a  great  quantity  of  mer- 
cury. Owing  to  the  accurate  adaptation  of  the  two  tubes,  it  is  unnecessary  to  use 
the  greasy  materials  usually  employed  to  secure  the  perfect  adjustment  of  glass 

1  The  instrument  is  manufactured  by  the  optician  Biichi,  in  Bern. 


Fig.     59.— Sahli's    pocket 
mercury  manometer. 


SPHYGMOMANOMETRY  {TONOMETRY).  137 

stop-cocks,  and  the  mercury  is  consequently  kept  in  much  better  condition.  When 
the  instrument  is  to  be  employed,  the  elongation  a  6  is  inserted,  and  the  pelotte  of 
V.  Basch's  instrument  (preferably  the  enlarged  form,  as  described  upon  page  134  ; 
see  Fig.  58)  is  connected  with  c  by  a  tube.  The  pressure  exercised  upon  the 
artery  by  the  pelotte  is  transmitted  to  the  shorter  branch  of  the  manometer.  The 
elongated  branch  is  so  divided  that  it  gives  the  pressure  directly  in  centimeters, 
every  half-centimeter  being  marked  as  a  unit.  In  such  a  manometer,  as  is 
well  known,  the  pressure  is  obtained  by  multiplying  the  height  of  the  ascending 
column  by  two,  because  the  mercury  falls  exactly  as  far  in  one  branch  as  it  rises  in 
the  other.  The  manometer  must  be  accurately  filled  with  mercury  to  the  zero 
mark.  The  ampulla  e  is  for  the  purjjose  of  preventing  the  throwing  of  the  mer- 
cury out  of  the  shorter  branch  by  a  sudden  diminution  of  pressure,  and  the  am- 
pulla b  acts  in  a  similar  manner  when  the  pressure  is  suddenly  increased  by  careless 
manipulation  of  the  pelotte.  The  instrument  may  be  packed  and  transported  by 
removing  the  elongating  tube  a  b,  and  plugging  the  openings  a  and  c  with  rubber 
corks.  I  formerly  employed  glass  stop-cocks  for  this  purpose,  but  owing  to  their 
fragility  and  the  necessity  of  using  a  lubricant  to  render  them  air-tight,  I  have 
found  that  they  were  not  well  adapted  to  the  purpose.  The  entire  instrument  may 
be  packed  in  a  handy,  well-cushioned  case,  which  is  made  large  enough  to  also 
hold  the  pelotte  for  von  Basch's  instrument. 

Since  the  mean  blood-pressure  is  so  important  for  diagnosis,  a.s  well  as  for  de- 
termining the  efiiciency  of  certain  therapeutic  agents,  it  is  very  fortunate  that  so 
many  physiologists  have  recently  turned  their  attention  toward  devising  some  simple 
and  accurate  method  of  measuring  it.  Such  methods  have  been  described  by  Mosso, 
Hurthle,  v.  Frey,  Eiva-Rocci,  and  Gartner. 

The  Riva-Rocci  and  the  Gartner  instruments  are  the  only  ones  which  have 
proved  to  be  practically  valuable.  The  detailed  descriptions  of  the  others  in 
previous  editions  of  this  book  have  consequently  been  omitted  in  the  present  one. 
The  principle  of  Eiva-Rocci' s  sphygmomanometer  ^  is  the  same  as  that  of  v. 
Basch's.  It  measures  the  amount  of  pressure  necessary  to  obliterate  the  pulse 
peripheral  to  a  point  of  constriction.  A  pneumatic  pressure  is  used  as  in  v. 
Basch's  instrument.  The  practically  important  modification  consists  in  substituting 
for  the  single  pelotte  to  press  upon  the  artery  a  pneumatic  cuff  which  encircles  the 
upper  arm,  and  the  cavity  of  which  connects  with  a  rubber  bulb.  Since  the  upper 
arm  contains  only  a  single  bone,  inflation  of  the  cuff  will  interrupt  all  the  arterial 
supply  to  the  forearm  in  a  perfectly  equal  way. 

The  cufl^  should  be  made  of  some  firm  mackintosh  cloth,  or,  if  of  elastic  rubber, 
it  should  be  securely  fastened  to  a  lining  of  material  which  will  not  stretch.  This 
is  to  prevent  the  loss  of  a  part  of  the  pressure  from  any  eccentric  inflation  or  dis- 
tention of  the  wall.     Fig.  60  represents  the  apparatus. 

The  i^atient's  upper  arm  is  inserted  into  the  cuff  (a).  The  latter  is  connected 
with  a  mercury  manometer  {b),  and  through  it  with  a  double  rubber  bulb  (c).  By 
pumping  at  c  the  cuff"  can  be  made  to  encircle  the  upper  arm  tightly,  and  the  amount 
of  pressure  employed  can  be  read  in  mm.  of  mercury  upon  the  vertical  tube  of  the 
manometer.  This  pressure  is  increased  until  the  radial  pulse  disappears.  The  cuff", 
about  4  cm.  wide,  should  be  so  adjusted  as  to  fit  the  arm  rather  snugly  without 
compressing  it.  The  latter  purpose  is  accomplished  by  a  clamp,  as  is  rej^resented 
in  Fig.  60.  The  instrument  was  tested  experimentally  both  by  Riva-Rocci  and  by 
Gumprecht.^  The  muscles  should  be  well  relaxed,  because  compression  through 
thick  muscles  does  not  affect  the  result.  The  same  objection  applies  to  the  ])rinci- 
ple  involved  in  this  method  as  was  mentioned  in  discussing  v.  Basch's  instrument 
(p.  1 35).  The  amount  of  pressure  found  depends  not  only  upon  the  median  arterial 
pressure,  but  also  very  decidedly  upon  the  energy  of  the  pulse  wave,  and  with  it 
upon  the  size  of  the  pulse  volume.  For  these  reasons,  and  perhaps  also  partly  on 
account  of  the  resistance  to  compression  which  the  muscles  of  the  upper  arm  afford, 

^  Riva-Rocci,  Un  nuovo  sfigmomanonietro,  Torino,  1896 ;  Frascati  e  Comp.  Tecnica 
della  sfigmomanometria,  Gnz.  Med.,  di  Torino,  1897,  Nos.  9  and  10. 
^  Zeits.f.  klin.  Med.,  1900,  vol.  xxxix.,  parts  5  and  6. 


138     ARTERIAL  PULSE,  PALPATION,  SPHYGMOQRAPHY,  ETC. 

the  figures  which  the  writer  has  found  in  a  great  many  attempts  have  always  been 
very  high.  Normal  individuals  furnish  a  value  of  150  to  160  mm.  Hg.,  and  the 
arteriosclerotic  and  nephritic  as  high  as  230  to  250  mm.,  or  even  higher.  Although 
all  these  values  may  be  relatively  too  high,  nevertheless  the  instrument  possesses  a 
distinct  advantage  in  being  purely  objective  as  compared  with  v.  Basch's  (see  ^.  135). 
This  may  be  realized  by  making  several  tests,  one  after  the  other,  when  it  will  be 
seen  that  they  are  almost  invariably  the  same.  This  is  especially  apt  to  be  the  case 
if  at  each  attempt  the  pressure  is  raised  beyond  the  point  at  which  the  pulse  cannot 
be  felt,  and  then,  when,  as  a  result  of  the  yielding  of  the  rubber  tubes  and  connec- 
tions, the  pressure  falls  slowly,  the  point  is  noted  at  which  the  pulse  begins  to  appear 
again.  In  this  way  the  attention  is  not  distracted  by  the  need  of  pumping,  and 
the  method  is  still  more  objective  and  quite  exact.  Of  course,  for  a  control  it  is 
advisable  to  note  the  point  at  which  increasing  jiressure  causes  the  pulse  to  vanish. 
The  writer  has  frequently  attempted  to  supplant  the  palpation  of  the  pulse  by  the 
objective  method  of  sphygmography,  making  short  curves  at  different  pressures  until 
the  needle  makes  but  a  straight  line.  It  has  advantages  in  demonstrating  to  a  clinic. 
One  caution  should  be  added.     Pronounced  congestion,  pain,  and  even  cutaneous 


Fig.  60.— Riva-Rocci's  sphygmomanometer. 


hemorrhage  may  result  from  employing  the  instrument  to  measure  very  high  press- 
ure— e.  g.,  above  230  mm. 

The  transportable  mercury  manometer  of  Sahli,  described  upon  p.  136,  may  also 
be  employed  in  connection  with  the  Riva-Rocci  pneximatic  arm-band,  rendering  this 
excellent  instrument  much  handier  and  more  practical. 

Led  by  v.  Recklinghausen,^  a  number  of  authors  have  pointed  out  that  the 
cuff  of  Riva-Rocci's  instrument  is  too  narrow.  They  came  to  this  conclusion  from 
the  fact  that  different  pressure  values  are  obtained  when  a  wider  cuff  is  emi^loyed. 
It  is  clear  that  if  the  cuff  is  too  narrow  the  inflation  produces  a  marked  distortion, 
both  of  the  cuff  itself  and  of  the  surface  of  the  arm,  which  endangers  the  trans- 
mission of  the  aerostatic  pressure,  since  a  certain  fractional  part  of  the  manometric 
.  pressure  is  consumed  in  producing  the  aerostatic  tension  of  the  cuff  and  the  tension 
of  the  tissues  pressed  upon.  The  cuff  of  the  original  Riva-Rocci  instrument  was  4^ 
cm.  in  width.  These  authors  now  demand  a  cuff  32  cm.  wide.  It  is  clear,  however, 
that  this  not  only  makes  the  instrument  more  clumsy,  but  also  renders  the  closure  of 
the  cuff  more  difficult  and  less  secure.  Additional  errors  also  arise  from  the  fact  that 
such  a  broad  cuff  does  not  act  upon  an  approximately  cylindric  surface,  owing  to 

^  V.  Recklinghausen,  Arch.  f.  exper.  Pathol,  u.  Pharm.,  1901,  vol.  xlvi.,  parts  1  and  2; 
Hansen,  Deiii.  Arch.  /.  klin.  Med.,  1900,  vol.  Ixvii. 


SPHYGMOMANOMETRY  {TONOMETRY).  139 

the  irregular  contour  of  the  arm.  Martin '  has  found  that  a  cuff  10  cm.  in  width 
suffices  for  all  cases.  In  the  writer' s  opinion  a  great  deal  depends  upon  the  manner 
in  which  the  cuff  is  applied.  If  the  cuff  is  emptied  and  applied  accurately  to  the 
skin  without  the  exercise  of  any  pressure,  cuflFs  only  5  to  6  cm.  in  width  remain 
so  flat  during  inflation  that  the  transmission  of  the  pressure  is  complete  and  the 
results  are  as  accurate  as  they  can  well  be  from  the  nature  of  the  procedure.  We 
should  banish  the  illusion  that  this  procedure  is  of  equal  value  with  manometry 
upon  the  exposed  and  divided  artery. 

Gartner's  tonometer  ^  depends  upon  a  similar  principle.  It  estimates  the  press- 
ure which  is  required  to  interrupt  the  peripheral  circulation.  Gartner  makes  use 
of  the  color  of  the  ti^)  of  the  finger  instead  of  feeling  the  j)ulse  to  determine  the 
condition  of  the  peripheral  circulation.  His  instrument  consists  of  a  small  pneu- 
matic compression  ring,  whose  cavity  is  connected  with  a  mercury  or  spring  man- 
ometer and  with  a  rubber  bulb.  The  pneumatic  ring  is  constructed  of  a  metal 
hoop  1  cm.  high  and  2J  cm.  in  diameter.  A  rubber  membrane  lines  this  hoop, 
and  with  the  latter  surrounds  an  air  space  communicating  with  the  manometer  and 
bulb.  The  pneumatic  ring  is  first  slipped  over  the  second  phalanx  of  the  little 
finger  without  pressure.  The  projecting  end  phalanx  is  then  made  bloodless  by 
a  rubber  compressor  like  a  glove  finger,  or  by  a  ring  cut  out  of  a  rubber  tubing, 
rolled  upon  the  finger  as  far  as  the  pneumatic  ring.  This  compression  is  kept  up 
UJitil  the  pressure  in  the  pneumatic  ring  has  been  raised  by  means  of  the  bulb 
sufficiently  to  keep  the  blood  from  returning  to  the  finger  ;  then  the  compressor 
is  removed.  The  finger-tip  now  appears  as  pale  as  a  corpse.  By  gradually  releas- 
ing the  pressure  from  the  rubber  bulb  the  finger  becomes  colored  again.  As  a 
matter  of  fact,  the  finger  assumes  a  cyanotic  color,  and  so  facilitates  the  differentia- 
tion. This  is  because  the  veins  will  still  be  compressed  at  the  moment  the  digital 
arteries  open  under  the  arterial  blood-jsressure.  This  pressure  at  which  the  blood 
again  streams  into  the  finger  can  be  regarded  as  equivalent  to  the  blood-pressure  in 
the  digital  arteries.  In  cases  where  the  capillaries  of  the  finger-tip  are  much 
contracted,  it  may  happen  that  the  finger-tip  will  not  be  properly  colored  after 
the  release  of  the  pressure  on  the  arteries.  In  such  cases  Gartner  accomplished 
his  purpose  by  relaxing  the  tonus  of  the  fine  vessels  by  producing  an  artificial 
congestion  by  a  pressure  of  20  to  40  mm.,  Hg.,  with  the  pneumatic  ring  for  a 
half  minute,  and  so  paralyzing  the  vessels  just  before  repeating  the  test.  Gartner 
assumes  that  the  pressure  in  the  small  digital  arteries  difiers  but  little  from  that 
in  the  radial.  Of  course,  the  measurement  will  be  decidedly  influenced  by  the 
height  of  the  fingers,  so  that  he  recommends  that  the  test  be  undertaken  with 
the  fingers  at  the  height  of  the  heart.  Without  question,  Gartner's  instrument 
offers  certain  advantages  over  Riva-Rocci'  s.  One  of  the  most  important  consists 
in  the  avoidance  of  the  unfortunate  confusion  between  the  static  and  dynamic 
conception  of  both  Riva-Rocci' s  and  v.  Basch's  instruments.  Even  here,  how- 
ever, although  the  pulse  wave  plays  an  insignificant  part,  it  is  not  the  mean 
blood-pressure  which  is  measured,  but  a  blood-pressure  which  closely  approximates 
the  maximum.  Another  advantage  seems  to  the  writer  to  be  that  it  depends  ujjon 
relations  which  are  appreciated  by  the  keenest  of  our  senses — namely,  the  sense 
of  sight. 

Gartner  also  considers  that  the  resistance  of  the  arterial  wall,  which  especially 
in  arteriosclerosis  plays  so  important  a  part,  influences  the  measurement  less  in  the 
small  finger  arteries  than  in  the  large  vessels.  Another  advantage  is  that  the 
patient  does  not  have  to  be  undressed  when  Gartner's  method  is  employed.  The 
normal  pressure  values  Gartner  has  estimated  vary  between  90  arid  105  mm. 
There  is  only  one  objection  to  his  method,  and  he  does  not  deny  it,  nor  has  he  been 
able  to  obviate  it  as  yet.  This  is  that  the  readings  are  decidedly  influenced  by 
the  resistance  of  the  tissues  of  the  finger-tips.     This  resistance  is  very  different  in 

1  Munch.  Med.  WocL,  1903,  No.  24,  p.  1021. 

^G.  Gilrtner,  Ueber  einen  neuen  Blutdruckmesser  (Tonometer),  Wien.  Med.  Presse, 
1899,  jSTo.  26.  L.  Schulmeister  (Vienna)  and  F.  Hugershofif  (Leipzig)  make  the  instru- 
ments. 


140     ARTERIAL  PULSE,  PALPATION,  SPHYGMOGRAPHY,  ETC. 

a  laborer's  hand  and  in  a  lady's  hand.  In  the  writer's  opimon  this  source  of 
error  is  so  considerable  that  it  discounts  the  value  of  the  entire  procedure,  and 
the  description  of  certain  technical  modifications  of  this  method  ^  will  consequently 
be  omitted,  since  they  do  not  obviate  this  chief  fault. 

[Within  the  last  few  years  the  usefulness  of  blood-pressure  determi- 
nation has  been  quite  generally  recognized  in  America.  Both  here  and 
in  England  new  instruments  have  been  brought  forward,  some  of  which 
represent  a  distinct  advance  over  any  of  those  previously  mentioned, 
and  merit  separate  description. 

Hill  and  Barnard's  sphygmometer^  appeared  a  little  after  Eiva-Rocci's, 
and  uses  the  same  method  of  circular  compression.  It  does  not,  how- 
ever, measure  the  pressure  required  to  obliterate  the  pulse  (systolic  or 
maximum  pressure),  but,  like  Mosso's,  the  point  of  maximal  pulsation 
(diastolic  or  minimal  pressure).  This  is  accomplished  by  the  employ- 
ment of  a  delicate  spring  tambour,  graduated  in  mm.,  Hg.,  as  the  man- 
ometer (Fig.  61)  shows  the  apparatus.     The  cuff,  a  hollow  bag,  4|^  cm. 


Fig.  61.— Hill  and  Barnard's  sphygmometer. 

wide,  with  an  outer  leather  armlet,  is  buckled  around  the  arm,  and 
connected  with  the  manometer  by  a  screw-joint.  The  pressure  is  then 
raised  by  means  of  the  hand-pump  until  the  needle  shows  diminishing 
excursions  on  the  dial.  Then,  by  unscrewing  a  valve  in  the  stem  of  the 
pump,  the  pressure  is  allowed  to  fall  gradually,  while  the  needle  is  closely 
watched.  Its  oscillations  increase  for  a  time  to  a  maximum,  then,  after 
remaining  the  same  for  a  short  time,  rapidly  decrease.  The  last 
point  at  which  they  remain  maximal  represents  the  minimum  arterial 
pressure,  as  already  described.  Hill  thought  that  the  midpoint  of  maxi- 
mum oscillation  was  equivalent  to  the  mean  arterial  tension,  but  this 
has  been  proved  inaccurate.  The  instrument  is  well  constructed,  light, 
and  compact.  It  has  two  great  drawbacks.  One  is  the  narrowness  of 
the  cuff,  for  reasons  which  will  follow.     The  other  is,  that  so  delicate 

1  See  Martin,  Milnch.  med.  Wock,  1903,  No.  24,  p.  1021. 

2  Hill,  L.,  Barnard,  H.,  Rrit.  Med.  Jour.,  1897,  vol.  ii.,  p.  904.  Made  by  J.  Hicks, 
London ;  Agents  for  the  United  States,  Oelschlager  Bros.,  42  East  23rd  St.,  New  York 
City. 


SFHYGMOMANOMETE  Y  {TONOMETR Y.) 


141 


a  manometer  needs  constant  standardizing  by  comparison  with  a  mer- 
cury one,  and  soon  becomes  inaccurate. 


Fig.  62.— Riva-Rocci  sphygmomanometer  as  modified  by  Cook. 


To    ln}litor 

Fig.  63.— Erlanger's  sphyguiomaiiometer. 


Hill  and  Barnard's  so-called  ixx'ket  sphygmometer  is  hardly  more 
than  a  clinical  toy.     Oliver's  dynamometer^  cannot  be  recommended 
1  Oliver,  George,  Jour,  of  PhynioL,  1897-98,  vol.  xxii,  p.  51. 


142     ARTERIAL   PULSE,   PALPATIOy,  SPHYGMOGRAPHY,   ETC. 

because  it  possesses  all  the  faults  of  v.  Basch's  method  of  applying  the 
pressure  by  a  pad  over  the  artery. 

In  America,  Cook  rendered  a  great  service  by  so  modifying  the  Riva- 
Rocci  apparatus  as  to  make  it  inexpensive  and  easily  carried/  thus  se- 
curing for  it  a  much  more  extended  apj^lication.  His  instrument  so 
closely  resembles  its  oirginal  in  the  technic  of  its  use  that  it  needs  no 
further  description. 

Two  American  instruments  are  now  made  with  a  12  cm.  cuff,  Er- 
langer's  and  Janeway's.  The  former  ^  is,  undoubtedly  the  most  accurate 
and  valuable  sphygmomanometer  yet  constructed.  It  gives  readings  both 
of  systolic  (maximum)  and  diastolic  (minimum)  pressure,  and  therefore 
makes  possible  the  calculation  of  exact  mean  arterial  pressure.  Fig.  63 
shows  the  apparatus  in  perspective. 

Besides  the  manometer,  compressing  armlet,  and  inflator  it  contains 
a  somewhat  elaborate  reading  mechanism  and  iNy^mographiondrum. 
This  mechanism  consists  of  the  tambour,  the  interior  of  which  is  con- 
nected with  the  air  chamber  inside  the  glass  bulb  G.  This  air  chamber 
has  no  other  openings  while  the  record  is  being  made,  but  automatically 


Fig.  fi4.— Janeway's  sphygmnmanometer. 

connects  with  the  outer  air  throiigh  the  tube  E  and  the  stop-cock  C 
when  rapid  changes  in  pressure  are  made,  ^vhich  might  damage  the  tam- 
bour. The  ptilse  waves  are  transmitted  through  the  tube  to  "PS" 
and  cause  variations  in  volume  of  the  rubber  bulb  B.  These  pulsations 
of  B  are,  of  course,  reproduced  by  the  air  within  C,  and  thus  carried 
to  the  tambour,  which  inscribes  them  on  the  smoked  cylinder.  The 
purpose  of  the  rubber  bulb  B  is  to  shield  the  tambour  from  too  sudden 
and  great  variations  of  pressure.  The  stop-cock  is  an  important  mech- 
anism, but  cannot  be  described  intelligently  without  mechanical  draw- 
ings. It  is  easily  understood  from  the  instrument  itself.  Unfortu- 
nately this  apparatus  is  too  bulky  to  be  carried  far,  and  is  more  com- 
plicated than   desirable   for   strictly  clinical  Mork.      For   purposes  of 

Cook,  Jour.  Am.  Med.  Assoc,  1903,  vol.  xL,  p.  1199. 
crer.  J.,  Am.  Jour,  oj  Physiol.,  1904,  vol.  x..  Proceed,  of  Am.  Physiol.  Soc,  p.  14. 


2  K-lan 


SPHYGMOMANOMETR  Y  {TONOMETR  Y). 


143 


physiologic  experiment  on  human  beings,  and  whenever  very  accurate 
readings  of  both  pressures  are  desired,  it  should  be  the  choice. 

Janeway's  sphygmomanometer'  is  shown  in  Fig.  64.  Its  special  feature 
is  the  portable  U-tube  manometer  attached  to  a  case,  into  which  it  folds 
for  carrying.  The  whole  when  closed  measures  lOJ  x  f  x  If  in.,  and 
with  cuff  and  inflator  weighs  2  J  pounds.  The  armlet  is  a  hollow  rub- 
ber bag,  12x18  cm.,  loosely  covered  and  attached  to  an  outer  leather 
cuff,  15  X  33  cm.,  which  fastens  by  two  straps  with  friction  buckles. 
For  inflation  a  Politzer  bag  with  valve  is  used.  £"  is  a  stop-cock  pro- 
vided with  a  needle  valve,  by  which  the  pressure  can  be  reduced  gradu- 
ally. The  method  of  getting  the  systolic  pressure  is  practically  the 
same  as  with  Riva-E,occi's  sphygmomanometer,  the  pressure  being 
raised  by  squeezing  the  inflator  until  the  radial  pulse  is  lost,  then 
gradually  lowered  until  it  returns.      The  reading  at  the  moment  of 


Fig.  65. — Stanton's  sphygmomanometer. 


return  represents  the  systolic  pressure.  In  addition,  an  approximate 
determination  of  the  diastolic  pressure  can  be  made  by  noting  the  press- 
ure at  which  the  mercury  shows  the  greatest  pulsation  (see  sphyg- 
momanometer). This  is  done  by  allowing  the  pressure  to  fall  5  to 
10  mm.  at  a  time  after  the  return  of  the  pulse  has  been  detected,  and 
observing  at  least  10  pulsations  at  each  point.  After  a  certain  level  (in 
normal  pulses  25  to  40  mm.  below  the  systolic  pressure)  the  extent  of 
the  oscillations  diminishes  rapidly.  The  lowest  point  at  which  it  re- 
mains maximal  is  the  diastolic  lateral  pres.sure.  The  estimation  of  the 
two  pressures  is  the  only  clinical  method  of  computing  mean  arterial 
pressure,  and  has  considerable  diagnostic  value  in  cases  of  aortic  insuf- 

^  T.  C.  Janeway,  The  Clinical  Study  of  Blood-pressure,  New  York,  1904,  D.  Apple- 
ton  &  Co. ,  p.  89. 


144        VISIBLE  PHENOMENA    OF  MOTION  IN  THE   VESSELS. 

ficiency  and  hypertension,  where  the  elevation  of  systolic  is  much  more 
marked  than  that  of  diastolic  pressure. 

The  remaining  American  instrument,  Stanton's,^  is  shown  in  Fig. 
65.  The  manometer  consists  of  a  metal  cistern  (C)  connected  with  a 
glass  upright  tube  and  scale  (D),  which  can  be  unscrewed  for  carrying. 
The  armlet  is  a  hollow  rubber  bag,  3^  in.  (8  cm.)  wide  and  16  in. 
long,  closed  at  both  ends,  and  attached  to  an  outer  cuflp  of  thick  canvas, 
reinforced  by  tin  strips.  While  it  has  not  the  width  necessary  for  ab- 
solute accuracy,  it  nevertheless  suffices  for  the  vast  majority  of  cases. 
A  single  rubber  bulb  is  used  for  inflation.  At  A  is  a  stop-cock,  and  at 
B  a  screw  valve  for  the  gradual  lowering  of  pressure.  With  this 
sphygmomanometer  systolic  pressure  may  be  measured  and  diastolic 
pressure  approximately  estimated,  as  already  described  with  Janeway's 
apparatus.  It  is  a  portable  and  convenient  clinical  instrument. — 
T.  C.  J.] 


VISIBLE  PHENOMENA  OF  MOTION  IN  THE  VESSELS. 

CAPILLARY  PULSE, 

UxDEE  normal  conditions  the  blood  flows  smoothly  and  without  a 
pulse  in  the  capillaries,  because  the  resistance  in  the  smallest  arteries 
completely  deprives  the  pulse  wave  of  its  energy  at  this  point,  or  because, 
as  V.  Frey  and  Krehl  believe,  the  pulse  wave  is  completely  reflected 
centripetally  (see  p.  117  et  seq.).  Under  some  conditions,  however, 
the  pulse  is  transmitted  to  the  capillaries,  and  becomes  evident  to 
inspection  in  the  form  of  a  pulsating  reddening  and  blanching  of  the 
parts  in  question.  Whatever  facilitates  the  entrance  of  a  pulse  wave 
into  the  capillary  areas,  or  whatever  renders  the  flow  into  the  veins  dif- 
ficult, will,  of  course,  favor  the  production  of  a  capillary  pulse.  The 
larger  the  pulse  wave  and  the  more  it  approaches  the  type  of  "  pulsus 
celer,"  the  more  the  conditions  for  a  capillary  pulse  are  favored.  A 
capillary  pulse  is  sometimes  observed  over  hyperemic,  and  especially 
over  inflammatory,  areas — e.  g.,  over  felons.  Very  frequently  the 
patient  himself  appreciates  the  increased  pulsation  in  inflammatory 
parts  as  a  throbbing  pain.  The  capillary  pulse  due  to  a  pulsus  celer, 
especially  in  aortic  insufficiency,  is  of  far  greater  interest.  This  is  a 
very  common,  although  not  a  constant,  sign  in  this  valvular  lesion.  It 
is  perhaps  best  appreciated  by  observing  the  alternate  blusliing  and 
pallor  at  the  finger-nail.  Sometimes  enough  pressure  upon  the  anterior 
part  of  the  nail-bed  to  blanch  the  nail  brings  out  the  margin  between 
red  and  white  which  oscillates  with  systole.  The  capillary  pulse  in 
aortic  insufficiency  may  be  very  frequently  appreciated  at  other  places 
which  are  characterized  by  their  redness — e.  g.,  ears,  lips,  cheeks. 

1  W.  B.  Stanton,  Univ.  of  Penna.  Med.  Bull.,  1903,  vol.  xv.,  p.  466. 


RESPIRATORY  PHENOMENA    OF  MOTION  IN  THE   VEINS.     145 

A  clean  glass  slide  lightly  pressed  upon  the  extended  lower  lip  will 
sometimes  bring  out  the  capillary  pulse  when  it  cannot  be  appreciated 
at  the  finger-nail.  Another  useful  device  is  to  rub  a  spot  upon  the 
forehead  until  it  is  hyperemic  and  then  look  for  an  alternation  of  red- 
ness and  pallor. 

Contrary  to  many  statements,  a  capillary  pulse  is  by  no  means  path- 
ognomonic of  aortic  insufficiency.  Any  condition  which  will  produce 
a  "  pulsus  celer "  (exophthalmic  goiter,  fever,  chlorosis)  will  be  apt  to 
show  a  capillary  pulse.  Even  in  health  it  may  sometimes  be  observed. 
Yet  although  not  absolutely  pathognomonic  of  aortic  insufficiency,  it  is 
so  common  in  this  lesion  and  so  rare  in  other  conditions  that  the  sign 
really  possesses  considerable  diagnostic  significance.  The  sign  becomes 
most  distinct  during  the  stage  of  compensation.  The  retinal  vessels 
will  also  show  a  visible  pulsation  by  the  ophthalmoscope  w^hen  a  capillary 
pulse  is  visible  elsewhere. 

RESPIRATORY  PHENOMENA  OF  MOTION  IN  THE 

VEINS, 

The  respiratory  variations  in  the  interior  of  the  thorax,  as  is  well 
known,  influence  the  venous  circulation  very  distinctly.  Inspiration 
favors,  expiration  retards  the  flow  of  venous  blood.      This  influence  is 


Fig.  66.— Veii'jus  engorgement  during  forced  expiration— case  of  plitliisis  (New  York  ruv 

Hospital). 

ordinarily  not  evident  in  the  visible  veins  with  superficial  breathing, 
but  forced  breathing  will  produce  an  inspiratory  diminution  and  expi- 
ratory increase  in  these  veins,  and  if  they  are  already  distended  bv  con- 
gestion the  change  will  become  still  more  evident.  Both  conditions  are 
usually  present  in  dyspnea. 

10 


146 


VISIBLE  PHENOMENA    OF  MOTION   IN  THE   VESSELS. 


Intrathoracic  variations  in  pressure  become  more  distinct  during 
coughing  or  other  exertions  of  abdominal  pressure.  The  intrathoracic 
pressure  then  becomes  markedly  positive.  A  coughing  paroxysm  or 
straining  after  a  deep  inspiration  produces  a  prolonged  distention  and  a 
subsequent  sudden  collapse  of  the  veins,  most  plainly  seen  in  the  neck. 
When  this  periodic  congestion  is  frequently  repeated,  especially  in 
patients  who  suffer  from  chronic  cough,  a  permanent  dilatation  of  the 
veins,  especially  of  the  jugular,  may  result,  so  that  with  coughing  or 
straining  not  only  is  cyanosis  very  marked,  but  the  whole  lower  portion 
of  the  neck  becomes  swollen.  The  "bulbs"  of  the  jugular  vein  may 
appear  a»  large  swellings,  either  just  inside  or  outside  of  the  insertion 
of  the  sternocleidomastoid  (Fig.  66).     The  bulging  of  the  supraclavic- 


FiG  67.— Enlargement  of  jugular  vein  in  a  case  of  leukemia  with  enlarged  mediastinal  glands 
(Dr.  Joseph  Collins,  New  York  City  Hospital). 


ular  fossse  during  a  cough,  therefore,  should  not  always  be  regarded  as  a 
distention  of  the  lung  apices  (p.  98  et  seq.). 

In  very  rare  cases  the  reverse  condition  is  observed — i.  e.,  a  disten- 
tion of  the  veins  during  inspiration  and  a  collapsing  or  a  diminution 
during  expiration  ;  this  always  suggests  that  during  inspiration  some 
mechanical  compression  of  the  veins  exists  within  the  chest  interior. 
This  phenomenon  has  been  described  as  a  sign  of  fibrinous  mediastinitis, 
like  the  pulsus  paradoxus  (see  p.  126).  It  may,  however,  depend  upon 
the  effect  of  inspiratory  pressure  or  traction  upon  the  large  veins  leading 
to  the  heart,  due  to  interference  with  the  mobility  of  the  thoracic  con- 
tents (pericarditis,  pleuritis,  mediastinal  tumors). 


DIFFERENT  VARIETIES  OF   VENOUS  PULSE.  147 


DIFFERENT  VARIETIES  OF  VENOUS  PULSE. 

DIFFERENTIATION  OF  VENOUS  PULSATION  FROM  ARTERIAL 

PULSE. 

When  the  distended  veins  become  distinctly  visible  (in  venous  pulse 
the  external  jugular  veins  are  chiefly  concerned),  it  is  generally  a  simple 
matter  to  distinguish  between  their  pulsation  and  that  of  the  neighboring 
arteries.  The  pulsation  of  some  deeply  seated  vein  (internal  jugular) 
which  cannot  be  directly  observed  is  much  more  difficult  to  determine. 
But  even  then  the  venous  pulse  can  be  easily  recognized,  particularly  by 
the  large  area  of  pulsation  involved  corresponding  to  the  large  size  of 
the  vein,  also  by  the  slow,  undulating  transmission  of  the  beat,  and  by 
the  very  moderate  amount  of  power  to  be  felt  in  the  pulsation,  depend- 
ing upon  the  slight  amount  of  tension  of  the  venous  contents.  If  the 
pulsation  is  transmitted  from  an  artery  to  a  vein,  compression  of  the 
vein  will  not  affect  the  pulsation  peripheral  to  the  point  of  compression, 
and  sometimes  the  resulting  congestion  will  make  the  pulsation  even 
more  distinct.  An  accentuation  of  the  pulsation  from  compression 
otherwise  occurs  only  with  the  very  rare  penetrating  pulse  (see  p.  152). 


PHYSIOLOGIC  VENOUS  PULSE. 

(Negative  Venoas  Pulse;  Systolic  Venous  Collapse;  Venous  Undulation;  Negative 
Centrifugal  Venous  Pulse;  The  Presystolic  Variety  of  the  Negative  Venous 
Pulse.) 

The  arterial  pulse  wave  usually  disappears  in  the  capillaries — i.  e.,  it 
is  reflected  centripetally  (see  p.  144  et  seq.),  so  that  the  blood  no  longer 
pulsates  but  flows  uniformly  in  the  venous  radicals.  Nevertheless  under 
both  physiologic  and  pathologic  conditions  peculiar  pulsations  synchro- 
nous with  cardiac  action  are  frequently  observed  in  the  greater  veins 
lying  near  the  chest  (almost  exclusively  in  the  jugular  veins). 

In  the  following  sections  we  shall  describe  several  pathologic  varie- 
ties of  this  pulsation.  One  type  of  venous  pulse  must,  however,  be 
considered  absolutely  physiologic,  because  it  is  constantly  observed  after 
exposing  the  vein  in  healthy  animals,  and  because  perfectly  normal  indi- 
viduals sometimes  show  it.  That  this  venous  pulse  is  not  observed  in 
everybody  is  due  to  the  fact  that  in  some  people  the  jugular  veins  are 
not  visible  or  are  seen  only  with  considerable  difficulty.  Conversely, 
this  physiologic  venous  pulse  can  naturally  be  seen  with  especial  readi- 
ness if  the  veins  have  become  more  noticeably  distended  by  congestion. 

The  physiolof/ie  venous  pulse  can  be  distinguished  from  the  pathologic 
varieties  to  be  considered  later  by  the  circumstance  that  compression 
of  the  vein  by  the  finger  obstructs  the  pulsation  above  the  point  of 
pressure,  while  below  the  compression  the  pulsation  either  disappears  or 
diminishes,  but  never  increases.  This  central  obliteration  or  diminution 
of  the  pulse  wave  proves  beyond  a  doubt  that  the  pulse  wave  is  not  thrown 


148         VISIBLE  PHENOMENA    OF  MOTION  IN  THE    VESSELS. 

back  into  the  veins  from  the  heart.  The  peripheral  disappearance  of  the 
pulse  wave  proves  that  it  cannot  be  a  wave  transplanted  from  an  artery  to 
the  vein.  The  only  remaining  hypothesis  is  that  the  cardiac  activity  does 
not  force  the  blood  back  into  the  veins,  but  that  the  continuous  blood- 
current  is  rhythmically  retarded  and  accelerated.  This  type  of  a  ve- 
nous pulse  is  generally  called  a  negative  venous  pulse,  because  it  depends 
upon  the  transmission  of  a  negative  trough  or  suction  wave  from  the 
heart  to  the  vein  (see  below).  It  is  also  sometimes  termed  an  undula- 
tion on  account  of  its  appearance.  Probably  the  reason  that  the  undu- 
lation does  not  cease  entirely  centrally  from  the  point  of  compression, 
as  we  should  naturally  expect  from  our  supposition  of  its  origin,  is 
because  it  is  almost  impossible  to  compress  the  vein  sufficiently  to  pre- 
vent the  influx.  The  diminution  may  be  rendered  more  distinct  by  com- 
pressing the  subclavian  as  well  as  the  jugular  vein.  The  internal  jugular 
should  always  be  compressed,  never  the  external  jugular  alone.  The 
fact  that  the  venous  valves  are  intact  does  not  in  any  way  prevent  the 
transmission  of  the  physiologic  venous  pulse  toward  the  periphery  (e.  g., 


Fig.  68.— Physiologic  (negative)  venous  pulse  (Riegel). 

from  the  "  bulbus  "  to  the  vena  jugularis),  because  it  is  a  negative  wave 
motion  which  traverses  the  vein  in  the  direction  of  the  valve  openings, 
according  to  the  laws  of  wave  motion.^ 

Fig.  68  represents  a  sphygmogram  of  the  curves  of  the  carotid  pul- 
sation taken  simultaneously  with  the  curves  of  the  physiologic  venous 
pulsation  (Riegel).  The  latter  is  both  visible  and  palpable  in  the  ex- 
ternal as  well  as  in  the  internal  jugular.  Comparing  the  two,  it  is  evi- 
dent that  the  venous  collapse  corresponds  to  the  rise  of  the  carotid 
pulse,  or,  roughly  expressed,  the  physiologic  venous  pulse  is  cardiodias- 
tolic.     Hence  the  name  "  systolic  venous  collapse." 

If  we  neglect  the  peculiar  wave  (c')  in  the  ascending  limb  of  the 
venous  curve,  the  normal  venous  pulse  can  be  easily  explained  by  as- 
suming that  the  venous  reflux  depends  largely  upon  the  condition  of 
the  right  auricular  contraction.  For  auricular  diastole  (ventricular 
systole)  seems  to  favor  the  reflux,  and  auricular  systole  (ventricular 
diastole)  seems  to  check  it.  Estimating  the  time  relations  in  Fig.  68 
shows,  however,  that  any  such   simple  explanation   is  insufficient  and 

^  Of.  Tigerstedt,  Lehrbuch  der  Physiologic  des  Kreislaufes,  1893,  p.  367. 


DIFFERENT   VARIETIES   OF   VENOUS  PULSE.  149 

impossible.  Besides,  other  influences  synchronous  with  the  heart  beat 
aifect  the  venous  qirculation — viz.,  first  the  state  of  contraction  of  the 
right  ventricle  or  the  suction  effects,  and  second  the  effect  of  the  so-called 
auxo-  and  raeiocardia — /.  e.,  the  intrathoracic  variations  in  pressure 
produced  by  the  systolic  diminution  and  diastolic  increase  in  the  size 
of  the  heart.  Although  cardiac  systole  does  exert  a  certain  amount  of 
suction  and  the  diastole  exerts  pressure  upon  the  interior  of  the  thorax, 
it  is  impossible  to  explain  the  alternation  of  the  venous  with  the  arterial 
pulse  without  considering  all  the  other  factors  which  have  any  influence. 

Before  submitting  his  own  explanation,  the  writer  wishes  to 
insert  the  following  in  connection  with  Fig.  68  :  The  point  a,  where 
the  carotid  wave  begins  to  rise,  does  not  correspond  (as  is  generally 
accepted)  to  the  commencement  of  ventricular  systole,  but  to  the  begin- 
ning of  the  expulsion  time.  The  beginning  of  systole  must  therefore 
be  located  a  little  earlier.  Point  a'  in  the  venous  pulse  curve  corre- 
sponds to  the  same  moment  of  time  as  the  point  a  in  the  carotid  curve. 
Beginning  at  this  point,  we  can  explain  the  venous  pulse  as  follows  :  At 
the  moment  (a)  the  total  volume  of  the  heart  is  diminished,  meiocardia 
occurs  and  an  intrathoracic  suction  action  is  combined  with  it ;  at  the 
same  time  the  auricle  dilates,  and  consequently  the  conditions  for  the 
flow  of  venous  blood  are  the  most  favorable.  A  venous  collapse  ex- 
pressed in  line  a'  b'  is  therefore  the  natural  eff'ect  and  explains  itself. 
The  diastole  of  the  ventricle  begins  a  little  beyond  the  point  6,  at  a 
point  not  indicated  upon  the  descending  limb  of  the  carotid  curve. 
From  this  point  it  is  difficult  to  explain  the  curve,  because  during  ven- 
tricular diastole  various  contradictory  influences  affect  the  flow  of  ve- 
nous blood  into  the  veins — viz.,  the  diastolic  suction  power  of  the  right 
ventricle,^  diastolic  auxocardia,  with  an  exactly  opposite  action,  further 
the  contraction  of  the  ventricle,  which  backs  up  the  blood  in  the  veins  at 
the  end  of  diastole,  and  finally  the  part  of  ventricular  systole  (called 
the  closure  time)  which  immediately  precedes  the  ascending  limb  of  the 
carotid  curve,  which  really  does  prevent  the  entrance  of  the  blood, 
although  it  does  not  diminish  the  intrathoracic  pressure. 

All  these  factors,  except  the  suction  power  of  the  ventricle,  tend  to 
obstruct  the  venous  flow  and  to  produce  the  congestion  in  the  jugular 
veins  expressed  in  the  ascending  limb  h'  a' ,  which  fades  only  at  the 
onset  of  the  expulsion  time.  The  secondary  elevation  at  (c')  of  the 
ascending  limb  is,  however,  not  explained.  Its  position  corresponds 
very  satisfactorily  with  the  supposition  that  it  is  due  to  the  presystolic 
contraction  of  the  right  auricle  producing  a  backing-up  in  the  veins." 

We  must,  however,  be  well  acquainted  with  its  peculiarities  to  avoid 
confounding  it  with  the  two  following  varieties  of  venous  pulse.  It  is 
evident  from  our  explanation  of  its  origin  that  to  recognize  the  diastolic 
character  of  the  venous  pulse  it  is  essential  to  contrast  the  height  of  the 
venous  pulse  apex  with  the  apex  of  the  carotid  pulse  {i.  e.,  in  regard  to 

'  Expressed  better,  the  diastolic  release  of  the  obstacle  to  the  blood's  entrance. 
'  Compare  the  scheme  of  the  time  sequence  of  the  cardiac  phases,   in   Bernstein, 
Lehrbuch  der  Physioloc/ir,  1894,  p.  61,  Fig.  13. 


150        VISIBLE  PHENOMENA   OF  MOTION  IN  TEE   VESSELS. 

the  time)  and  not  with  the  cardiac  apex  beat.  This  is  because  the  apex 
beat  of  the  heart  coincides  with  the  "  closure  time,"  and  so  still  belongs 
to  auxocardia,  and  more  nearly  corresponds  in  point  of  time  to  the  apex 
of  the  venous  pulse  than  does  that  of  the  cardiac  pulse. 

(See  p.  152  for  further  assistance  in  distinguishing  the  physiologic 
from  the  pathologic  venous  pulses.) 

It  has  been  shown  by  Riegel  that  an  accentuated  negative  venous 
pulse  can  occur  under  pathologic  conditions  from  an  increased  contrac- 
tion of  the  auricle.  In  these  cases  the  presystohc  serration,  .correspond- 
ing to  the  auricular  contraction,  is  the  larger,  and  may  be  so  pronounced 
that  the  entire  venous  pulse  has  the  character  of  a  presystolic  pulse. 
This  variety  is  seen  particularly  in  marked  degrees  of  venous  congestion 
and  in  cases  of  pericardial  exudates. 

Although  it  was  formerly  supposed  that  liver  pulsation  always 
belonged  to  the  category  of  the  so-called  positive  centrifugal  venous 
pulse  (see  following  paragraph),  Volhard  has  shown  that  it  is  very  fre- 
quently such  an  accentuated  negative  venous  pulse  as  has  just  been 
described.  To  obtain  his  proof  he  employed  the  procedure  of  mano- 
metric  comparison  described  on  p.  152. 

POSITIVE  CENTRIFUGAL  1   (REGURGITATING)   VENOUS  PULSE; 
LIVER  PULSATION. 

A  positive  centrifugal  venous  pulse  is  only  observed  with  tricuspid 
insufficiency.  It  arises  in  this  valvular  lesion  because  during  systole 
the  blood  is  forced  back  into  the  right  auricle,  and  from  there  into  the 
veins.  Its  elevation  corresponds  to  cardiac  systole,  as  will  be  readily 
recognized  by  a  simultaneous  sphygmographic  representation  of  the 
jugular  and  carotid  pulse. 

A  positive  venous  pulse  curve  differs  considerably  from  a  negative 
venous  pulse  curve.  A  few  secondary  elevations  are  to  be  seen  in  its 
ascending  limb,  probably  because  the  factors  which  produce  the  physio- 
logic venous  pulse  are  felt  here,  too,  and  so  interfere  with  the  actual 
regurgitation  ;  perhaps  also  because  the  positive  venous  pulse,  although 
it  is  systolic,  does  really  pi'ecede  the  onset  of  the  carotid  beat  a  little.  Of 
course,  the  regurgitation  of  the  blood  through  the  insufficient  tricuspid 
valve  begins  at  the  beginning  of  systole — i.  e.,  at  the  "  closure  time  " 
(here  with  reference  to  the  right  ventricle),  and  not,  like  the  arterial  pulse, 
at  the  "  expulsion  time."  Hence,  it  would  naturally  precede  the  arterial 
pulse  a  little. 

If  the  valves  at  the  upper  end  of  the  jugular  bulb  close  properly, 

1  The  term  centrifugal  venous  pulse  has  only  one  meaning  here.  The  positive  cen- 
trifugal pulse  corresponds  to  a  positive  (lise)  wave  of  centrifugal  couree,  and  is  con- 
trasted with  a  positive  centripetal  pulse,  which  comprises  a  positive  wave  of  centripetal 
course.  At  the  same  time  the  pathologic  venous  pulse  of  tricuspid  insufficiencv  consid- 
ered here  as  a  centrifugal  pulse  should  hardly  be  contrasted  with  the  physiologic  variety 
considered  as  a  centripetal  pulse,  because  the  latter  is  also  centrifugal — /.  c,  it  also  pro- 
ceeds from  the  heart,  and  passes  through  the  trunk  of  the  vein  toward  the  periphery. 
The  only  difference  between  the  positive  centrifugal  venous  pulse  discussed  here  and 
the  phys'iologic  or  negative  pulse  consists  in  the  fact  that  in  the  latter  a  negative  wave 
(trough)  is  transmitted  centrifugaliy. 


DIFFERENT  VARIETIES  OF  VENOUS  PULSE.  151 

the  positive  pulse  will  be  chiefly  apparent  in  the  bulb  (bulbous  pulse). 
There  may,  however,  be  a  slight  wave  transmitted  to  the  periphery, 
because  the  closure  of  the  bulbous  valves  only  prevents  the  actual  regur- 
gitation of  blood  and  not  its  wave-like  motion.  The  latter,  a  positive 
wave,  in  closing  the  bulb  valves  produces  above  them,  from  the  backing 
up,  a  positive  w^ave  of  exactly  the  same  shape.  Consequently,  by  care- 
fullv  watching  a  bulbous  pulse  we  can  appreciate  that  the  veins  do  pulsate 
above  the  bulb  valves,  but  decidedly  less  than  below.  The  difference  is 
that  as  far  as  the  valves  a  real  backward  motion  or  regurgitation  of  the 
blood  can  be  plainly  observed,  but  above  the  valves  only  the  w^ave 
motion  started  by  the  reflux.  Under  such  conditions  a  distinct  systolic 
tone  may  sometimes  be  produced  over  the  bulbous  valves  by  the  shock  of 
the  regurgitated  blood  (jugular  valve  sound,  see  Auscultation  of  the 
Veins).  V^ery  frequently,  however,  as  the  result  of  congestion,  the 
venous  valves  become  insufficient,  so  that  the  positive  venous  pulse  may 
be  seen  just  as  distinctly  in  the  upper  part  and  in  the  small  branches  of 
the  jugular  vein  as  over  the  bulb  itself. 

Another  difference  between  the  positive  centrifugal  venous  pulse  and 


Fig.  69.— Positive  centrifugal  (regurgitating)  venous  pulse  (Riegel). 

the  negative  physiologic  venous  pulse  is  that  the  rise  of  the  former 
occurs  approximately  at  the  same  time  as  that  of  the  carotid  pulse. 
Again,  when  the  pulsating  vein  is  compressed,  the  positive  centrifugal 
venous  pulse  persists,  and  sometimes  even  becomes  accentuated  centrally, 
but  disappears  peripherally  from  the  seat  of  pressure. 

The  appearance  of  the  regurgitating  venous  pulse  is  not  infrequently 
limited  to  the  jugular  vein  ;  but  in  ])ronounced  cases  the  veins  of  the 
extremities  may  also  pulsate.  A  pulsation  in  the  liver  veins  is  especially 
important  in  the  diagnosis  of  tricuspid  insufficiency. 

The  liver  venous  pulse  can  be  appreciated  by  palpating  the  liver, 
which  is  usually  much  enlarged  in  tricuspid  insufficiency.  The  exam- 
iner should  palpate  as  far  as  possible  to  the  right  of  the  median 
line,  so  as  to  avoid  confusion  with  an  epigastric  pulsation  or  with  an 
aortic  pulsation,  which  is  sometimes  transmitted  to  the  liver.  (See  later 
section  upon  Palpation  and  Inspection  of  the  Cardiac  Kegion.)  To  avoid 
such  errors  it  is  especially  important  to  be  convinced  that  the  pulsation 
is  really  expansile — {.  e.,  that  the  volume  of  the  liver  increases  inter- 
mittently. This  can  generally  be  best  accomplished  by  firmly  grasping 
the  edge  of  the  liver,  or  by  employing  bimanual  palpation,  one  hand 


152         VISIBLE  PHENOMEXA    OF  MOTION  IN   THE    VESSELS. 

behind  pressing  the  liver  forward  against  the  other  hand  in  front.  Ad 
arterial  liver  pulse  sometimes  occui's  in  aortic  insufficiency  as  a  result 
of  the  "pulsus  celer."  It  can  be  distinguished  from  the  venous  liver 
pulse  only  by  a  careful  consideration  of  all  the  other  conditions. 

The  writer  once  demonstrated  an  inflammatory  liver  pulse  over  the  left  lobe  of 
the  liver  as  the  result  of  a  cholangitis  following  gall-stone  colic.  Duroziez's 
double  murmur  (see  later)  was  heard  over  this  lobe.  The  pulsation  and  the  mur- 
mur both  disappeared  after  several  weeks,  and  the  autopsy  revealed  a  purulent 
cholangitis  at  the  place  in  question  and  several  miliary  abscesses  in  the  liver. 

POSITIVE  CENTRIPETAL  OR  PENETRATING  VENOUS  PULSE. 

This  rare  type  of  venous  pulse  is  produced  when  the  arterial  wave  possesses 
sufficient  force  to  penetrate  the  capillaries  and  transmit  a  pulsating  motion  to  the 
venous  radicals.  The  phenomenon  depends  upon  conditions  similar  to  those  pro- 
ducing the  capillary  pulse,  and  has  been  found  chiefly  in  aortic  insufficiency. 
Quincke,  however,  believes  that  a  capillary  pulse  does  not  always  accompany  a 
penetrating  venous  pulse ;  but,  on  the  contrary,  that  we  may  be  unable  to  appre- 
ciate the  pulse  wave  in  the  capillaries  because  it  is  spread  over  too  great  an  area, 
whereas  the  constriction  that  the  venous  radicals  under  favorable  pressure  condi- 
tions oppose  to  the  course  of  the  current  may  cause  the  pulse  to  again  become 
visible.  This  type  of  venous  pulse  occurs  especially  with  an  arterial  ' '  pulsus 
celer."  It  does  not  appear  in  the  jugular  vein,  but  in  the  small  veins  of  the 
extremities.  Compression  will  obliterate  the  pulse  in  the  central  portion,  but 
not  in  the  peripheral  part  of  the  vein. 

DIASTOLIC  VENOUS  COLLAPSE  (Friedreich). 

This  very  rare  phenomenon  was  described  by  Friedreich  in  connection  with 
systolicr  etraction  of  the  cardiac  region  from  pericardial  adhesions.  (See  later 
Palpation  and  Inspection  of  the  Cardiac  Region. )  The  diastolic  recession  of  the 
chest-wall  produces  a  diastolic  suction  within  the  thorax,  and  this  is  supposed  to 
cause  the  veins  to  collapse.  It  is,  so  to  speak,  the  reverse  of  the  negative  or 
physiologic  venous  pulse.  In  the  latter  the  vein  is  distended  during  diastole ;  in 
the  phenomenon  described  by  Friedreich  the  distention  occurs  during  systole. 
Therefore  it  may  be  easily  confounded  with  the  positive  centrifugal  (regurgitating) 
venous  pulse,  which  is  also  systolic.  Compressing  the  vein  will,  however,  readily 
settle  the  question,  for  the  diastolic  venous  collapse  acts  not  like  a  positive  centrif- 
ugal, but  like  a  negative  venous  pulse — ;'.  e.,  it  disappears,  or  is  at  least  much 
diminished,  centrally  to  the  point  of  compression. 

VOLHARD'S  PROCEDURE  FOR  DETERMINING  THE  PHASES  OF  THE 
VENOUS  PL^LSE;  PRACTICAL  DIFHCULTIES  IN  DISTINGUISHING 
THE  DIFFERENT  KINDS  OF  VENOUS  PULSE ;  COMBINED  VENOUS 
PULSE. 

In  view  of  the  great  difficulty  in  recognizing  the  phases  of  a  venous  pulse  by 
the  eye  and  hand,  and  the  technical  details  necessary  for  its  graphic  representation, 
Volhard  ^  has  furnished  a  clever  and  simple  procedure  by  means  of  which  we  can 
easily  determine  the  time  of  a  venous  pulse  in  reference  to  the  carotid  pulsation. 
By  means  of  small  glass  funnels,  one  of  which  is  placed  over  the  pulsating  vein 
(or  the  liver)  and  the  other  upon  the  carotid,  Volhard  transmits  the  movements 
of  the  pulse  to  two  water  manometers  which  are  filled  with  differently  colored 
fluids  and  placed  side  by  side.  It  can  then  easily  be  determined  whether  the 
fluids  are  displaced  in  the  same  or  in  opposite  directions.  The  quickness  of  the 
movement  is  also  an  indication  as  to  whether  we  have  to  do  with  a  positive  or 
with  a  negative  pulsation  (collapse)  of  the  vein.  On  account  of  the  influence  of 
'  Congr.f.  inn.  Med.,  1902,  p.  402. 


PERCUSSION.  153 

inertia  the  water  must  be  at  the  same  level  in  both  manometers.  The  length  of 
the  column  of  air,  however,  is  immaterial,  since  the  air  waves  are  transmitted 
with  the  same  velocity  as  sound.  In  the  author' s  experience  the  procedure  some- 
times gives  very  clear  results,  but  it  frequently  fails  owing  to  the  difficulty  of 
separating  the  venous  pulse  completely  from  the  transmitted  movement  of  the 
carotid. 

Although  the  preceding  distinctions  apparently  render  the  differentiation  of 
the  different  kinds  of  venous  pulse  perfectly  plain,  we  are  nevertheless  frequently 
confused  in  practice,  especially  because  many  venous  pulses  are  combined  phe- 
nomena. It  has  already  been  noted  that  the  positive  regurgitating  venous  pulse 
is  frequently  combined  with  the  signs  of  the  physiologic  venous  pulse  because, 
naturally,  with  a  tricuspid  insufficiency  the  physiologic  undulations  of  the  veins 
would  not  disappear.  The  typical  character  of  the  positive  regurgitating  venous 
pulse  must  then  be  determined  by  means  of  the  time  relation  of  the  pulse  to  the 
cardiac  phases  and  by  the  results  of  the  compression  test.  Even  the  physiologic 
venous  pulse  is  frequently  deformed  because  the  carotid  pulse  imparts  itself  to  the 
venous  contents  and  antagonizes  the  venous  pulse,  both  in  its  time  phase  and  in  the 
relation  to  the  action  to  the  compression  test.  In  many  of  these  cases  it  is  absolutely 
impossible  to  determine  definitely  the  nature  of  the  venous  pulse. 


PERCUSSION. 

PERCUSSION  IN  GENERAL;  INSTRUMENTS. 

The  examination  of  the  human  body  by  means  of  percussion  (or 
striking)  plays  an  especially  important  role  in  the  modern  diagnostic 
methods  of  internal  medicine.  The  condition  of  the  or^an  or  orrans 
underlying  the  spot  percussed  is  determined  or,  at  least,  inferred  from 
the  sound  produced.  We  accredit  the  discovery  of  this  method  to  the 
Vienna  physician  Auenbrugger,  for  in  the  year  1761  a  description  of  it 
appeared  in  his  work,  Inventum  Novum.  However,  the  method  was  not 
generally  employed  until  after  Corvisart,  Napoleon  I.'s  body  physician, 
translated  Auenbrugger's  work  into  the  French  (1808)  and  appended 
extensive  observations  of  his  own  as  commentaries.  Manifold  modifica- 
tions, theoretic  confirmations,  and  symptomatic  improvements  were  then 
added  to  the  method  by  a  great  number  of  authors,  of  whom  we  need  only 
mention  Piorry,  the  inventor  of  the  pleximeter ;  Barry,  the  inventor 
of  the  percussion  hammer ;  Wintrich,  Skoda,  and  Traube.  Hence, 
although  the  method  is  already  more  than  a  century  old,  it  really  only 
became  the  common  property  of  physicians  during  the  second  half  of 
the  nineteenth  century.  To-day  percussion  and  auscultation  have  be- 
come the  corner-stone  of  diagnosis.  The  student  must  learn  both  at  the 
very  beginning  of  his  clinical  experience. 

There  are  copntless  methods  of  percussion.  Originally  only  imme- 
diate percussion  was  employed — i.  e.,  the  striking  of  the  surface  of 
the  body  directly  with  the  tips  of  the  fingers.  But  where  the  body- 
covering  is  soft  such  a  method  will  elicit  only  indistinct  and  impure 
sounds,  and  therefore  to-day  we  almost  exclusively  use  mediate  per- 
cussion— i.  e.,  either  a  finger  of  the  other  hand  or  a  specially  constructed 


154  PERCUSSION. 

instrument — the  "  pleximeter  " — is  inserted  between  the  striking  finger 
and  the  surface  of  the  body.  The  "  plexor  "  is  a  small  hammer  furnished 
with  a  rubber  tip.     It  may  be  substituted  for  the  striking  finger. 

In  mediate  percussion  we  may  use  either  :  (1)  Finger-finger  percus- 
sion, (2)  finger-pleximeter  percussion,  or  (3)  plexor-pleximeter  percussion. 

Individual  taste  or  habit  w^ill  generally  determine  a  preference  for 
one  of  these  methods.  There  are  certain  differences  and  advantages  in 
each  of  them,  although  we  may  be  skilful  or  awkward  with  any  one  of 
them.  The  finger-finger  percussion  is  the  most  difficult  to  learn  ;  but  in 
many  cases  it  furnishes  more  accurate  results  than  the  pleximeter  percus- 
sion, because  the  inherent  note  of  the  pleximeter  is  liable  to  confuse  the 
percussion  tone.  Consciously  or  unconsciously,  the  sense  of  touch  in  the 
finger-finger  percussion  aids  the  sense  of  hearing  (palpation  percussion).^ 
But  the  chief  advantage  is  that  the  physician  is  independent  of  instru- 
ments, which  may  be  readily  forgotten,  mislaid,  or  broken.  The  finger 
pleximeter,  and  especially  the  plexor-pleximeter  percussion  methods, 
are  much  easier  to  learn,  and  greater  differences  of  sound  may  be  more 
readily  demonstrated  and  appreciated  by  a  larger  circle  of  listeners; 
nevertheless,  a  percussion  note  which  is  loud  enough  to  be  heard  at 
considerable  distance  is  generally  faulty  (see  below).  A  physician 
should  be  familiar  with  all  three  methods  ;  and  he  should  be  able  to 
control  his  own  results  by  applying  first  one  and  then  the  other,  for 
despite  the  utmost  care  and  great  skill,  the  subjective  character  of  the 
method  often  in  difficult  cases  leaves  a  doubt  in  the  mind  of  the  exam- 
iner. A  plexor  and  pleximeter  are  of  no  great  advantage  in  the  em- 
ployment of  the  plexor-pleximeter  method  (p.  158),  because  we  can 
substitute  a  bit  of  wood,  a  pencil,  or  the  like  for  the  flexor,  and  a  coin 
or  another  bit  of  wood  for  the  pleximeter. 

In  certain  cases — e.  g. ,  for  determining  slight  pathologic  dulness  in  the  chest 
or  abdomen  or  for  differentiating  the  deep  cardiac  dulness — mediate  percussion  is  to 
be  recommended  as  a  control.  The  examiner  thus  avoids  too  strong  pressure  of 
the  pleximeter  or  of  the  finger  of  the  left  hand,  a  very  common  fault  with  begin- 
ners. Mediate  percussion  is  generally  made  by  striking  with  the  tips  of  the  four 
fingers  and  thumb  of  the  right  hand  arranged  like  a  pyramid.^  In  percussing  the 
lung  apices  beneath  the  clavicles  the  bone  serves  as  a  pleximeter,  and  the  middle 
finger  of  the  right  hand  as  the  plexor. 

Only  continued  practical  experience  can  teach  the  technic  of  percus- 
sion, and  but  few  rules  are  worth  stating. 

The  percussion  stroke  should  be  made  perpendicular  to  the  surface 
of  the  part  percussed.  In  finger  percussion  the  nail  of  the  percussing 
finger  should  be  cut  short,  and  the  blow  should  be  struck  with  the  pulp 
of  the  last  phalanx  in  such  a  manner  that  not  only  the  direction  of  the 
stroke  but  also  the  axis  of  the  last  phalanx  is  perpendicular  to  the  plex- 
imeter and  to  the  surface  of  the  body  part  percussed.  A  perpendicular 
stroke  is  essential  for  producing  a  good,  equal  note.      It  is  especially 

'  [The  fine  appreciation  of  variations  in  resistance  to  the  pleximeter  finger  is  of  almost 
equal  importance  to  the  recognition  of  variations  in  resonance. — Ed.] 

'^  [Most  American  clinicians  use  the  middle  finger  of  the  right  hand  as  the  plexoi 
and  the  middle  or  first  finger  of  the  left  hand  as  the  pleximeter. — Ed.] 


QUALITY  OF  THE  PERCUSSION.  155 

difficult  for  the  beginner  unless  he  is  a  piano  player.  Both  in  plexor  and 
in  finger  percussion  the  stroke  should  be  light,  short,  and  elastic,  pro- 
duced by  merely  bending  the  wrist  joint,  at  the  same  time  avoiding  any 
cramped  position  of  the  hand  or  lingers.  Percussion  should  be  light 
or  superficial  and  even  (see  p.  163).  The  so-called  strong  or  deep  per- 
cussion should  also  be  quite  delicate,  so  that  the  note  cannot  be  heard  at 
any  great  distance. 

The  pleximeter — i.  e.,  the  linger  to  be  struck — should  be  placed  with 
its  palmar  side  upon  and  in  close  contact  with  the  surface  of  the  body 
and  parallel  to  the  border  to  be  differentiated.  Only  slight  pressure 
should  be  employed,  because  strong  pressure  even  with  light  (super- 
ficial) percussion  will  cause  a  diffuse  vibration  of  the  body,  and  so 
simulate  the  effect  of  a  stronger  (deep)  percussion. 

Instead  of  the  usual  pleximeter,  a  bit  of  firm,  gray  erasing  rubber, 
cut  about  1  cm.  wide,  1  cm.  thick  and  4  cm.  long,  will  answer  the  pur- 
pose well  if  the  physician  is  not  skilled  in  finger  percussion.  Like  the 
finger,  such  a  pleximeter  has  practically  no  intrinsic  curve ;  it  can  be 
easily  bent  to  conform  to  the  curves  of  the  chest-wall,  and  it  can  be 
struck  with  the  hard  end  of  the  hammer  or  with  the  finger. 

In  percussing  a  child's  body  very  much  less  force  must  be  used  than 
for  the  adult.     (See  Deep  and  Superficial  Dulness.) 

QUALITY  OF  THE  PERCUSSION. 

RESONANT  AND  DULL  TYMPANITIC  AND  NON-TYMPANITIC 
PERCUSSION  NOTES. 

Even  a  layman,  percussing  different  regions  of  the  body  surface,  is 
able  to  recognize  that  one  part  furnishes  a  resonant,  another  part  a  dull, 
note.  An  accurate  differentiation  between  resonant  and  dull  notes,  or 
between  different  grades  of  resonance,  is  the  groundwork  of  percussion. 
A  typically  resonant  note  can  be  obtained  by  percussing  over  the  lung ; 
a  typical  dull  note,  by  percussing  over  great  muscle  masses — e.g.,  the 
thigh.  Experience  has  taught  us  that  resonant  notes  are  produced  over 
organs  containing  air ;  dull  notes  over  organs  without  air,  quite  irre- 
spective of  whether  they  are  solid  or  filled  with  fluid.  Therefore  per- 
cussion, on  the  one  hand,  defines  the  boundaries  of  the  different  organs  ; 
and,  on  the  other  hand,  by  changes  in  the  resonance  of  the  note,  deter- 
mines any  increase  or  decrease  of  air  contained  in  the  organ.  The  less 
air,  other  conditions  remaining  the  same,  the  duller  the  note.  The 
resonance  of  the  note  also  varies  decidedly  with  the  deep  diameter  of  the 
air-containing  organ — i.  e.,  the  diameter  in  the  direction  of  the  percus- 
sion stroke.  The  thicker  the  layer  of  air  the  more  resonant  the  note. 
The  influence  of  the  tension  of  the  wall  surrounding  the  air  cavity  upon 
the  resonance  of  the  note  will  l^  mentioned  later. 

We  apply  the  term  loud,  clear  or  resonant  as  contrasted  with  faint, 
dulled,  dull  or  flat  to  the  percussion  notes  of  the  ordinary  living  body. 
When  a  resonant  note  is  modified  by  a  dulled  note,  we  speak  of  the 
presence  of  dulness;  a  note  which   is  neither  very  resonant  nor  very 


156  PERCUSSION. 

dull  is  called  relatively  dulled  ;  an  absolutely  dull  note,  on  the  contrary, 
absolutely  dulled  ov  flat.  The  terms  absolute  and  relative  dulness  have  a 
corresponding  signification. 

In  defining  the  quality  of  a  percussion  note  many  modern  authors  employ  the 
terms  short  and  long  as  synonymous  with  dull  and  resonant.  Theoretically  this 
is  not  quite  correct,  because  the  latter  expressions  characterize  the  intensity  of  the 
note ;  whereas  short  and  long  refer,  on  the  contrary,  to  its  duration,  and  the  latter 
must  depend  upon  the  size  of  the  vibrating  mass.  The  length  of  a  musical  instru- 
ment' s  note  is  of  very  essential  importance  to  the  tone  and  value  of  the  instrument. 
A  musical  ear  can,  in  fact,  easily  dilFerentiate  this  peculiarity  of  duration  in  a  per- 
cussion note.  However,  in  the  relations  of  percussion  which  concern  us  a  resonant 
note  is  almost  always  long  and  a  dull  note  short.  The  exceptions  to  this  rule  have 
no  special  diagnostic  importance,  so  that  the  expressions  short  and  long  may  as  well 
be  eliminated. 

A  consecutive  series  of  note  qualities  range  in  countless  gradations 
between  the  two  limits  resonant  and  dull,  the  differences  depending  upon 
the  amplitude  of  the  note  vibrations.  There  are,  however,  other  very- 
important  differences  of  quality  which  we  must  heed  and  which  depend 
upon  variation  in  the  form  and  number  of  vibrations.  The  most  im- 
portant of  the  latter  is  the  distinction  between  tympanitic  and  non-tym- 
panitio  resonant  notes.  This  distinction  is  illustrated  by  comparing  in  a 
healthy  person  the  note  obtained  over  the  lung  with  that  obtained  over 
the  air-containing  abdominal  viscera.  The  pulmonary  note  is  resonant, 
but  not  tympanitic.  The  note  over  the  stomach  and  intestines  is  reso- 
nant, but  also  tympanitic.  Both  tympanitic  and  non-tympanitic  notes 
are  really  noises  in  the  purely  physical  sense ;  but  in  tympanitic  notes 
the  vibrations  are  sufficiently  periodic  (1  e.,  tuneful)  for  the  ear  to 
be  able  to  compare  their  number  with  the  number  of  vibrations  of 
other  sounds  ;  in  short,  to  be  able  to  recognize  a  certain  pitch.  This 
theoretic  differentiation  between  tympanitic  and  non-tympanitic  notes 
will  not  make  the  matter  much  clearer  to  a  beginner ;  but  in  a  practical 
demonstration  a  musical  ear  will  very  readily  appreciate  the  distinction 
between  the  resonant  but  non-tympanitic  lung  note  and  the  true  tym- 
panitic note  of  the  bowels.  No  sharply  defined  boundary  really  exists 
between  tympanitic  and  non-tympanitic  notes. 

Various  explanations  have  been  adduced  to  show  how  at  one  time 
an  air-containing  organ  furnishes  a  resonant  non-tympanitic  note,  and 
at  another  time  a  resonant  tympanitic  note  ;  but  most  of  these  explana- 
tions have  no  trustworthy  physical  basis  and  are  not  tenable.  Physicists 
have  thus  far  busied  themselves  very  little  with  this  acoustic  question. 

A  discussion  of  the  so-called  theories  of  the  tympanitic  and  non- 
tympanitic  notes  may  therefore  well  be  omitted,  and  merely  the  facts 
mentioned  as  to  when  the  non-tympanitic  note  of  an  air-containing 
organ  is  transformed  into  a  tympanitic  note,  and  vice  versd. 

Experience  teaches  us  that  a  non-tympanitic  note  will  be  transformed 
into  a  tympanitic  note  when  the  tension  of  the  air  within  the  organ 
diminishes — i.  e.,  when  its  wall  is  relaxed  ;  and  the  converse  is  also  true, 
that  with  an  increase  in  tension  a  tympanitic  will  be  transformed  into  a 
non-tympanitic  note.     If  we  inflate  a  pig's  bladder  while  at  the  same 


QUALITY  OF  THE  PERCUSSION.  157 

time  we  percuss  over  the  bladder,  we  shall  notice  that  up  to  a  certain 
point  of  distention  the  note  is  tympanitic,  but  with  further  inflation 
non-tympanitic.  During  the  transformation  of  a  non-tympanitic  into  a 
tympanitic  note  its  intensity  or  sonority  increases  ;  in  other  words,  the 
note  first  becomes  hyperresonant  before  it  becomes  tympanitic. 

The  essential  characteristic  of  a  tympanitic  note,  as  has  been  said,  is 
a  certain  definite  pitch,  so  that  naturally  we  can  distinguish  a  low  tym- 
panitic from  a  high  tympanitic  note,  and  gradations  between  the  two. 
Different  tone  heights  (pitch)  cannot  be  distinguished  easily  in  non- 
tympanitic  notes.  The  pitch  of  a  percussion  note  depends  upon  various 
factors,  above  all  upon  the  tension  of  the  wall  enclosing  the  air  space 
and  upon  the  size  of  the  latter. 

It  is  self-evident  that  more  than  one  of  the  qualities  discussed  may 
characterize  the  same  percussion  note.  Thus,  e.  g.,  we  may  speak  of  a 
relatively  dulled  high  tympanitic  note ;  or  of  a  resonant  low  tympanitic 
note. 

The  following  scheme  of  the  tone  qualities  described  above  may  be 

useful : 

resonant  (clear)  relatively  dulled        absolutely  dulled  (dull,  flat) 

(generally  long,  full)  (relatively  faint)  (generally  short,  dead). 

..A  ■       ..  ..A' 

tympanitic    non-tympanitic        tympanitic     non-tympanitic 

.A  .A 

high    low.  high     low. 

There  are  two  other  specific  tone  qualities  M^hich  must  be  mentioned 
— viz.,  metallic  resonance  and  the  "  crached-pot "  sound  or  cracked-pot 
resonance. 

METALLIC  RESONANCE. 

Metallic  resonance  means  a  peculiar  quality  of  the  percussion  note, 
which  is  best  characterized  by  its  name.  It  can  be  imitated  by  percuss- 
ing one's  own  distended  cheeks  with  a  plexor  and  pleximeter. 

Its  metallic  character  depends  upon  an  individual  metallic  overtone 
of  a  definite  pitch,  which  can  be  appreciated  sometimes  during  the  entire 
duration  ;  sometimes,  however,  only  at  the  end  of  the  sound.  In  the 
latter  case  we  speak  of  it  as  a  metallic  after-resonance. 

.We  are  especially  indebted  to  Wintrich  for  experiments  upon  metal- 
lic resonance.  He  showed  that  this  sound  arises  only  when  large  air 
spaces  are  percussed.  These  may  be  closed  or  open  ;  but  if  open 
the  orifice  must  be  relatively  narrow — i.  e,,  in  proportion  to  the  cross- 
section  of  the  cavity.  The  inner  surface  of  the  cavity-wall  must  be 
comparatively  smooth ;  because,  according  to  Wintrich,  metallic  reso- 
nance depends  essentially  upon  the  reflection  of  the  air  waves  which 
percussion  sets  into  vibration  within  the  cavity.  This  produces  the 
high  inharmonious  overtones  responsible  for  the  metallic  character  of 
the  sound.  The  thinner  the  walls  the  easier  the  metallic  character  can 
be  appreciated. 

If  the  walls  of  the  cavity  are  yielding  (flexible),  metallic  resonance 
will  not  result  unless  they  are  under  a  certain  moderate  tension.      Again, 


158  PERCUSSION. 

a  cavity  must  be  of  a  certain  size  to  produce  metallic  resonance  ;  accord- 
ing to  Wintrich,  its  greatest  diameter  must  be  at  least  6  cm.  Small 
cavities  very  rarely  furnish  metallic  resonance. 

The  metallic  resonance  noted  in  percussing  the  normal  human  body 
is  in  most  cases  so  faint  that  it  can  be  appreciated  only  Avhen  the  ear 
is  very  near  or  is  connected  with  the  percussed  area  by  means  of  -a 
stethoscope  (auscultatory  percussion).  The  easiest  way  to  appreciate 
metallic  resonance  is  by  means  of  the  "  stick-pleximeter  "  method.  In 
this  method  Ave  percuss  with  the  handle  of  the  plexor  upon  a  bit  of 
stick,  a  coin,  or  some  other  firm  object  placed  upon  the  body,  and  at  the 
same  time  auscult  with  the  stethoscope  in  the  immediate  neighborhood. 
By  the  reverberation  of  its  high  overtones  the  resulting  shrill  noise 
seems  particularly  to  favor  the  production  of  a  metallic  resonance. 
Metallic  resonance  may  accompany  non-tympanitic  as  well  as  tympanitic 
notes ;  but  in  the  former  case  it  can  be  appreciated  only  by  the  aid  of 
the  stick-pleximeter  method  of  percussion. 

Metallic  resonance  can  be  elicited  sometimes  over  physiologic  cavi- 
ties— e.  g.,  the  stomach  and  intestines  ;  sometimes  over  pathologic  col- 
lections of  air — e.  g.,  lung  cavities,  pneumothorax,  pneumopericardium. 

If  the  metallic  resonating  cavity  contains  fluid  as  well  as  air,  change 
of  the  patient's  position  may  alter  the  pitch  of  the  metallic  resonance. 
This  is  because  its  pitch  depends  partly  upon  the  greatest  diameter  of 
the  air  cavity,  which  would  be  altered  by  the  shifting  of  the  relative 
positions  of  the  fluid  and  the  air  (see  p.  213). 

CRACKED-POT   RESONANCE. 
(Bruit  de  Pot  Fele;  Noise  of  the  Spinning-top,  of  the  Chink  of  Coins.) 

This  peculiar  clanging  or  rattling  percussion  noise  can  be  simulated 
by  filling  the  hand  with  coins,  shutting  it  tight  enough  to  allow  only  a 
slight  space  for  the  coins  to  move,  and  then  shaking  the  hand ;  or,  in 
another  way,  by  clasping  the  hands  together  firmly,  leaving  a  slight  air 
space  between,  and  then  striking  the  back  of  one  hand  against  the  knee. 
The  force  of  the  blow  will  expel  some  air  through  the  narrovr  chink 
between  the  hands.  Another  inethod  is  to  strike  a  hollow  rubber  ball 
with  a  narrow  opening  vigorously  enough  to  expel  some  air  with  each 
stroke.  Such  experiments,  as  well  as  the  conditions  in  the  chest  which 
are  responsible  for  the  phenomenon,  make  it  probable  that  the  cracked- 
pot  sound  observed  in  man  is  a  stenotic  murmur,  made  by  the  percussion 
blows  expelling  air  quickly  through  a  narrow  slit-like  opening.  (See 
p.  213  for  its  diagnostic  significance.) 


TOPOGRAPHIC  PERCUSSION. 


159 


TOPOGRAPHIC  PERCUSSION. 

PERCUSSION  CHARTS;  SUPERFICIAL  AND  DEEP  DULNESS  OF 
ORGANS;  LIGHT  AND  STRONG  PERCUSSION;  SITUATION  OF 
THE  ORGANS;    ORIENTATION  POINTS  AND  LINES. 

Topographic  percussion  means  the  determination  of  the  boundaries 
of  the  organs  of  the  body  by  means  of  percussion.  By  this  method  we 
attempt  to  project  the  boundaries  of  the  organs  upon  the  body  surface ; 
and  to  represent  these  relations  conveniently  in  the  history  sheets  the 


Horizontal 
Mamillary  line. 


Fig.  70.— Chart  of  anterior  bodv-half. 


borders  are  sketched  upon  a  chart  of  the  human  body,  with  a  skeleton 
drawn  in.side.  Fig.«.  70,  71,  and  72  show  such  percussion  charts.  Per- 
haps they  would  be  still  more  convenient  if  they  were  double  the  size. 
Since  every  man's  skeleton  is  not  of  the  same  shape,  it  is  advisable  to 
represent  by  some  mark  {e.  g.,  a  cross)  the  boundary  points  which  are 


160 


PERCUSSION. 


quite  normal  in  their  relation  to  the  skeleton  (see  Fig.  79).     Such  a 

chart  is  rarely  absolutely  accurate. 

The  possibility  of  employing  topographic  bounding  of  organs  which 

are  situated  in  part  one  over  the  other  depends  upon  the  fact  that  some  are 

filled  with  air  and  some  are  solid.     A  solid  organ  gives  a  dull,  a  hollow 

organ  a  resonant,  note.  In  rare 
cases  the  qualitative  variations  of 
the  resonant  note  can  be  utilized 
for  defining  the  boundaries.  For 
example,  we  can  differentiate  the 
resonant  but  non-tympanitic  note 
of  the  lung,  or  the  low  tympan- 
itic note  of  the  stomach,  from 
the  high  tympanitic  note  of  the 
intestine.  But  naturally  the  dif- 
ferences are  often  very  slight,  and 
the  qualities  of  the  resonant  notes 
merge  into  each  other  without 
sharp  boundaries,  so  that  the  dis- 
tinction is  by  no  means  easy. 

The  first  essential  for  utiliz- 
ing topographic  percussion  is  to 
localize  the  percussion  stroke. 
Where  the  boundaries  to  be 
defined  are  superficial — that  is, 
where  they  lie  directly  under  the 
body-wall — the  lightest  possible 
percussion  will  evidently  suc- 
ceed best.  As  soon  as  we  per- 
cuss more  vigorously,  the  vibra- 
tions will  be  strongly  transmitted 
over  the  boundaries,  producing 
a  mixed  note.  Therefore,  it  is  a 
good  general  rule  that  to  appre- 
ciate superficial  boundaries  tee 
should  percuss  as  lightly  as  pos- 
sible. In  other  words,  the  per- 
cussion should  be  gentle  enough 
not  to  produce  any  note  at  all 
over  solid  tissues.  Then  the 
same  strength  of  percussion  will 
produce  a  very  plain,  resonant 
note  just  as  soon  as  we  encroach 

upon  the  edge  of  an  organ  containing  air — <?.  g.,  in  differentiating  the 

lower  lung  boundary  from  the  liver. 

This  light  percussion,  valuable  in  estimating  superficial  boundaries, 

is   called   superficial  percussion ;  and   the  dulness  mapped  out  by  the 

method  is  called  superficial  dulness.     It  is  the  easiest  for  the  beginner 


Fig.  71.— Chart  of  left  lateral  body -half. 


TOPOGRAPHIC  PERCUSSION.  161 

to  differentiate.  Its  position  and  extent  generally  correspond  quite 
accurately  to  the  position  of  the  part  of  the  organ  which  is  next  to  the 
body-wall. 

Special  attention  should  he  directed  to  another  point  in  determining 
the  superficial  boundaries.  The  skilled  observer  instinctively  heeds  it ;  but 
the  beginner,  despite  his  best  endeavor  to  percuss  lightly,  disregards  it,  and 
so  fails  in  a  correct  differentiation.     It  is  not  only  necessary  to  percuss 


Posterior  median  line. 


Fig.  72.— Chart  of  posterior  body-half. 

lightly,  but  the  pleximeter,  or  the  finger  of  the  left  hand  serving  this  pur- 
pose, should  be  brought  into  very  light  contact  tvith  the  surface  of  the  body. 
The  mere  loeight  of  the  finger  is  sufficient.  Firm  pressure  of  the  pleximeter 
(or  finger")  will  simulate  the  effect  of  strovg  piercussion,  because  the  vibrations 
will  penetrate  much  more  intensely  further  into  the  depths  and  to  the  sides, 
and  so  jjrevent  a  linear  localization  of  the  boundary  between  two  superficial 
organs,  the  one  containing  air  and  the  other  solid. 
11 


162  PERCUSSION. 

In  many  cases  the  boundaries  of  organs  which  we  wish  to  differ- 
entiate lie  in  the  deeper  parts — e.  g.,  most  of  the  heart  is  covered  by 
the  lungs,  and  yet  it  is  very  desirable  to  determine  its  size  by  percussion. 
Naturally  this  is  a  much  more  difficult  differentiation  than  that  of  super- 
ficial boundaries.  Light  percussion  will  be  useless.  On  the  contrary, 
the  blow  must  penetrate  the  tissues  to  the  depths  of  the  organ  in  ques- 
tion, in  order  to  obtain  tone  differences  sufficient  to  furnish,  at  least 
approximately,  conclusions  upon  the  position  of  the  deep-lying  boun- 
daries. The  intensity  of  the  note  will  also  depend  upon  the  thick- 
ness of  the  layer  of  air  that  we  percuss.  The  more  air-containing 
tissue  that  is  set  in  vibration,  so  much  louder  (more  resonant)  the  note.^ 
If  a  6  (Fig.  73)  represents  a  cross-section  through  the  anterior  wall  of 
the  thorax,  and  c  d  one  through  the  heart,  then  by  vigorous  percussion  in 
the  direction  of  the  arrows  e  and  /  the  elliptic  shaded  areas  will  be  set  in 
vibration.  Weil  has  named  such  an  area  "  the  acoustic  sphere  of  action." 
This  acoustic  sphere  of  action  at  e  will  be  entirely  within  lung  tissue,  but 
at/  partly  in  the  solid  heart  and  partly  in  lung  tissue.  Hence,  a  smaller 
volume  of  air-containing  lung  will  be  set  in  vibration  by  percussing  at 


Fig.  73.— The  acoustic  spheres  of  action  of  the  blow  in  deep  percussion— origin  of  tiie  deep 

rill  1  nticc 


dulness 

/than  at  e,  so  that  the  note  over /will  sound  somewhat  fainter,  or,  as 
we  say,  relatively  dulled. 

It  should  be  remembered  that  repeated  forcible  percussion  in  certain 
cases  increases  the  resonance.  The  probable  explanation  of  the  phenom- 
enon is  that  the  continued  forcible  blows  excite  a  "  lung  reflex  " — in  other 
words,  a  localized  temporary  emphysema — in  response  to  the  irritation 
of  the  blows.  The  position  of  this  relative  dulness  will,  under  some 
circumstances,  enable  us  to  mark  out  the  organs  which  are  situated  rpore 
deeply.  Such  percussion,  necessarily  stronger  than  superficial  percussion, 
is  called  strong  or  deep  jwrcussion,  and  the  corresponding  dulness,  deep 
dulness. 

The  percussion  stroke  in  superficial  pei'cussion  is  light  and  should 
include  as  small  a  sphere  of  action  as  possible  ;  but  the  strength  of 
stroke  in  deep  percussion  should  be  so  adjusted  that  its  sphere  of  action 
will  reach,  to  the  deep-lying  organs,  as  is  shown  in  Fig.  73.  It  is  very 
difficult  for  a  beginner  to  arrive  at  the  correct  strength  of  percussion. 
It  requires  long  practice.     A  helpful  suggestion  is  that  the  strength  of 

^  According  to  the  law  that  the  intensity  of  the  note  equals  tlie  mass  ninUiplied  by 
the  square  of  the  velocity.  In  consequence  of  the  inertia  of  tlie  vibrated  mass,  the 
tone  will  also  be  fuller;  that  is,  the  sound  will  last  longer  (see  p.  155). 


TOPOGRAPHIC  PERCUSSION.  163 

percussion  should  be  so  adjusted  as  to  produce  the  most  intense  dulness 
and  to  make  the  diiFerences  between  the  notes  as  plain  as  possible. 

The  beginner  will  err  again  by  percussing  too  strongly,  just  as  in  super- 
ficial percussion  (^p.  155).  To  bring  out  deep  dulness,  one  should  not 
p)ercuss  the  pjatient  with  all  pjossible  strength  and  shake  the  greater  jjart 
of  the  thorax,  as  negative  or  untrustworthy  results  are  obtained  by  such  a 
method.  Ordinarily  the  stroke  should  be  only  a  little  more  vigorous  than 
is  necessary  to  map  out  the  superficial  dulness.  The  pressure  used  in  apply- 
ing the  pleximeter  (or  the  finger  of  the  left  handj  to  the  body-wall  should 
be  only  a  little  stronger  than  for  supterficial  dulness. 

From  what  has  been  said  above,  it  is  clear  how  impossible  it  is  to 
demonstrate  the  finer  results  of  percussion  to  listeners  at  a  distance.  A 
percussion  strong  enough  for  this  purpose  furnishes  most  incorrect  re- 
sults, and  is  admissible  only  for  demonstrating  quite  coarse  diiFerences. 

Weil's  explanation  is  now  apparently  generally  accepted — viz.,  that 
the  deep  dulness  of  organs  depends  only  upon  the  volume  of  the  air- 
containing  part  which  is  set  in  vibration.  It  was  formerly  believed 
that  the  solid  organs  themselves  not  only  produced  a  slight  tone,  but 
were  also  capable  of  partially  dulling  the  loud  resonant  tone  of  the 
neighboring  air-containing  organs.  According  to  this  hypothesis  the 
deep  dulness  depended  upon  the  dulling  influence  of  the  solid  organs  in 
the  neighborhood  of  those  filled  with  air.  Weil  has  experimentally 
proved  that  such  dulling  influence  does  not  exist. 

The  necessary  strength  of  the  percussion  stroke  naturally  depends  not 
only  upon  the  nature  and  the  position  of  the  surrounding  organs,  but  upon 
the  thickness  of  the  body-wall  covering.  For  example,  the  inferior 
lung  boundary  can  ordinarily  be  easily  distinguished  from  the  liver  by 
very  light  percussion,  but  not  in  very  fat  or  edematous  patients,  because 
then  the  acoustic  sphere  of  action  of  the  percussion  does  not  penetrate 
beyond  the  thick  layer  of  the  thoracic  wall.  In  such  cases  only  very 
vigorous  percussion  can  bring  out  a  clear,  plain  lung  tone,  and  at  best 
the  superficial  as  well  as  the  deeper  boundaries  are  very  difficult  and 
sometimes  impossible  to  map  out. 

If  we  only  percuss  lightly  enough  and  with  slight  pleximeter  press- 
ure superficial  dulness  is  frequently  quite  intense.  For  this  reason  it  is 
often  called  absolute  dulness.  On  the  other  hand,  deep  dulness  is  never 
complete  or  absolute,  and  hence  is  called  relative  dulness. 

The  designations  absolute  and  relative  dulness  should  be  av^oided  in 
topographic  percussion,  because  in  mapping  out  organs  it  is  much  more 
important  to  know  whether  a  dulness  is  obtained  by  deep  or  by  super- 
ficial percussion  than  "svhether  it  is  more  or  less  intense.  Des])ite  light 
percussion,  superficial  dulness  will  not  be  absolute  if  the  air-containing 
surroundings  are  set  in  vibration. 

It  is  easier  to  teach  practically  the  other  essentials  to  the  technic  of 
topographic  percussion  than  to  describe  them.  In  mapping  out  an  or- 
gan the  beginner  should  compare  the  note  in  two  places,  one  of  which 
plainly  lies  outside  and  the  other  inside  the  edge  of  the  organ  to  be  de- 
fined.    He  should  then  percuss  between  these  two  places,  gradually 


164  PERCUSSION. 

advancing  the  pleximeter  parallel  to  the  edge  to  be  determined  until 
one  point  of  the  boundary  is  determined  and  marked  upon  the  skin 
with  a  pencil.  In  a  similar  way  other  points  of  the  boundary  are 
marked,  and  finally  all  are  joined  by  a  line  which  will  correspond  pretty 
accurately  to  the  edge  of  the  organ.  Such  a  line  can  be  represented 
schematically  (as  described  above)  upon  a  chart. 

For  rapid  and  comprehensive  registering  of  the  results  of  percus- 
sion we  use  in  the  Bern  Clinic  different  colored  pencils.  We  repre- 
sent the  superficial  dulness  obtained  by  light  percussion  by  blue ;  the 
deep  dulness  obtained  by  strong  percussion  by  red.  The  intensity 
of  the  dulness  is  expressed  by  varying  the  intensity  of  the  color.  A 
dulness  appreciable  both  to  deep  and  superficial  percussion  is  repre- 
sented by  a  mixed  red  and  blue  color.  Even  color  tones  and  evenly 
mixed  colors  are  easily  made  by  using  very  soft  pastel  pencils  and  a 
leather  stump.  In  order  to  distinguish  the  boundaries  of  organs  which 
are  palpable  from  those  which  we  obtain  by  percussion,  the  former  are 
denoted  by  a  continuous  black  line.  This  method  of  representation  is 
followed  throughout  this  book. 

A  comprehension  of  the  topographic  results  of  percussion  naturally 
presupposes  an  exact  knowledge  of  normal  visceral  topography.  Many 
anatomic  facts  relative  tq  the  position  of  organs  do  not,  of  course,  apply 
accurately  to  such  relations  in  the  living  body,  because  the  position  of  the 
organs  is  markedly  influenced  by  the  breathing,  and  because  even  the 
median  vital  position  of  the  thorax  and  of  the  diaphragm  is  quite  diflPerent. 
from  that  in  the  cadaver.  This  is  especially  noticeable  in  the  position  of 
the  lung  edges.  In  tlie  first  place  the  lung  boundaries  in  the  cadaver 
assume  an  entirely  individual  equilibrium,  on  account  of  the  elastic  rela- 
tions of  the  thorax  and  of  the  lungs,  the  rigidity  of  the  respiratory 
muscles,  etc.  This  is,  or  at  least  may  be,  essentially  different  from  the 
median  position  in  the  living.  The  cadaveric  position  of  the  lung  edges 
is  generally  that  of  exaggerated  expiration.  Frozen  sections,  inserting 
needles  through  the  lung  edges  before  opening  the  thorax,  or  cutting 
windows  in  the  thoracic  wall  without  disturbing  the  costal  pleura,  fur- 
nish correct  results.  All  other  anatomic  testimony  is,  in  the  nature  of 
things,  worthless,  because  as  soon  as  the  thorax  is  opened  the  lungs  are 
retracted,  tending  to  assume  a  position  of  equilibrium.  Topographic 
percussion  is  therefore  a  valuable  aid  to  anatomists  for  determining  the 
anatomic  position  of  organ  boundaries  during  life.  The  plates  illus- 
trating the  position  of  the  viscera  in  this  book  are  taken  from  the  classic 
plates  of  Luschka  and  the  models  of  Ferber.^  They  have  been  drawn 
especially  for  clinical  purposes  to  show  the  median  position  of  the  mova- 
ble organs,  and  with  particular  attention  to  the  sources  of  error  men- 
tioned above.     The  reader  is  recommended  to  study  Ferber's  models. 

Symington's^  cross-sections  or  D  wight's  Frozen  Sections  of  a  Child 
illustrate  the  topographic  relations  in  the  cliild. 

^  Situsphantom  der  Organe  der  Brust  und  oberen  Bauchgegend,  Bonn,  Max  Cohen  & 
Son,  1877. 

'^  Topographic  Anatomy  of  the  Child,  Edinburgh,  1887. 


TOPOGRAPHIC  PERCUSSION. 


165 


Figs.  74—76  reproduce  outlines  from  Luschka's  plates.  To  orient 
the  positions  of  the  borders  to  the  skeletal  points,  the  ribs  and  the  ver- 
tebral spines  are  counted.  Here  it  is  well  to  remember  :  The  second 
rib  is  usually  marked  upon  the  sternum  by  the  angle  of  Ludwig ;  it  is 
ordinarily  the  highest  rib  which  we  can  plainly  grasp  between  the  fingers 
from  in  front.     Generally  the  first  rib  is  almost  hidden  beneath  the  clav- 


Aorta. 


,-Pulin.  art. 


Heart. 

Lung  borders. 


—  Boundaries  of  the  pleurse  and  of  the  incisurse  interlobulares  of  the  lung. 

"■"" — "  stomach^ 

••••»••»»••>»»«  Liygr.       >-and  line  of  diaphragm. 

Fig.  74.— Position  of  the  thoracic  and  upper  abdominal  viscera  from  in  front :  a  b.  Boundary 
of  right  pleural  cavitj^ ;  c  d,  boundary  of  left  pleural  cavity  ;  ef,  edge  of  right  lung ;  cj  h,  edge  of 
left  lung;  i,  upper  incisura  lobularis  (right  lung) :  k,  lower  incisura  lobularis  (right  lung) ;  !,  left 
incisura  loljularis  ;  'm  n  right,  «  o  lovrer,  p  o  left  border  of  heart ;  q,  mediastinal  sinus  situated 
between  the  pleural  boundaries  and  the  incisura  eardiaca  of  the  anterior  edge  of  the  left  lung; 
r,  highest  point  of  the  liver,  overlapped  by  lung;  s,  lower  edge  of  liver;  t  pars  eardiaca,  u  pars 
pylorica,  v  small  curvature,  w  large  curvature,  of  the  stomach  (modified  from  Luschka-Weil). 


icle.  The  lowest  of  the  ribs  which  is  directly  attached  to  the  sternum  (true 
ribs)  is  the  seventh.  The  first  of  the  "  floating  ribs  " — i.  e.,  those  with  tlieir 
tips  freely  suspended — is  the  eleventh.  In  counting  the  vertebral  spines 
we  generally  begin  with  the  seventh  cervical.  Its  prominence  when  the 
head  is  bent  forward  (vertebra  prominens)  makes  it  easy  to  recognize. 
Where  three  vertebral  spines  are  quite  prominent  in  this  region,  the 


166 


PEBGUSSION. 


seventh  is  usually  in  the  middle.  Where  the  seventh  cannot  be  posi- 
tively determined,  the  vertebra  should  be  counted  from  below — i.  e., 
from  the  fifth  lumbar  vertebra  upward.  The  lower  angle  of  the  scapula, 
wdth  the  arms  hanging,  ordinarily  corresponds  to  the  seventh  rib  and 
the  seventh  dorsal  vertebra.     The  base  of  the  xiphoid  cartilage  can  be 


•^——^^^-—^  Pulmonary  border. 

.-•___._____  Pleural  boundary  and  incisurEe  interlobulares. 

••....-...-i.....  Stomach  and  kidney. 

• "  Liver  and  spleen. 

Fig.  75.— Position  of  the  thoracic  and  upper  abdominal  viscera  from  the  left  side :  a  b,  Lower 
edge  of  the  left  lung ;  a  c,  lower  boundary  of  the  pleural  cavity  ;  d  e,  incisura  interlobularis  ;  /, 
edge  of  the  left  lobe  of  the  liver;  n  posterior,  ft  anterior  end  of  the  spleen  in  its  oval  form,  in 
the  rhomboid  form  it  pushes  itself  in  between  the  anterior  (g  I)  and  the  posterior  {p  K)  edge  of  the 
piece  (I  h) ;  k,  convex  edge  of  the  left  kidney  ;  I,  splenic  lung  angle  :  m,  splenic  kidney  angle  :  n, 
the  part  of  the  greater  curvature  of  a  moderately  distended  stomach  lying  against  the  wall 
(from  Luschka-Weil). 

utilized  in  topography,  but  its  tip  varies  considerably  in  length  and 
position,  and  is  therefore  unreliable. 

Besides  the  skeletal  parts  we  make  use  of  so-called  orientation  lines. 
These  are  vertical  lines  which  intersect  the  ribs  at  certain  angles.  They 
are  the  follo\ving  (see  Figs.  70,  71,  and  72): 

1.  The  anterior  and  the  posterior  median  line. 

2.  The  right  and  the  left  sternal  line — draAvn  vertically  through  the 
edges  of  the  sternum. 

3.  The  right  and  the  left  parasternal  line — drawn  halfway  between 
the  sternal  border  and  the  nipple. 


TOPOGRAPHIC  PERCUSSION.  3  67 

4.  The  right  and  the  left  mammillary  line  (or  nipple  lines) — drawn 
perpendicularly  through  the  nipple. 

5.  The  middle,  the  anterior,  and  the  posterior  axillary  line — drawn 
through  the  middle,  the  anterior,  and  the  posterior  edge  of  the  axilla. 

6.  The  right  and  the  left   scapular    line — drawn    perpendicularly 
through  the  inferior  angle  of  the  scapula,  with  the  arm  hanging  down. 

The  position  of  the  mammillary  line  is  inconstant  both  in  men  and 
in  women.     The  so-called  midclavicular  line,  which  is  dropped  perpen- 


Lung  borders. 

Pleural  boundaries  and  incisurse  interlobulares. 

Kidney. 

Liver  and  spleen. 


Fig.  76.— Position  of  the  viscera  from  behind:  ah,  Lower  lung  border;  c  rf,  lower  pleural 
boundary  ;  c  and  /,  incisure  interlobulares  ;  at  ig)  on  the  right  side  it  is  divided  into  the  sulcus 
interlobularis  dextra  superior  and  inferior ;  h,  spleen ;  i,  lower  liver  edge ;  k,  left  kidney ;  I,  right 
kidney  (from  Lusehka-Weil). 

diciTlarly  from  the  middle  of  the  clavicle,  is  therefore  a  more  accurate 
landmark.  A  horizontal  mammillary  line  is  sometimes  employed  ;  that 
is,  a  horizontal  line  on  the  surface  of  the  thorax,  drawn  through  the 
nipples.  Its  position  is,  of  course,  influenced  by  the  height  of  the 
nipples.  In  men  these  are  usually  found  to  be  between  the  fourth  and 
fifth  or  upon  one  of  these  ribs  (rarely  between  the  £fth  and  the  sixth 
ribs),  about  10  cm.  distant  from  the  lower  thoracic  edge,  and  about  16 
cm.  from  the  lower  edge  of  the  clavicle. 


168 


PERCUSSION. 


The  terms  used  in  topographic  anatomy  are  usually  serviceable  in 
topographic  percussion — such  as  supra-  and  infraclavicular  grooves, 
supra-  and  infraspinatous  fossae,  interscapular  space,  epigastrium,  hypo- 
chondrium,  mesogastrium,  hypogastrium,  etc.  (see  Figs.  77  and  78). 


TOPOGRAPHIC  PERCUSSION  OF  THE  LUNGS. 

NORMAL  LUNG  BORDERS. 

The  boundaries  of  the  lungs  move  normally  with  respiration  ;  hence 
we  must  distinguish,  on  the  one  hand,  an  expiratory,  and,  on  the  other, 
an  inspiratory  position.      This   distinction  is  especially  important  for 


Fig.  77.— Topographic  areas  of  trunk— anterior  view. 

determining  the  mobility  of  the  lung  edges.  In  general,  the  median 
position  of  the  lung  borders  when  the  patient  breathes  superficially  is 
sufficient  for  most  purposes.  The  excursions  of  the  lungs  are  then 
hardly  greater  than  the  limits  of  error  which  are  inherent  in  percussion. 
The  boundaries  designated  as  normal  correspond  to  such  a  median  posi- 
tion of  the  lung  edges. 

We  usually  determine  the  inferior  boundaries  of  the  patient's  right 
lung  (the  lung-liver  boundary)  anteriorly  while  he  is  lying  down ;  pos- 
teriorly, while  he  is  sitting  or  standing.  Such  a  boundary  line  inter- 
sects the  parasternal  and  midclavicular  lines  at  the  upper  edge  of  the 
sixth  rib ;  the  axillary  lines,  at  the  eighth  to  ninth  ribs ;  the  scapular 


TOPOGRAPHIC  PERCUSSION. 


169 


Fig.  78. — Topographic  areas  of  trunk— posterior  view. 


Fig.  79.— Normal  percussion  boundaries  of  the  lungs,  liver  and  spleen,  and  Traube's  space- 
anterior  view. 


170 


PERCUSSION. 


lines,  at  the  tenth  rib  ;  the  posterior  median  line,  at  the  eleventh  verte- 
bral spine.  The  border,  therefore,  runs  very  nearly  horizontal  (see 
Figs.  79  and  80). 

The  precordial  edge  of  the  left  lung  forms  a  segment,  within  which 
the  heart  lies  directly  against  the  thoracic  wall.  This  segment  corre- 
sponds to  the  so-called  superficial  carcUae  dulness  (Figs.  79  and  85).  The 
border  of  the  lung  bounding  this  area  lies  above  at  the  left  edge  of  the 
sternum,  upon  the  fourth  rib,  and  runs  from  there  horizontally  to  the  left ; 


Fig. 


-Percussion  boundaries  of  the  lung,  liver  and  spleen,  and  Traube's  space— from  the 
left  side. 


at  the  parasternal  line  it  curves  downward  to  the  level  of  the  sixth  rib. 
and  then  takes  the  same  course  as  the  inferior  border  of  the  right  lung. 
For  practical  purposes  we  may  assume  that  the  inferior  lung  edge,  with 
the  exception  of  this  segment  over  the  heart,  follows  practically  a  hori- 
zontal course  upon  both  sides.  The  edge  of  the  left  lung  can  be  easily 
and  accurately  diiferentiated  by  the  superficial  cardiac  dulness ;  but 
farther  to  the  left  the  loud,  resonating  stomach  is  a])t  to  confuse  the 
percussion.  From  the  axillary  line  backward  the  defining  of  the  edge 
of  the  lung  becomes   easier  again,  because  the  spleen,  the  powerful 


TOPOGRAPHIC  PERCUSSION. 


Ill 


muscular  masses  of  the  quadratus  lumborum,  and  the  lumbar  limb  of 
the  diaphragm  lie  below  the  lung. 

The  anterior  lung  borders  run  almost  vertically  beneath  the  sternum 
(Fig.  74).  It  is  impossible  to  percuss  them,  because  only  a  small  space 
exists  between  them,  and  because  an  exact  localization  of  the  percussion 
stroke  upon  the  sternum  is  very  difficult.  The  bone  vibrates  to  per- 
cussion more  or  less  as  a  whole,  like  a  great  pleximeter,  and  transmits 
the  vibration  widely  over  the  surface.  The  superficial  cardiac  dulness 
can  be  percussed  accurately  only  when  a  considerable  part  of  that  bone 
overlies  or  is  bounded  by  a  dull-sounding  tissue  (see  Figs.  88,  91). 
For  this  reason  the  right  border  of  the  superficial  cardiac  dulness  ordi- 


FiG.  81.— Apical  percussion  :  Lines  above  clavicle  at  normal  height. 


narily  corresponds  to  the  left  edge  of  the  sternum,  and  hence  has  little 
diagnostic  importance. 

The  apices  of  the  lungs  form  slightly  voluminous  cones  covered  by 
very  thick  layers  of  muscle,  which  render  the  upper  pulmonary  bounda- 
ries much  more  difficult  to  determine  as  linear  projections  than  the  lower. 
Moreover,  the  trachea  lies  in  such  close  proximity  to  the  lung  apices  that 
percussion  is  very  liable  to  set  this  in  vibration.  Hence  the  difficulty 
of  properly  percussing  the  apices.  Figs.  79  and  81  represent  the 
boundary  lines  of  the  lung  apices  in  individuals  who  are  neither  too 
muscular  nor  too  fat.  The  highest  point  of  the  upper  lung  border  lies 
from  3  to  5  cm.  above  the  clavicle. 

[In  a  recent  paper  ^  Dr.  R.  W.  Philip,  Physician  to  the  Victoria 
Hospital  for  Consumption,  has  called  attention  to  the  significance  of 
'  Practitioner,  London,  vol.  xvii.,  1903. 


172 


PERCUSSION. 


the  supraclavicular  triangle  in  relation  to  early  apical  changes.  He 
believes,  from  a  large  number  of  observations,  that  the  mean  of  lung 
resonance  above  the  clavicle  is  at  least  1 J  in.  (4  cm.) ;  that  frequently 
it  is  over  2  in.  (5J  cm.). 

Assuming  that  lung  resonance  may  be  determined  in  the  healthy 
subject  over  an  area  of  three  fingers'  breadth  above  the  clavicle.  Dr. 
Philip  believes  that  apical  changes  are  often  overlooked  by  limiting 
percussion  to  a   single  finger's   breadth  above  the  clavicle,  a  method 


Fig.  82.— Apical  percussion;  Line  above  left  clavicle  1V$  cm.  below  normal ;  left  apex  dull 
(New  York  City  Hospital). 

which  obtains  with   many  examiners.     The  editors'   experience  corre- 
sponds with  Dr.  Philip's. 

The  accompanying  photographs  (Figs.  81-83)  illustrate  a  normal 
extent  of  pulmonary  resonance  above  both  clavicles ;  a  decided  limita- 
tion of  the  resonance  above  the  left  clavicle  in  a  case  of  pulmonary 
tuberculosis  at  the  left  apex  ;  and  the  method  of  percussing  the  apices 
from  behind.  AVe  have  intentionally  omitted  any  reference  to  so-called 
"  tidal  percussion  of  the  apices."  Its  value  has  not  been  settled  beyond 
dispute. — Ed.] 

The  lung  borders  vary  somewhat  according  to  the  age  of  the  patient.  For  ex- 
ample, in  old  people  the  lung-liver  boundary  is  situated  somewhat  lower  (about 
one  intercostal  space ) .  The  superficial  cardiac  dulness  is  often  somewhat  dimin- 
ished and  situated  about  one  intercostal  space  lower  than  in  young  adults.  This 
change  depends  upon  the  diminished  elasticity  of  the  senile  lung.  Many  authors 
denote  this  change  as  senile  emphysema,  provided  nothing  else  abnormal  is  de- 
tected.    The  writer  doubts  if  such  nomenclature  is  correct,  and  has  been  unable 


TOPOGRAPHIC  PERCUSSION. 


173 


to  determine  a  higher  level  of  the  pulmonary  edge  in  children  than  in  perfectly 
healthy  adults.^ 

ACTIVE  AND  PASSIVE  MOBILITY  OF  THE  LUNG  BORDERS  UNDER  NORMAL 
AND  UNDER  PATHOLOGIC   CONDITIONS. 

Vigorous  respiration  will  depress  the  luDg  borders  several  centimeters 
during  inspiration  and  elevate  them  the  same  distance  during  expiration 
[active  mobility').  Percussion  will  very  plainly  demonstrate  this.  In  the 
axillary  line  the  extreme  positions  of  the  lung  border  may  reach  4  cm. 


Fig.  83.— Method  of  apical  percussion. 

above  and  below  the  mean,  so  that  the  total  excursion  may  be  as  much 
as  8  cm.  Litten's  diaphragm  phenomenon  (p.  78  6^  seq.)  is  the  visible 
expression  of  such  excursions.  Deep  inspiration  may  almost  or  entirely 
obliterate  the  superficial  cardiac  dulness. 

Change  in  a  patient's  position  will  demonstrate  a  jjossive  mohiUty 
of  the  lungs.  Changing  from  the  dorsal  decubitus  to  the  erect  posture 
may  elevate  the  lung-liver  boundary  (or  very  rarely  depress  it).  In 
some  cases  no  change  is  noted.  This  variable  result  probably  depends 
upon  the  preponderance  of  one  of  two  opposing  factors  which  influence 
the  position  of  the  diaphragm  :  1,  the  weight  of  the  liver ;  and  2,  the 
increased  abdominal  pressure  due  to  the  contraction  of  the  abdominal 
muscles  in  the  upright  posture.  If  the  abdominal  walls  are  tense  enough 
to  contract  vigorously  in  sitting  and  stauding,  a  slightly  higher  position 
of  the  inferior  lung  boundary  seems  to  be  the  rule,  because  the  intra- 

^  Sahli,  Die  topographische  Percussion  im  Kindesalier,  Bern,  Dalp'scbe  Buchhandlung 
(now  Schmid,  Franche  and  Cie.),  1881. 


174 


PEECUSSION. 


abdominal  pressure  will  be  increased.  Whereas  if  the  abdominal  walls 
are  relaxed — e.g.,  with  the  characteristic  pendulous  abdomen — the  oppo- 
site effect  will  be  observed,  because  the  weight  of  the  liver  will  depress 
the  diaphragm.  Changing  from  the  dorsal  decubitus  to  a  lateral  posture 
will  depress  the  pulmonary  border  of  the  uppermost  lung  about  3  or  4  cm. 
at  the  axillary  lines.  A  deep  inspiration  while  this  position  is  retained 
may  bring  the  border  about  9  cm.  lower  than  in  the  dorsal  decubitus  with 
median  respiratory  position ;  and  with  a  full  expiration  the  lung  border 
may  under  some  circumstances  make  an  excursion  of  as  much  as  13  cm. 
By  means  of  all  these  different  types  and  degrees  of  lung  mobility,  it  is 
generally  possible  to  demonstrate  the  clinically  important  sign  of  dimin- 


FiG.  84.— Normal  percussion  boundaries— from  behind. 

ished  or  absent  lung  mobility.  The  mobility  of  the  lung  border  is  dimin- 
ished in  (1)  pulmonary  emphysema  and  in  (2)  par^iaZ  consolidations  of  the 
lung.  Although  the  percussion  note  may  not  be  noticeably  dulled  if 
these  consolidations  are  scattered,  such  a  condition  may  be  suspected 
from  the  immobility  of  the  border.  (3)  Firm  pleuritic  adhesions  be- 
tween pulmonary  and  costal  pleura  also  prevent  mobility. 

Some  examiners  attempt  to  demonstrate  pleuritic  adhesions  of  the 
lung  edge  by  percussing  below  the  border  determined  during  quiet 
breathing  while  the  patient  breathes  deeply.  If  the  loudness  of  the 
note  is  much  increased  with  inspiration,  they  then  claim  that  the  lung 
edges  are  freely  mobile.  This  method  of  examination,  according  to  the 
author's  experience,  often  causes  error.     Even  if  the  lung  is  quite  adhe- 


TOPOGRAPHIC  PERCUSSION.  175 

rent,  the  intensity  of  the  note  beneath  the  lung  border  is  abnost  certain 
to  increase  during  inspiration.  Such  an  increase  does  not  necessarily 
prove  a  descent  of  the  boundary,  but  merely  suggests  a  thickening  or 
an  inflation  of  the  lung  edge.  In  other  words,  a  greater  accumulation 
of  air  at  or  near  the  pulmonary  edge  influences  the  note  below  it, 
because  even  with  the  lightest  percussion  it  is  not  possible  to  absolutely 
localize  the  percussion  stroke. 

A  much  better  method  for  demonstrating  mobility  of  the  pulmo- 
nary border  is  to  determine  the  boundary  in  the  position  of  extreme 
inspiration  while  the  patient  holds  his  breath,  mark  it  on  the  chest,  and 
then  do  the  same  during  extreme  expiration. 

ABNORMAL  POSITION  OF  THE  LUNG  BOUNDARIES. 

Under  pathologic  conditions  the  lung  boundaries  may  be  extended 
as  well  as  contracted. 

Extension  of  the  lung  boundaries  occurs  in  emphysema,  where  the 
lung-liver  boundary  may  reach  down  to  the  eighth  rib  in  the  right  mid- 
clavicular line,  to  the  ninth  or  tenth  rib  in  the  axillary  line,  and  to  the 
twelfth  vertebra  behind  in  the  posterior  median  line ;  in  fact,  quite  to 
the  inferior  limit  of  the  thorax.  The  emphysematous  increase  may 
sometimes  be  plainly  demonstrated  even  at  the  lung  apex,  and  over  the 
superficial  cardiac  dulness,  which  may  be  either  entirely  or  almost  oblit- 
erated. Both  the  active  and  the  passive  mobility  of  the  borders  in 
emphysema  are  diminished  on  account  of  the  permanent  inspiratory 
position  of  the  diaphragm  and  a  certain  fixity  of  the  lung  so  character- 
istic of  the  disease.  Emphysema  ordinarily  is  developed  upon  both 
sides,  and,  as  a  rule,  quite  uniformly ;  but  a  partial  emphysema  does 
occur  (perhaps  incorrectly  called  vicarious  emphysema),  in  which  the 
changes  are  localized  at  the  lung  borders.  Even  in  the  common  type 
of  pulmonary  emphysema  the  pulmonary  distention  is  not  always  uni- 
form. Frequently  percussion  shows  that  the  emphysema  is  limited  to 
the  region  over  the  heart,  whereas  the  inferior  lung  border  is  not  any 
lower  than  normal.  This  is  often  seen  in  fat  or  dropsical  individuals, 
apparently  because  the  increased  abdominal  contents  crowd  the  diaphragm 
upward. 

In  a  similar  manner  the  pulmonary  boundaries  are  also  extended  in 
attacks  of  bronchial  asthma  and  in  obstructive  bronchitis  because  there 
is  a  greater  resistance  to  the  emptying  than  to  the  filling  of  the  lungs. 
For  analogous  reasons,  when  a  bronchus  is  narrowed  the  afi'ected  pul- 
monary lobe  is  dilated. 

Certain  cardiac  affections,  particularly  mitral  lesions,  lead  to  pulmo- 
nary dilatation,  the  lungs  being  permanently  engorged  with  blood  and  in 
the  condition  of  so-called  cardiac  lung  rigidity ;  brown  induration  is 
usually  present  as  well.  The  lungs  in  these  cases  resemble  those  of 
emphysema,  since  they  are  dilated,  their  elasticity  is  partly  lost,  and 
they  make  but  slight  excursions. 

The  lung  borders  in  enteroptosis  (p.  192)  are  nearly  always  depressed. 

Retraction  of  the  lung  border  results  from  the  crowding  of  the  lung 


176  PERCUSSION. 

edges  by  the  neigbboring  parts.  1.  The  diaphragm  will  be  pushed 
upward  by  all  conditions  which  increase  the  intra-abdominal  pressure — 
e.g.,  meteorism,  ascites,  abdominal  tumors  (especially  if  situated  at  the 
convexity  of  the  liver).  Negative  intrathoracic  pressure  will  therefore 
be  diminished  ;  so  the  lungs  must  be  retracted,  not  only  upward,  but 
concentrically  in  all  directions,  from  in  front  backward  and  toward  the 
hilus,  even  enough  to  expose  the  heart  to  a  considerable  extent.  2.  An 
enlarged  heart  (or  a  pericardium  filled  with  fluid)  can  also  crowd  the 
lungs  aside  enough  to  increase  the  superficial  cardiac  dulness.  (See 
Heart  Percussion.)  If  such  a  crowding  is  very  marked,  the  resulting 
diminution  of  negative  intrathoracic  pressure  will  elevate  the  inferior 
lung  borders.  3.  All  processes  associated  with  a  pulmonary  shrinking 
may  occasion  a  retraction  of  the  lung  boundaries — e.  ^.,  the  chronic 
forms  of  tuberculosis,  which  produce  a  connective-tissue  retraction  of 
the  lungs  ;  and  cases  of  pleurisy  in  which,  after  the  absorption  of  the 
exudate,  the  expansion  of  the  compressed  portion  of  the  lung  is  pre- 
vented by  the  formation  of  a  firm  connective-tissue  coating.  The  shrink- 
ing usually  proceeds  concentrically  in  such  conditions,  so  that  the  lungs 
are  often  retracted  on  all  sides  ;  that  is,  as  much  over  the  heart  as  at  the 
inferior  borders,  and  sometimes  even  at  the  upper  borders,  toward  the 
hilus.  Chronic  tuberculosis  frequently  leads  to  a  retraction  of  the  pul- 
monary apex.  Therefore  the  demonstration  of  a  unilateral  low  position 
of  the  superior  lung  border  is  of  special  importance  for  the  early  diag- 
nosis of  apical  tuberculosis.  (See  Editor's  Note,  p.  172,  and  Fig.  81.) 
We  must  remember  that  the  normal  positions  mentioned  above  are 
only  averages,  and  that  abnormally  long  or  short  chests  would  naturally 
modify  the  position  of  the  lung  borders  in  relation  to  the  ribs,  while 
the  condition  could  in  no  way  be  considered  pathologic.  Errors  in  this 
respect,  especially  in  relation  to  the  diagnosis  of  emphysema,  frequently 
occur  in  practice.  They  cannot  be  avoided  by  definite  rules,  but  only 
by  practical  experience  and  by  the  development  of  a  geometric  vision. 

TOPOGRAPHIC  PERCUSSION  OF  THE  HEART. 

NORMAL  SUPERFICIAL  AND  NORMAL  DEEP  CARDIAC  DULNESS. 

Superficial  cardiac  dulness  is  the  dulled  area  which  corresponds  to 
the  segment  of  the  left  lung  about  the  heart  (Figs.  79  and  85).  Its 
extent  really  tells  more  about  the  position  of  the  lung  edge  than  about 
the  size  of  the  heart.  Nevertheless,  if  the  heart  is  enlarged  or  if  the 
pericardium  becomes  distended  with  fluid,  the  edges  of  the  lung  will  be 
pushed  back  and  the  superficial  cardiac  dulness  increased.  Certain  cau- 
tions are  necessary  to  prevent  mistakes  in  estimating  the  size  of  the 
heart  or  pericardium  from  the  extent  of  this  superficial  cardiac  dulness. 
For  example,  despite  an  enlarged  heart,  the  superficial  cardiac  dulness 
is  not  necessarily  increased  in  emphysema,  even  when  the  lung  edges 
in  the  neighborhood  of  the  heart  are  fixed  by  pleuritic  adhesions.  The 
deep  dulness  is  more  important  in  estimating  the  size  of  the  heart  and 
the  contour  of  the  pericardium.     The  deep  cardiac  dulness  will  never 


TOPOOBAPHIC  PERCUSSION. 


177 


be  very  intense,  but  is  always  modified  (a  so-called  relative  dulness). 
The  beginner  often  finds  it  very  difficult  to  determine.  The  superficial 
cardiac  dulness,  on  the  contrary,  is  frequently  absolute,  and  therefore 
easier  for  the  beginner's  ear  to  appreciate.  Both  varieties  of  dulness 
should  therefore  be  mapped  out  upon  the  chest.  The  superficial  often 
confirms  the  results  of  the  deep  percussion. 

The  form  and  size  of  the  superficial  dulness,  also  called  the  small 
cardiac  dulness,  have  already  been  described  in  the  section  on  Topo- 
graphic Percussion  of  the  Lungs  (see  Fig.  79,  p.  169  et  seq.).  Fig.  85 
represents  the  relations  of  the  superficial  and  the  deep  or  great  cardiac  dul- 
ness in  the  average  healthy  adult.     The  boundaries  of  the  latter  run  from 


Fig.  85. — Superficial  and  deep  cardiac  dulness  under  normal  conditions. 


the  upper  edge  of  the  third  left  rib  nearly  parallel  to  the  border  of  the 
superficial  cardiac  dulness,  bend  toward  the  left  in  a  bow-shape,  with 
the  convexity  outward,  become  perpendicular  slightly  inside  the  mid- 
clavicular line,  and  end  near  this  point  at  the  apex  beat.  The  heart 
is  bounded  below  by  the  liver,  so  that  the  deep  dulness,  like  the  super- 
ficial, merges  into  the  hepatic  dulness  and  cannot  be  differentiated  from 
it.  Where  the  liver  is  covered  by  intestines  filled  with  air,  or  where  it 
is  pushed  upward  to  the  right,  superficial  percussion  will  generally  evoke 
a  loud  tympanitic  tone  just  below  the  heart.  Most  authors  limit  the 
right  boundary  of  the  deep  dulness  at  the  left  sternal  border ;  never- 
theless, according  to  the  writer's  experience,  the  majority  of  healthy 
adults  show  a  slight  dulness  up  to  the  right  sternal  border  (Fig.  85). 
But  in  many  cases  the  whole  extent  of  the  sternum  furnishes  such  a 

12 


178  PERCUSSION. 

loud  tone  that  the  deep  cardiac  dulness  is  really  limited  by  the  left 
sternal  border.  (See  Topographic  Percussion  of  the  Lungs.)  These 
individual  peculiarities  depend  upon  the  vibration  of  the  sternum,  upon 
the  thickness  of  the  layer  of  lung  covering  the  heart,  etc.  In  determin- 
ing the  upper  borders  of  the  deep  dulness,  the  fact  that  the  sternum  trans- 
mits the  blow  so  deeply  necessitates  a  light  percussion. 

Both  the  superficial  and  the  deep  dulness  are  smaller  in  the  aged 
than  in  younger  adults,  because  the  lungs  of  old  people  cover  the  heart 
more  extensively.  In  children  both  varieties  of  dulness  are,  on  the  con- 
trary, larger,  because  the  amount  of  lung  tissue  which  covers  the  heart 
is  thinner,  and  so  the  sphere  of  acoustic  action  of  the  percussion  blow 
reaches  the  solid  organ  earlier.  This  distinction  is  shown  by  comparing 
Figs.  73  and  86. 

Fig.  73  pictures  the  relation  of  the  acoustic  sphere  of  action  of  the 
percussion  blow  in  adults ;  Fig.  86,  in  children.  In  the  latter  it  is 
plain  that  the  deep  dulness  will  sometimes  be  larger  than  the  organ 
itself ;  whereas  in  adults,  and  even  more  noticeably  in  older  people,  per- 
cussion can  only  include  a  portion  of  the  entire  size  of  the  heart.     Long 


Fig.  86.— Relations  of  the  size  of  the  acoustic  sphere  of  the  action  of  the  percussion  blow  in 


children  (see  Fig.  73) 

practice  will  prevent  mistakes,  but  even  then  we  must  employ  the  other 
examination  methods,  such  as  palpation  of  the  apex  beat. 

Variations  of  the  thoracic  dimensions  in  different  individuals  make 
the  conclusions  to  be  drawn  from  deep  cardiac  percussion  still  more 
doubtful.  The  heart  boundaries  are  ordinarily  mapped  out  in  accord- 
ance with  the  orienting  lines  of  the  body — e.  g.,  the  position  of  the  left 
border  of  the  heart  in  reference  to  the  mammillary  line.  This  some- 
times leads  to  erroneous  conclusions.  Although,  as  a  rule,  the  left 
border  of  the  deep  cardiac  dulness  lies  somewhat  inside  the  mammillary 
line,  it  is  self-evident  that  if  the  mammillary  line  is  pushed  inward  even 
a  normal  heart  would  reach  outside.  Even  the  midclavicular  line  is 
not  absolutely  constant,  because  the  length  of  the  clavicle  varies,  and 
■with  it  the  breadth  of  the  thorax.  If  the  sternum  is  broad,  a  dulness  be- 
yond the  right  sternal  edge  would  be  more  significant  than  if  the  sternum 
is  narrow.  Hence  the  importance  of  the  absolute  size  of  the  cardiac 
dulness.  At  the  Bern  Clinic  we  always  measure  its  horizontal  diameter 
in  the  third  and  fourth  intercostal  spaces,  and  the  distance  of  the  left 
and  right  margins  of  dulness  from  the  anterior  median  line.  Riess  ^  has 
1  Zelt.f.  klin.  Med.,  1888,  vol.  xiv.,  p.  12. 


TOPOGRAPHIC  PERCUSSION.  179 

estimated  the  normal  figures  from  averages  upon  a  large  number  of 
measurements  in  medium-sized  healthy  adults,  as  follows  : 

Distance  of  the  right  border  of  the  deep  cardiac  dulness  from  the 
anterior  median  line  :  Third  intercostal  space  2|  cm. ;  fourth  intercostal 
space  3f  cm. 

Distance  of  the  left  border  of  the  deep  cardiac  dulness  from  the 
median  line :  Third  intercostal  space  4|  cm.  ;  fourth  intercostal  space 
7i  cm. 

Total  width  of  the  deep  cardiac  dulness  :  Third  intercostal  space  7^ 
cm. ;  fourth  intercostal  space  11;^  cm. 

These  figures  seem  to  the  writer  rather  too  small. 

Cardiac  percussion  can  sometimes  be  simplified  by  directing  the 
patient  to  bend  forward  or  to  take  a  deep  inspiration. 

Before  an  attempt  to  estimate  the  deep  cardiac  dulness  in  women  with  promi- 
nent breasts,  the  patient  or  a  nurse  must  first  push  the  left  mamma  upward  and  to 
the  left. 

ACTIVE  AND  PASSIVE  MOBILITY  OF  THE  SUPERFICIAL  AND  DEEP  CARDIAC 

DULNESS. 

The  heart  borders,  like  those  of  the  lungs,  change  their  position 
actively  with  respiration  and  passively  with  change  of  the  patient's 
position.  Active  mobility  concerns  only  the  respiratory  overlapping 
of  the  heart  by  the  lung  edges,  whereas  passive  mobility  influences  the 
position  of  the  heart  as  well  as  of  the  lung  borders. 

The  boundaries  described  above  are  estimated  during  quiet  breathing 
in  the  dorsal  decubitus.  Deep  inspiration  diminishes  the  size  of  both 
superficial  and  deep  cardiac  dulness  more  or  less  decidedly.  Forced 
expiration  produces  the  opposite  effect,  and  in  rare  cases  may  bring  the 
superficial  dulness  to  the  right  of  the  right  sternal  edge,  the  right  edge 
of  the  lung  retreating  so  far.  Therefore  percussion  during  forced  ex- 
piration (without  exerting  abdominal  pressure)  will  sometimes  reveal 
the  true  size  of  a  heart  which  is  extensively  covered  by  the  lungs. 

In  the  left  lateral  posture  the  heart  falls  to  the  left  and  displaces  the 
anterior  edge  of  the  left  lung.  The  anterior  edge  of  the  right  lung  is 
only  exceptionally  found  beyond  the  left  sternal  edge,  because  its  excur- 
sion is  normally  limited  by  the  line  of  the  pleura  beneath  the  sternum 
(see  Fig.  74).  Therefore  in  left  lateral  positions  both  the  superficial 
and  the  deep  cardiac  dulness  are  increased  to  the  left. 

In  right  lateral  positions  the  opposite  displacement  occurs.  Both 
the  deep  and  the  superficial  dulness  will  reach  beyond  the  right  of  the 
sternum,  while  the  superficial  dulness  to  the  left  of  the  sternum  may 
entirely  disappear. 

Changing  from  the  recumbent  to  the  sitting  posture  does  not  produce 
any  constant  change  in  the  form  or  size  of  the  cardiac  dulness.  Both 
the  superficial  and  the  deep  dulness  may  seeui  somewhat  more  intense 
in  the  upright  posture.  If  the  patient  bends  forward  both  are  increased, 
because  the  heart  pushes  the  lungs  aside,  approximating  itself  more 
completely  to  the  anterior  thoracic  wall.     Where  emphysema  or  thick 


180  PEBCUSSWN. 

thoracic  walls  obscure  the  percussion  in  the  recumbent  posture,  sitting 
up  and  bending  forward  may  be  helpful.  To  prevent  mistakes  the 
patient  must  be  careful  not  to  bend  sidewise  or  twist  his  back,  for  we 
must  remember  that  in  such  a  position  a  normal  heart  will  furnish  a 
broader  and  more  intense  dulness. 

The  absolute  measures  of  the  mobility  of  the  superficial  and  the 
deep  cardiac  dulness  vary  so  much  with  the  individual  that  the  figures 
would  be  superfluous. 

PATHOLOGIC  CHANGES  IN  THE   SUPERFICIAL  AND  DEEP  CARDIAC 

DULNESS. 

Diminution   of   tlie   Superficial   and   Deep   Cardiac  Dulness. 

In  advanced  emphysema,  in  left-sided  pneumothorax,  in  pneumocardiay. 
and  in  precordial  emphysema  both  the  superficial  and  the  deep  cardiac 
dulness  may  be  either  diminished  or  entirely  disappear.  The  cardiac 
atrophy  which  is  sometimes  observed  at  the  autopsy  table  is  too  slight 
to  be  recognized  by  percussion.  Ernp>hysema  also  causes  an  especially, 
low  position  of  the  cardiac  dulness,  on  account  of  the  deep  position  of 
the  diaphragm.  Frequently  no  deep  cardiac  dulness  can  be  made  out, 
and  the  superficial,  if  present,  may  appear  only  at  the  fifth  or  even  the 
sixth  rib.  In  left-sided  pneumothorax  we  should  expect  that  at  least 
a  part  of  the  superficial  cardiac  dulness  would  persist,  because  the 
normal  division  line  of  the  pleurae,  which  would  divide  the  superficial 
cardiac  dulness  in  half,  shifts  (Fig.  74).  As  a  matter  of  fact,  however, 
left  pneumothorax  almost  always  dislocates  the  heart,  the  division  line, 
and  with  it  the  mediastinum,  so  far  to  the  right  that  the  superficial 
cardiac  dulness  to  the  left  of  the  sternum  may  entirely  disappear.  In 
right-sided  pneumothorax  (Fig.  99)  the  air  resonance  may  overlap  the 
left  edge  of  the  sternum,  in  consequence  of  the  mediastinum  being 
pushed  to  the  left,  so  that  the  superficial  cardiac  dulness  will  appear  to 
be  narrowed  from  the  right.  The  demonstration  of  cardiac  dislocation 
(p.  188)  will  suggest  and  explain  this  condition.  Percussion  elicits  an 
abnormally  resonant  metallic  note  (often  tympanitic)  over  the  area  of 
cardiac  dulness  in  pneumopericardium  and  p>recordial  emphysema.  The 
pericardial  sac  in  the  former  ordinarily  contains  fluid  as  well  as  air ; 
this  becomes  evident  when  the  patient  sits  up,  for  the  lower  portion 
of  the  abnormally  resonant  area  becomes  dull,  the  fluid  following  the 
laws  of  gravity.      (The  auscultatory  signs  will  be  mentioned  later.) 

With  marked  gaseous  distention  of  the  intestine  or  of  the  stomach, 
even  careful  percussion  may  elicit  a  tympanitic  note  over  the  area  of 
superficial  cardiac  dulness,  because  the  vibrations  are  transmitted  to  the 
abdominal  contents.  But  very  gentle  percussion,  in  which  the  plex- 
imeter  is  applied  only  by  its  own  weight,  and  perhaps  best  with  the 
patient  bending  forward,  will  probably  enable  us  to  demonstrate  the 
superficial  cardiac  dulness,  and  so  to  differentiate  tympanites  from  the 
overlapping  of  the  heart  by  air-containing  tissue.  A  deep  cardiac  dul- 
ness in  such  cases  is  difficult,  if  not  impossible,  to  obtain. 


TOPOGRAPHIC  PERCUSSION. 


181 


Enlargement  of  the  Superficial  and  Deep  Cardiac  Dulness. 

Enlargement  of  the  Cardiac  Dulness  from  Abnormalities 
of  the  I/Ung"  Borders. — Both  the  superficial  and  the  deep  cardiac 
dulness  will  be  increased  if  the  heart  pushes  back  the  anterior  lung 
boundary,  or  if  some  anatomic  process  in  the  latter  (infiltration  or 
atelectasis)  adds  a  dull  tone  of  its  own  to  the  cardiac  dulness.  The 
increase  of  cardiac  dulness  does  not  then  depend  upon  any  alteration  of 
the  heart's  size.  Such  conditions  can  be  properly  interpreted  only  by 
carefully  considering  the  entire  clinical  picture,  and  by  making  use  of 
other  methods  of  examination.  The  most  frequent  examples  are  jndmo- 
naiy  contraction  and  the  concentric  retraction  of  the  lung,  or  an  upward 
dislocation  of  the  diaphragm  from  marked  ascites,  meteorism,  and  the 
like  (see  pp.  175  and  176). 

Increase  of  the  Cardiac  Dulness  from  Actual  Increase 
of  the  Si^e  of  the  Heart  or  of  the  Pericardial  Contents. — 
Here  the  superficial  and  the  deep  cardiac  dulness  are  generally  increased 


Fig.  87.— Precordial  buli^in.Lr:  I'.nlar.L'rd  ln^ail  and  liver;  <liiiil)l{.'  mitral  Ir^iini;  jiercussion 
boundaries  outlined  by  dutteil  lines.  This  picture  doe.s  not  bring  out  the  marked  precordial 
bulging  which  was  v^ry  evidLiit  in  looking  at  the  patient.  The  width  of  the  cardiac  dulness  at 
the  nipple  line  was  21  cm.  (New  York  City  Hospital). 


correspondingly  unless  an  emphysema  or  adhesions  of  the  pulmonary 
border  complicate  the  picture  (p.  176),  In  the  event  of  such  a  com- 
plication the  superficial  cardiac  dulness  may  be  much  less  enlarged  than 
the  deep ;  both  may  remain  small ;  or  even  neither  may  be  increased, 


182  PERCUSSION. 

on  account  of  the  marked  covering  of  the  heart.  In  this  way  even 
considerable  cardiac  enlargement  might  escape  clinical  demonstration. 

The  superficial  cardiac  dulness  is  very  important  in  demonstrating 
cardiac  enlargement,  because  the  beginner  finds  it  much  easier  to  esti- 
mate than  the  deep  dulness  ;  because  there  is  less  chance  for  a  subjective 
variation ;  and  because  in  decided  cardiac  enlargement  or  increase  of 
pericardial  contents  on  account  of  the  considerable  lung  retraction  the 
entire  cardiac  dulness  frequently  becomes  superficial. 

Actual  Enlargement  of  the  Heart. — The  heart  is  pathologically 
enlarged  both  by  hypertrophy  of  its  walls  and  by  dilatation  of  its  cavi- 
ties. The  extent  of  the  former  enlargement  must,  of  course,  be  limited. 
The  latter  will  be  much  greater  and  more  easily  recognized.  If,  while 
the  chambers  of  a  heart  retain  their  normal  size,  its  walls  increase 
about  0.5  cm.  in  thickness  from  simple  hypertrophy,  this  would  pro- 
duce a  difPerence  of  only  1  cm.  in  the  width  of  the  heart.  Now,  as  a 
matter  of  fact,  we  cannot  percuss  accurately  enough  to  appreciate  1  or 
2  cm.  increase  in  cardiac  size,  nor  do  we  practically  ever  see  post  mor- 
tem as  much  hypertrophy  as  0.5  cm.  unless  complicated  with  dilatation. 
Evidently,  then,  any  enlargement  of  cardiac  dulness  which  can  be 
demonstrated  by  percussion  must  depend  upon  the  dilatation  of  the 
cavities,  whether  there  is  any  coexisting  hypertrophy  or  not. 

An  appreciable  enlargement  of  cardiac  dulness  due  to  a  pure  hypertrophy  of 
the  heart — i.  e. ,  one  unassociated  with  dilatation — is,  however,  sometimes  observed 
in  very  rare  cases,  particularly  in  chronic  nephritis.  In  such  cases  a  diagnosis  of 
pure  hypertrophy  must  be  supported  by  other  examination  methods  (increased 
force  of  apex  beat,  high-tension  pulse,  accentuated  second  tone  (see  below)). 

The  cardiac  dulness  may  be  increased  in  all  directions  or  only  in  one 
direction.  We  naturally  sup})ose  a  dislocation  of  the  left  border  of  car- 
diac dulness  to  the  left  to  depend  upon  a  dilatation  of  the  left  ventricle  ; 
a  dislocation  of  the  right  border  to  the  right,  upon  a  dilatation  of  the 
right  ventricle ;  an  increase  upward,  upon  a  dilatation  of  the  auricles  or 
of  the  great  vessels.  But  the  autopsy  table  has  shown  so  many  excep- 
tions that  these  conclusions  are  by  no  means  sure — e.  g.,  marked  dilata- 
tion of  the  left  ventricle  may  increase  the  cardiac  dulness  upward  without 
there  being  any  dilatation  of  the  auricles  or  of  the  great  vessels  ;  because, 
if  the  ventricle  is  dilated,  the  oblique  position  of  the  heart  pushes  the 
dulness  upward.  The  clinical  findings  might  very  often  induce  us  to 
assume  a  dilatation  of  the  left  ventricle  when  the  dulness,  as  a  matter  of 
fact,  depends  only  upon  a  dilatation  of  the  right  ventricle,  or  vice  versa  ; 
or,  again,  to  assume  that  only  one  ventricle  is  enlarged,  whereas 
the  autopsy  shows  that  both  share  equally  in  the  enlargement.  The 
reason  of  this  is  that  any  dilatation  of  one  chamber  of  the  heart  must 
secondarily  dislocate  the  entire  heart.  Thus,  dilatation  of  the  right  ven- 
tricle increases  the  dulness  not  only  to  the  right,  but  often  to  the  left, 
pushing  the  left  ventricle  in  that  direction.  The  position  of  the  medi- 
astinum is  a  factor  in  the  difference  of  pressure  at  either  side — i.  e.,  in  the 
two  pleural  cavities — so  that  the  actual  position  of  a  heart  with  dilated 
cavities  is  a  complicated  result  of  its  own   enlargement  and  of  the 


TOPOGRAPHIC  PERCUSSION. 


183 


diiference  of  pressure  at  the  two  sides  of  the  mediastinum,  which  dif- 
ference is  equalized  by  a  dislocation  of  the  mediastinum  together  with 
the  heart.  To  make  the  matter  still  more  complicated,  the  resistance  to 
cardiac  dislocation  is  by  no  means  equal  in  all  cases.  Great  differences 
are  caused  by  the  varying  resistance  of  the  mediastinum,  by  the  vary- 
ing amount  of  depression  of  the  convexity  of  the  diaphragm,  and  by 
individual  variations  of  the  prolongations  of  the  pericardium  upon  the 
great  vessel  trunks.  The  existence  of  such  differences  is  plainly  proved 
by  the  different  dislocations  of  the  heart  from  causes  acting  outside  of 
it  (pleural  exudates). 


Fig.  88. — Cardiac  dulness  with  dilatation  of  the  right  ventricle :  Dulness  is  especially  increased 

to  the  right. 

It  is  generally  more  difficult  to  demonstrate  enlargements  of  the 
right  heart  by  percussion  than  those  of  the  left,  because,  on  account 
of  the  notch  in  the  left  lung,  the  left  heart  is  more  accessible  to  per- 
cussion than  the  right,  which  is  covered  more  completely  by  lung  and 
by  the  sternum.  Besides,  the  right  ventricle  (Fig.  74)  rests  upon  the 
convexity  of  the  diaphragm,  so  that  if  that  chamber  dilates,  the  heart 
will  have  the  tendency  to  find  the  necessary  sjwce  in  the  left  thoracic 
cavity,  because  the  arch  of  the  diaphragm  would  present  too  great  a 
hindrance  to  its  enlarging  to  the  right.  Hence  a  moderate  dilatation  of 
the  right  ventricle  often  produces  only  a  dislocation  of  the  left  cardiac 
boundary  ;  while  it  requires  a  very  considerable  dilatation  of  the  right 
ventricle  to  increase  the  dulness  to  the  right  of  the  sternum.  The  most 
familiar  example  of  this  is  the  displacement  of  the  apex  beat  to  the  left 


184 


PERCUSSION. 


in  pure  mitral  stenosis,  where  the  left  ventricle  is  certainly  not  dilated 
Sometimes,  however,  the  enlargement  of  the  right  ventricle  (Fig.  88) 
can  be  definitely  demonstrated  to  the  right. 

So  many  exceptions  make  it  clear  that  a  diagnosis  of  the  enlarge- 
ment of  a  certain  cavity  cannot  be  determined  from  the  direction  of 
the  increase  of  cardiac  dulness  without  the  general  clinical  picture  and 
without  other  methods  of  examination.  The  position  of  the  apex  beat, 
as  we  shall  see  below,  is  perhaps  as  helpful  as  anything.  Figs.  88  and 
89  show  typical  examples  of  the  position  of  cardiac  dulness  in  dilatation 
of  the  right  and  of  the  left  ventricle. 


Cardiac  dulness  with  dilatation  of  the  left  ventricle. 


Enlargement  of  the  cardiac  dulness  upward  may  be  due  to  dilatation 
of  the  ventricles,  of  the  auricles,  or,  of  the  great  vessels.  Percussion 
will  frequently  differentiate  the  latter  two  from  the  former ;  if  the  in- 
crease of  the  dulness  upward  is  very  pronounced  (/.  e.,  in  proportion  to 
the  lateral  enlargement),  or  if  it  assumes  the  form  of  a  projection  from 
or  an  appendage  to  the  ordinary  form  of  cardiac  dulness,  it  is  to  be 
referred  to  dilatation  of  the  auricles  or  great  vessels. 

Fig.  90  presents  such  an  example,  and  illustrates  the  importance  of 
determining  by  cardiac  percussion  the  relation  of  the  superficial  to  the 
deep  dulness  in  enlargement  of  the  heart.  Figs.  88  and  89  show  an 
enlargement  outward,  with  the  borders  of  superficial  and  deep  dulness 
practically  parallel  to  each  other,  so  that,  as  under  normal  conditions, 
the  superficial  dulness  is  entirely  surrounded  (except  below)  by  a  strip 


TOPOGRAPHIC  PERCUSSION. 


185 


of  relative  dulness.  lu  Fig.  90  the  borders  of  the  superficial  and  of 
the  deep  dulness  merge  above  and  near  the  apex,  so  that  there  is 
only  a  superficial  dulness.  This  illustrates  a  reasonably  frequent  occur- 
rence. It  results  from  the  enlarged  heart  crowding  back  the  lung 
edges,  so  that  the  heart  lies  directly  against  the  thorax,  and  natu- 
rally furnishes  only  a  superficial  dulness.  In  Fig.  90  the  left  auricle 
has  pushed  the  border  of  the  lung  so  far  aside  that  this  chamber  and 
the  pulmonary  artery  both  lie  close  against  the  chest-wall.  The  less 
markedly  dilated  left  ventricle  is  still  partly  covered  by  the  lung  ;  hence, 
outside  of  the  superficial  dulness,  a  slight  relative  or  deep  dulness  per- 
sists.    In  Fig.  90  the  intensity  and  the  superficial  character  of  the  ex- 


Deep  cardiac 

dulness. 


Pulmonarypulse, 
visible  and  pal- 
pable. Palpable 
diastolic  valvu- 
lar shock. 


Pulsation  of  the 
auricle,  visible 
and  palpable. 


Deep  cardiac 
dulness. 


Fig.  90.— Dilatation  of  the  left  auricle  and  left  ventricle,  with  an  exposure  of  the  pulmonary  artery, 
in  a  case  of  mitral  insuf&ciency. 


tensive  dulness  above,  contrasted  with  the  amount  of  the  dulness  to  the 
left,  the  characteristic  appendage  to  the  normal  superficial  cardiac  dul- 
ness upward,  and  the  results  of  palpation  mentioned  in  the  figure, 
should  suggest  the  diagnosis  of  a  dilatation  of  the  left  auricle  or  of  the 
pulmonary  artery. 

Fig.  91  represents  a -marked  dilatation  of  the  right  auricle  and  right 
ventricle  in  tricuspid  insufficiency.  Here  again  the  lungs  are  pushed 
so  far  aside  that  the  dulness  is  superficial,  and  the  left  edge  and  the 
apex  of  the  heart  lie  perfectly  free.  Above  and  to  the  left  a  small 
zone  of  relative  dulness  remains. 

It  can  be  seen  in  this  figure,  just  as  in  Fig.  88,  that  the  superficial 
dulness  includes  all  the  lower  part  of  the  sternum.     Hence  the  dulness 


186 


PEECUSSION. 


can  be  well  defined  above,  although  normally  it  is  difficult  to  deter- 
mine by  percussion  the  solid  from  the  air-containing  parts  (see  p.  171) 
beneath  the  sternum. 

From  the  bulging  of  the  cardiac  dulness  upward,  as  in  Figs.  90  and 
91,  percussion  cannot  always  decide  whether  the  auricles  or  the  great 
arteries  are  responsible  for  the  enlargement.  The  other  relations,  es- 
pecially the  kind  of  pulsation  over  the  area,  will  then  assist  in  settling 
the  condition.  (See  Palpation  and  Inspection  of  the  Heart  Eegion.) 
The  percussion  results  in  Fig.  92  are,  however,  sufficiently  character- 
istic to  justify  the  diagnosis  of  a  dilatation  of  the  aorta. 

Fluid  Effusion  in  the  Pericardium. — When  fluid  accumulates  in 
the  pericardium,  whether  as  a   result   of  general  dropsy  or  of  inflam- 


FiG.  91.— Dilatation  of  the  right  auricle  and  right  ventricle  in  a  case  of  tricuspid  insufiBciency. 

mation  of  the  serous  membrane,  its  cavity  becomes  more  and  more  dis- 
tended and  the  edges  of  the  lung  are  pushed  aside,  just  as  by  the  en- 
larged heart.  If  the  pericardium  lies  against  the  thorax-wall,  percussion 
elicits  a  superficial  (absolute)  dulness  ;  but  if  it  is  still  covered  by  the 
lungs  the  dulness  will  only  be  relative,  and  the  superficial  and  deep  dul- 
ness will  run  concentrically.  If  the  distention  of  the  pericardium 
is  very  marked,  the  lungs  will  be  pushed  aside  and  the  entire  dul- 
ness will  be  superficial,  just  as  in  marked  cardiac  enlargement  (see  p. 
184).  The  form  and  the  position  of  the  cardiac  dulness  enlarged  by 
pericardial  effusions  are,  from  the  anatomic  conditions,  generally  very 
characteristic  (Fig.  88).  The  specific  gravity  of  the  effusion  is  always 
lower  than  that  of  the  heart  itself;  therefore,  with  large  effusions — 
i.  e.,  if  the  lateral  portions  of  the  pericardium  are  filled — the  fluid  will 


TOPOGRAPHIC  PERCUSSION. 


187 


occupy  the  upper  portion  of  the  cavity,  and  the  heart  itself  the  lower. 
Even  relatively  slight  eifusious  will  increase  the  cardiac  dulness  in 
the  dorsal  decubitus,  because  the  fluid  is  then  collected  against  the  an- 
terior thoracic  wall.  If  the  patient  is  slightly  raised  from  the  recum- 
bent posture,  the  fluid  first  collects  at  the  superior  bulging  of  the  peri- 
cardium, in  the  neighborhood  of  the  great  vascular  trunks,  beneath  the 
upper  end  of  the  sternum,  and  there  pushes  the  lungs  aside.  There- 
fore, quite  early  in  pericardial  effusions,  the  cardiac  dulness  reaches  high 
up  under  the  sternum  or  in  its  neighborhood  and  assumes  a  character- 
istic triangular  shape,  with  a  blunt  apex  above  and  a  broad  base  below. 
This  triangular  form  is  nothing  more  than  the  expression  of  the  shape 
of  the  portion  of  the  dilated  pericardium  which  lies  against  the  anterior 


Fig.  92.— Cardiac  percussion  results  in  a  case  of  diffuse  dilatation  of  the  aorta  from  aortic 
insufficiency ;  dilatation  of  the  left  ventricle. 

thoracic  wall,  and  since  the  pericardium  is  wider  at  its  diaphragmatic 
portion  than  at  the  great  vessels,  the  lungs  are  pushed  farther  aside  at 
the  lower  part  than  at  the  upper  part.  Pericardial  distention  shows 
especially  plainly  at  the  so-called  cardiohepatic  angle  (Fig.  74) ;  for  the 
lung  is  very  early  pushed  aside  to  the  right  of  the  sternum,  and  so 
changes  this  angle,  normally  about  90°,  to  a  much  more  obtuse  angle.^ 
An  erect  posture  makes  tlie  dulness  broader  and  lie  some\vhat  lower 
than  in  the  dorsal  decubitus  (if  tlie  effusion  is  larger),  because  the  fluid, 
following  gravity,  flows  more  forward.  Adhesions  of  the  pericardium 
may  prevent  the  application  of  any  rules  for  determining  the  shape  of 
the  pericardial  dulness. 

^  [This  sign  has  been  emphasized  in  the  diagnosis  of  pericardial  effusions  in  children, 
by  Rotch,  of  Boston. — Ed.] 


188  PERCUSSION. 

The  same  depression  of  the  upper  borders  of  dulness  during  the  sitting  post- 
ure has  been  observed  in  actual  enlargement  of  the  heart  fi-om  valvular  lesions. 
Therefore  we  cannot  always  diagnose  a  pericardial  efiusion  from  the  alteration  in 
dulness  noted  above  in  the  change  of  posture  from  lying  to  sitting.  The  action 
of  gravity  upon  the  enlarged  heart  may  depress  the  diaphragm  and  so  cause  a 
lower  position,  or  it  may  be  that  more  venous  blood  is  retained  in  the  lower  half 
of  the  body  in  the  erect  posture,  so  that  the  auricles  are  not  as  completely  filled. 
But  if  the  erect  posture  j)roduces  a  broadening  of  the  lower  jDart  of  the  dulness, 
it  is  certainly  more  suggestive  of  a  pericardial  effusion  than  if  it  produces  a  mere 
•depression  of  its  uj)per  border. 

DISLOCATION   OF  THE  HEART  DULNESS  IN  TOTO. 

The  position  of  the  movable  organs  of  the  thoracic  and  abdominal 
cavities  is  the  result  of  the  muscular  and  elastic  forces  pushing  or  pull- 
ing them  on  all  sides  and  of  the  given  limitations  to  their  power  of 
movement.  The  position  of  the  heart  is  essentially  due  to  the  position 
of  equilibrium  in  which  the  mediastinum  is  held  between  the  two  pleural 
■cavities  and  to  the  position  of  the  diaphragm.  Any  change  of  the  dia- 
phragmatic position  or  any  disturbance  of  the  equality  of  pressure  between 
the  two  pleural  cavities  will  produce  a  dislocation  of  the  heart. 

If  a  dislocation  of  the  diaphragm  develops  slowly,  the  dislocation  of  the 
Leart  will  be  especially  marked,  because  a  gradual  stretching  overcomes  the 
resistance  which  makes  a  dislocation  of  that  part  of  the  diaphragm  upon 
which  the  heart  rests  so  difficult  (fixation  of  the  central  tendon  by  the 
mediastinum,  esophagus,  aorta),  Meteorism,  ascites,  and  voluminous 
abdominal  tumors  push  the  heart  upward ;  emphysema  and  collections  of 
fluid  or  air  in  the  pleural  cavities,  downward. 

If  the  negative  pressure  in  one  pleural  cavity  becomes  less  markedly 
negative,  or,  still  more,  if  it  becomes  positive,  the  heart  will  be  pushed 
toward  the  side  where  the  absolute  pressure  is  less — e.  g.,  large  collec- 
tions of  air  or  fluid  in  one  pleural  cavity  dislocate  the  heart  to  the  opposite 
side.  Thoracentesis  generally  proves  that  an  effusion  which  dislocates  the 
heart  to  any  extent  is  under  positive  pressure ;  nevertheless,  an  effusion 
under  negative  pressure  would  exert  a  similar  dislocating  action.  For 
such  an  action  cloes  not  depend  upon  the  absolute  height  of  the  pressure, 
but  upon  the  difference  between  the  pressures  affecting  the  two  sides  of 
the  mediastinum.  The  heart  is  merely  pushed  to  one  side  until  this  dif- 
ference in  pressure  is  equalized.  The  practical  importance  of  this  fact, 
that  even  a  fluid  effusion  under  negative  pressure  may  dislocate  the 
heart,  is  the  warning  it  gives  us  always  to  avoid  the  risk  of  introducing 
air  into  a  chest  by  aspiration,  whether  the  heart  is  dislocated  or  not. 

Dislocation  of  the  heart  may  occur  not  only  when  the  negative 
pressure  on  one  side  becomes  less  negative  or  becomes  positive,  but  also 
when  it  becomes  still  more  markedly  negative.  Here  the  action  is  more 
that  of  suction  than  of  pressure,  and  is  observed  in  pleural  eflusions 
which  have  led  to  a  retraction  of  the  lungs.  As  the  exudation  becomes 
absorbed,  the  heart  is  drawn  over  toward  the  affected  side  to  fill  the  empty 
space.  In  fresh  pleurisy  the  heart  is  pushed  toivard  the  healthy  side.  In 
retraction  of  the  lung  from  other  causes  than  pleurisy — e.  g.,  from  inter- 


TOPOGRAPHIC  PERCUSSION.  189 

stitial  pneumonia  or  tuberculosis — the  heart  is  likewise  dislocated  to 
the  aiFected  side.  It  may  remain  there  permanently  from  continued 
tugging,  or  it  may  gradually  return  to  its  normal  position  from  a 
gradual  distention  of  the  lungs. 

There  is  no  law  to  determine  how  deformities  of  the  thorax  will  dis- 
locate the  cardiac  dulness. 

The  cardiac  dulness  in  situs  inversus  and  in  dextrocardia  lies  upon 
the  right  side,  forming  a  sort  of  reflected  mirror  picture,  symmetric  to 
its  normal  form  and  position. 

By  starting  from  the  normal  relations  we  can  easily  understand  the 
form  and  position  of  a  dislocated  cardiac  dulness.  Slight  dislocations 
(from  pleural  effusions,  etc.)  only  produce  a  lateral  displacement,  while 
marked  dislocations  occasion  both  a  lateral  and  a  pendulum  movement. 
On  account  of  the  normal  oblique  position  of  the  heart,  such  a  pendu- 
lum movement  probably  occurs  more  readily  in  dislocations  to  the  left ; 
whereas,  on  account  of  the  resistance  of  the  central  tendon  of  the  dia- 
phragm, a  similar  pendulum  dislocation  to  the  right  requires  much 
more  force.  The  results  of  pathologic  findings  and  the  experiments  of 
Ferber  ^  finally  settled  the  much  disputed  pendulum  movement  of  the 
dislocated  heart. 

In  the  ordinary  course  of  a  dislocated  heart  from  a  pleuritic  exuda- 
tion we  can  percuss  only  the  borders  of  the  latter  that  lie  opposite  the 
exudation,  because  the  dulness  of  the  exudation  merges  M'ith  the  cardiac 
dulness.  If  the  heart  is  dislocated  to  the  left,  the  left  edge  of  the 
heart  will  assume  tlie  same  position  as  in  left-sided  cardiac  dilatation. 
If  a  left-sided  exudation  dislocates  the  heart  considerably  to  the  right, 
the  right  cardiac  boundary  and  even  the  apex  beat  (exactly  as  in 
dextrocardia)  may  be  found  in  the  neighborhood  of  the  right  mam- 
millary  line  or  even  still  farther  outside.  Both  superficial  and  deep 
cardiac  dulness  will  be  found  to  the  right  of  the  sternum  ;  the  former 
will  merge  into  the  liver  dulness,  and  the  latter  will  run  around  the 
superficial  dulness,  in  the  shape  of  a  concentric  strip,  from  above  and 
to  the  right.  We  can  differentiate  the  result  from  dextrocardia,  by  the 
pleuritic  dulness  which  occupies  the  place  of  tlie  normal  heart  dulness ; 
from  situs  inversus,  by  the  normal  right-sided  position  of  the  liver. 

Fig.  97  shows  a  large  left-sided  pleural  exudate  dislocating  the  car- 
diac dulness  to  the  right ;  Fig.  99,  a  right-sided  pyopneumothorax 
pushing  the  cardiac  dulness  to  the  left.  From  these  figures  it  can  be 
seen  that  in  dislocation  of  the  heart  the  lung  edges  may  be  so  com- 
pletely pushed  aside  as  to  make  the  entire  cardiac  dulness  superficial, 
as  in  enlargements  of  the  heart  (see  p.  183)  and  pericardial  effusions 
(see  p.  186). 

If  the  heart  is  pushed  upward  by  a  distension  of  the  abdomen,  the 
cardiac  dulness  not  only  lies  higher,  but  also  a])pears  larger — i.  e., 
broader  than  normal.  This  is  partly  due  to  the  retraction  of  the  lung 
edges  away  from  the  heart  in  consequence  of  the  limitation  of  space  in 

^  "Die  physikalischen  Symptome  der  Pleuritis  exsudaliva,"  Habilitutionsfiekri/t,  Mar- 
burg, Elwert,  1875. 


190  PERCUSSION. 

the  thorax  (see  pp.  175,  176,  and  181).  The  heart  dulness  may  even 
be  twisted  by  a  sort  of  pendulum  movement  into  a  horizontal  position, 
because  the  apex  of  the  heart,  ^vhich  lies  upon  the  movable  portion  of 
the  diaphragm,  is  lifted  up  to  the  level  of,  or  even  higher  than,  the 
base. 

TOPOGRAPHIC  PERCUSSION  OF  THE  LIVER. 

NORMAL  LIVER  DULNESS. 

Oinicians  have  often  attempted  to  determine  a  superficial  and  a  deep 
dulness  for  the  liver  just  as  for  the  heart — i.  e.,  to  bound  the  anterior 
surface  lying  directly  against  the  thoracic  and  abdominal  wall,  and  to 
estimate  the  height  to  which  the  liver  in  the  dome  of  the  diaphi'agm  rises 
into  the  thorax.  The  latter  determination  would  be  of  very  little  value 
even  if  it  were  possible.  The  highest  point  of  the  liver  lies  far  removed 
from  the  anterior  thoracic  wall ;  and  in  large  persons  with  well-developed 
chests  it  is  too  remote  for  the  acoustic  range  of  the  percussion  blow. 
Again,  although  we  can  obtain  a  relative  dulness  (a  diminution  of  the 
fulness  of  the  tone)  above  the  lung-liver  boundary  corresponding  to  the 
wedge-shaped  form  of  the  lower  edge  of  the  lung,  yet  the  upper  limit 
of  this  dulness  will  almost  always  be  lower  than  the  highest  point  of 
the  liver.  But,  as  stated  above,  the  estimation  of  the  highest  point  of 
the  liver  is  of  little  value.  The  liver  is  applied  closely  to  the  dia- 
phragm, and  so  the  upper  liver  boundary  merely  coincides  with  the 
position  of  the  diaphragm,  and  we  can  determine  that  accurately  enough 
by  estimating  the  lung-liver  boundary'  and  the  liver  edge.  If  the  dia- 
phragm is  high,  the  lung-liver  boundary  and  the  liver  edge  are  always 
high.  If  the  diaphragm  is  low,  the  reverse  is  true.  The  lower  liver 
boundary,  which  is  generally  easy  to  determine  by  percussion,  usually 
shows  whether  the  organ  is  increased  or  diminished  in  size.  An  enlarge- 
ment of  the  liver  crowds  the  lower  liver  edge  correspondingly  down- 
ward ;  except,  though  rarely,  when  the  muscular  resistance  of  the 
diaphragm  is  diminished — e.  g.,  with  circumscribed  tumors  of  the  upper 
liver  surface,  abscesses,  or  echinococcus  cysts.  Even  here  the  estimation 
of  the  so-called  "  relative  liver  dulness  "  is  apt  to  be  so  unreliable  as 
to  be  of  little  value,  for  the  superficial  lung-liver  boundary  is  probably 
always  somewhat  crowded  by  such  a  growth. 

Ordinarily,  therefore,  we  are  contented  with  estimating  by  percussion 
the  part  of  the  liver  applied  to  the  abdominal  wall  and  situated  beneath 
the  edge  of  the  lung.  Under  favorable  circumstances  we  can  map  out 
a  superficial  dulness  such  as  is  pictured  in  Fig.  79.  At  the  sharp  edge 
of  the  liver  this  dulness  is  so  slight  that  only  very  light  percussion 
appreciates  the  dulled  note,  while  stronger  percussion  sets  the  underlying 
intestines  in  vibration.  In  the  same  way  very  light  percussion  is  essen- 
tial near  the  lung,  for  otherwise  the  resonant  tone  of  the  adjoining  lung 
tissue  obscures  the  dulness.  Stronger  percussion,  however,  brings  out 
very  clearly  the  superficial  liver  dulness  higher  up,  corresponding  to  the 
thickness  of  the  layer  of  the  liver  percussed.  The  upper  borders  of 
the  superficial  liver  dulness  coincide  with  the  lower  borders  of  pulmonary 


TOPOGRAPHIC  PERCUSSION.  191 

resonance.  They  can  be  plainly  demonstrated  from  the  front  to  the 
back.  The  lower  border  of  the  superficial  liver  dulness  ordinarily 
corresponds  to  the  left  boundary  of  the  superficial  cardiac  dulness,  inter- 
secting the  fifth  or  sixth  rib  between  the  left  parasternal  and  the  mam- 
millary  lines  (Fig.  79).  In  the  median  line  it  lies  halfway  between  the 
navel  and  the  base  of  the  xiphoid  process,  sometimes  even  higher.  In 
the  right  mammillary  line  it  reaches  the  edge  of  the  ribs  or  projects 
slightly  below  them,  and  it  lies  upon  the  tenth  rib  at  the  right  middle 
axillary  line.  All  these  measurements  refer  to  patients  who  are  breath- 
ing quietly  and  in  the  recumbent  posture.  The  inferior  edge  of  the 
liver  behind  can  not  usually  be  plainly  demonstrated  on  account  of  the 
thickness  of  the  muscle  layer. 

The  writer  protests  against  making  statements  about  the  absolute 
height  of  the  liver  dulness,  because  no  general  value  can  as  yet  be 
attached  to  such  measurements ;  but  in  concrete  cases  the  vertical 
diameters  of  the  liver  dulness  at  the  different  arbitrary  lines  should  be 
measured  in  order  to  recognize  any  changes  in  the  liver  size  during  the 
observation  of  the  same  case. 

ACTIVE  AND  PASSIVE  MOBILITY  OF  THE  LIVER  DULNESS. 

The  liver  dulness  also  possesses  an  active  mobility  with,  respiration,  and  a 
passive  mobility  with  an  alteration  of  the  patient's  position.  The  active  and 
passive  mobility  of  the  upper  edge  of  the  superficial  liver  dulness  coincides  with 
the  corresponding  mobility  of  the  pulmonary  border  (p.  173  et  seq.).  The  active 
mobility  of  the  lower  liver  border  corresponds  to  the  respiratoiy  mobility  of  the 
dome  of  the  diaphragm,  and  is  much  less  than  that  of  the  pulmonary'  border. 
When  a  patient  lies  upon  his  left  side,  the  passive  mobility  of  the  lower  liver  edge 
is  shown  by  a  depression  of  the  right  lobe.  When  he  lies  upon  the  right  side,  the 
reverse  occurs  (rotation  of  the  liver  about  a  sagittal  axis).  The  liver  is  more 
difficult  to  percuss  in  the  sitting  or  standing  posture,  on  account  of  the  increased 
tension  of  the  abdominal  walls.  The  lower  liver  edge  is  occasionally  elevated  in 
these  positions,  probably  because  the  increased  intra-abdominal  pressure  pushes 
the  liver  to  some  extent  upward.  If  the  abdominal  walls  are  lax,  the  weight 
of  the  liver  produces  the  reverse  etfect.     (See  Lung-liver  Boundary.) 

PATHOLOGIC  DISLOCATIONS  AND   GROSS   CHANGES  IN  THE  LIVER 

DULNESS. 

In  "  situs  inversus  "  the  liver  lies  in  the  left  upper  abdomen,  sym- 
metric with  its  normal  position.  Its  dulness  corresponds  to  the  reversed 
position.  Free  air  in  the  abdominal  cavity  nearly  obliterates  the  liver 
dulness,  because  the  air  will  be  collected  at  the  highest  points.  (See  the 
Section  upon  Comparative  Percussion  of  the  Abdomen.) 

Changes  of  the  Upper  Border  of  the  Superficial  I/iver 
Dulness. — The  upper  border  apparently  iies  higher  than  normal  if  a 
pathologic  dulness  from  the  thoracic  organs  (pleural  effusions  or  lung 
consolidation)  is  superimposed  upon  the  liver  dulness.  It  is  therefore 
necessary  to  resort  to  other  methods  of  examination  to  determine  whether 
it  is  a  genuine  high  liver  dulness  or  a  normal  liver  dulness  plus  a  patho- 
logic pulmonary  or  pleural  dulness  (see  below). 

The  upper  border  will  be  higher  if  the  liver  is  pushed  upward  hi 


192  PERCUSSION. 

toto — e.  g.,  by  increased  abdominal  tension.  In  this  case  the  liver  will 
ordinarily  be  rotated  about  a  frontal  axis,  so  that  its  inferior  edge  i& 
elevated  still  more  than  the  lung-liver  boundary,  and  the  vertical 
breadth  of  the  liver  dulness  appears  abbreviated  (angular  position  of 
the  liver).  If,  at  the  same  time,  the  liver  is  enlarged,  despite  its  being^ 
canted  upward,  the  lower  edge  may  stand  at  its  normal  place  or  even 
lower. 

Pulmonary  retraction  will  also  cause  a  higher  position  of  the  lung- 
liver  boundaries. 

A  mere  enlargement  of  the  liver  without  marked  increase  of  the  intra- 
abdominal pressure — i.  e.,  without  the  liver  being  pushed  upward — will 
not  ordinarily  cause  an  elevation  of  the  lung-liver  boundaries,  because 
the  organ  will  naturally  enlarge  in  the  direction  of  the  least  resistance 
and  not  against  the  diaphragm.  If  such  an  enlargement  of  the  liver 
occurs  so  rapidly  that  its  ligaments  are  not  quickly  enough  stretched,  a 
marked  increase  upward  will  result — e.  g.,  most  frequently  in  unequal 
enlargements  of  the  upper  surface  of  the  liver,  which  cause  a  localized 
pressure  (tumors,  echinococcus  cysts,  and  abscesses  of  the  convexity). 
In  most  of  these  cases,  however,  the  lower  edge  of  the  liver  will  alsa 
be  pushed  downward.  Subphrenic  abscesses  produce  practically  identical 
percussion  results  with  those  obtained  in  tumors  of  the  convexity. 

Emphysema,  either  by  crowding  the  diaphragm  m  toto  downward  or 
by  filling  the  pleural  sinus  more  completely  with  lung,  will  depress  the 
upper  border  of  the  superficial  liver  dulness  to  a  variable  degree, 
depending  upon  which  of  these  possibilities  is  present.  Pneumothorax 
effects  a  similar  result.  Lessening  of  the  intra-abdominal  pressure,  and 
exceptionally  enter ojdosis,  will  also  depress  the  upper  liver  border. 

Changes  in  the  iower  Border  of  the  Superficial  I^iver 
Dulness. — We  have  discussed  some  of  these  in  the  preceding  section. 
They  depend  either  upon  a  dislocation  of  the  liver,  a  change  in  its  size, 
or  upon  an  association  of  these  conditions.  A  careful  attention  to  the 
entire  clinical  picture  will  differentiate  these  different  conditions — e.  g., 
the  etiology  (alcohol,  anemia  versus  pleural  effusion,  ascites,  tympanites), 
the  accompanying  relations  (stasis),  a  palpatory  appreciation  of  altera- 
tions in  the  consistence  (cirrhosis,  carcinoma). 

If  the  dislocating  cause  evenly  affects  the  entire  upper  or  lower  sur- 
face, the  lower  edge  of  the  liver  will  be  pushed  upward  or  downward 
as  a  whole — i.  e.,  symmetric  and  parallel  to  its  former  position  (meteor- 
ism,  ascites,  emphysema).  If,  on  the  contrary,  the  pressure  acts 
unevenly,  the  organ  will,  by  virtue  of  its  attachments,  be  dislocated  in 
an  asymmetric  fashion. 

Accumulations  of  air  or  fluid  in  the  right  pleural  cavity  exceptionally 
rotate  the  liver  about  a  sagittal  axis.  Conversely,  a  left  pleuritic  or  left 
pericardial  effusion  will  sometimes  depress  the  left  half  of  the  liver. 
Similarly,  though  in  a  reversed  way,  a  one-sided  pulmonary  retraction 
will  elevate  the  liver. 

Solid  masses  beneath  the  liver  (packed  intestines,  tumors  of  the 
omentum,  of  the  colon,  of  the  stomach,  and  the  like)  may  increase  the 


TOPOGRAPHIC  PERCUSSION.  193 

liver  dulness  downward.     Palpation  or  a  carefully  repeated  examination 
generally  discloses  the  true  condition. 

Conversely,  intestines  distended  with  air,  overlying  the  liver  and 
hiding  part  of  it,  may  simulate  a  high  position  of  the  liver  edge. 


TOPOGRAPHIC  PERCUSSION  OF  THE  SPLEEN. 

NORMAL  SPLENIC  DULNESS ;  HALF-MOON-SHAPED  (TRAUBE'S)  SPACE. 

The  spleen  lies  in  the  left  hypochondrium,  between  the  ninth  and  the 
eleventh  rib  (Fig.  75).  Its  long  diameter  ordinarily  corresponds  to  the 
tenth  rib.  Its  posterior  extremity  is  situated  only  a  few  centimeters 
from  the  spinal  column.  Its  anterior  extremity  reaches  only  to  the 
middle  or,  at  most,  to  the  anterior  axillary  line.  In  relation  to  the 
course  of  the  ribs,  the  long  axis  of  the  organ  runs  from  behind  and 
above  forward  and  downward.  The  posterior  upper  third  of  the  spleen 
lies  hidden  under  the  edge  of  the  lung.  The  front  and  lower  two-thirds 
ordinarily  lie  against  the  thoracic  wall  unless,  as  very  frequently  hap- 
pens, intestines  have  pushed  in  between  the  thorax  and  the  spleen. 

Percussion  can  only  differentiate  that  portion  of  the  spleen  which  is 
uncovered  by  lung.  Hence,  it  merely  estimates  a  superficial  dulness 
which  can  be  accurately  determined  only  by  very  light  percussion  (see 
p.  160). 

To  map  out  the  free  part  of  the  spleen  as  perfectly  as  possible  by 
means  of  percussion,  the  patient  should  be  sitting,  standing,  or  lying 
somewhat  upon  the  right  side  (the  so-called  oblique  position),  because 
in  the  directly  recumbent  position  the  posterior  portions  of  the  spleen 
are  not  accessible  to  percussion.  The  right  oblique  position  has  the 
advantage  that  the  contents  of  a  well-filled  stomach  are  pushed  aside, 
and  so  do  not  simulate  an  enlarged  splenic  dulness. 

The  normal  splenic  dulness  in  the  sitting  or  standing  posture  is  pict- 
ured in  Fig.  80.  The  upper  boundary  of  the  dulness  corresponds  to 
that  portion  of  the  lung  edge  which  intersects  the  eighth  and  ninth  ribs, 
and  runs  from  the  middle  to  the  posterior  axillary  line.  The  anterior 
border  of  the  dulness  rarely  reaches  the  anterior  axillary  line  ;  in  adults 
it  is  about  5  cm,  distant  from  the  costal  margin.  The  dulness  reaches 
as  low  as  the  eleventh  rib.  Measured  in  the  long  axis  of  the  body,  the 
height  of  the  dulness  varies  between  5  and  6  cm.  Posteriorly  the 
splenic  dulness  merges  into  that  of  the  lumbar  region,  due  to  the  thick 
layers  of  muscles,  not  to  the  kidneys  (see  p.  195  et  seq.). 

The  splenic  dulness  is  but  sh'ghtly  dislocated  either  upward  or  down- 
ward in  changing  from  the  sitting  or  standing  to  the  reclining  posture. 
In  such  cases  it  follows  the  same  laws  as  the  liver  dulness,  and  moves 
as  a  whole  up  or  down  (see  p.  190).  The  anterior  boundary  then  usually 
remains  the  same.  The  s])lenic  dulness  is  only  slightly  dislocated  for- 
ward and  downward  in  the  ol^lique  and  lateral  postures,  because,  although 
the  left  lung  then  assumes  a  deeper  position,  at  the  same  time  more  of 
the  upper  part  of  the  spleen  is  covered  by  the  lung.     A  splenic  dulness 

13 


194  PERCUSSIOm 

which  projects  beyond  the  anterior  axillary  line,  even  in  the  oblique 
and  lateral  posture,  is  abnormal. 

The  beginner  should  practice  splenic  percussion  upon  patients  first 
in  one  position,  then  in  another,  in  order  to  control  the  results. 

It  is  useless  to  attempt  to  map  out  the  portion  of  the  spleen  lying  above  the 
edge  of  the  lung — ^.  e. ,  to  determine  a  deep  splenic  dulness.  The  spleen  is  a  com- 
paratively small  organ,  covered  outside  by  the  lung,  and  inside  in  contact  with  the 
stomach  and  intestines,  so  that  a  percussion  stroke  strong  enough  to  penetrate 
through  the  lung  would  set  the  tympanitic  stomach  into  vibration.  Besides,  the 
differentiation  of  that  part  of  the  spleen  covered  by  the  lung  has  no  practical  value, 
because,  just  as  in  the  case  of  the  liver,  any  alterations  can  be  easily  recognized 
in  the  parts  lying  free  (see  p.  190). 

Percussion  of  the  spleen  is  frequently  not  as  simple  as  the  above 
description  would  indicate.  The  spleen  may  be  abnormally  broad 
behind,  or  may  lie  abnormally  high,  so  that  it  practically  escapes  per- 
cussion, and  still  be  within  physiologic  limits  of  size.  With  meteorism, 
when  the  distended  intestines  push  the  spleen  upward  and  backward  or 
crowd  between  the  spleen  and  the  thoracic  wall,  the  vibration  of  such 
large  air-containing  cavities  may  make  it  almost  impossible  to  differ- 
entiate so  thin  a  solid  organ  as  the  spleen.  Again,  solid  or  fluid  stom- 
ach or  intestinal  contents  sometimes  simulate  a  splenic  dulness.  The 
right  oblique  position  will  generally  prevent  confusion  on  account  of 
stomach  contents,  and  repeated  examination  will  show  the  true  state  of 
affairs  in  regard  to  the  intestinal  contents.  Despite  every  care,  however, 
we  must  confess  that  palpation  is  very  much  more  trustworthy  than 
percussion  of  this  organ. 

Between  the  splenic  dulness  and  the  left  end  of  the  liver  dulness 
there  is  normally  a  tympanitic  area  due  to  the  stomach  or  intestines. 
This  space  is  bounded  above  by  the  lung  border,  below  by  the  free 
costal  margin,  and  is  called  the  half-moon-shaped  or  Traube's  space. 
It  is  important  in  the  diagnosis  of  left-sided  pleuritic  exudations  (Figs. 
79,  80,  and  95).  Percussion  cannot  always  diflPerentiate  this  space  above 
from  the  lung ;  but  then  a  boundary  line  can  always  be  constructed 
corresponding  to  the  edge  of  the  right  lung. 

PATHOLOGIC  GROSS  CHANGES  AND  DISLOCATIONS  OF  THE  SPLENIC 

DULNESS. 

Enlargement  of  the  spleen  is  ordinarily  evident  by  an  increase  in 
the  splenic  dulness  forward  and  downward  (Fig.  93).  If  the  splenic 
dulness  projects  forward  beyond  the  anterior  axillary  line,  or  if  its  ver- 
tical extent  in  adults  measures  more  than  7  cm.,  the  spleen  can  be 
considered  increased  in  size. 

Diminution  or  even  a  complete  disappearance  of  the  splenic  dulness  happens 
frequently  enough  in  perfectly  healthy  men  with  normal  spleens.  It  has  no  clini- 
cal importance. 

Pathologic  dislocations  of  the  spleen  are  of  slight  clinical  importance.  They 
are  mostly  difficult  to  demonstrate.  Although  pleural  effusions,  ascites,  meteor- 
ism,  and  tumors  may  dislocate  the  spleen,   percussion  will  rarely  be  of  much 


TOPOGRAPHIC  PERCUSSION. 


195 


help,  because  either  another  dulness  occupies  the  place  of  the  spleen,  or  else  there 
is  a  resonant  note  (meteorism). 

The  spleen  is  sometimes  dragged  downward  and  forward,  with  a  marked  dila- 
tation of  the  stomach,  by  stretching  the  ligamentum  gastrolienale.  It  will  then  be 
more  accessible  than  normally  to  percussion  and  palpation.  (See  later,  Examina- 
tion of  the  Stomach.) 

Large  pleural  effusions  occasioning  a  dulness  in  Traube's  space,  as  well  as  en- 


FiG.  93.— The  splenic  dulness  in  diflFerent  grades  of  splenic  enlargement  (a,  6,  c,  d). 

largements  of  the  liver,  may  cause  the  hepatic  and  splenic  dulness  to  merge  (see 
Fig.  95).  Under  these  circumstances  percussion  may  not  detect  even  enormous 
enlargements  of  the  spleen. 


TOPOGRAPHIC  PERCUSSION  OF  THE  KIDNEYS. 

The  anatomic  position  of  the  kidneys  (Fig.  76)  shows  how  impos- 
sible it  is  to  limit  their  boundaries  by  percussion.  Their  deep  position 
prevents  percussion  from  in  front,  and  the  thick  layers  of  muscles  behind 
produce  a  dulness  which  such  a  thin  structure  as  a  kidney  could  not 
increase.  If  we  percuss  a  patient  whose  kidney  has  been  removed,  we 
can  demonstrate  the  same  vertical  line  of  dulness  as  in  a  patient  Avith 
an  intact  kidney.  It  corresponds  to  the  outer  edge  of  the  sacrospinal 
muscles  and  has  nothing  to  do  with  the  kidney.  Large  renal  tumors 
aiford  an  intense  dulness  in  the  loins,  projecting  far  beyond  the  bound- 
aries of  the  sacrospinal  muscles.  If  the  tumor  has  pushed  the  other 
abdominal  viscera  aside  and  lies  against  the  abdominal  wall,  it  can  be 
demonstrated  from  in  front.  Here  it  is  of  special  diagnostic  importance 
to  demonstrate  by  percussion   that  the  colon  is  anterior  to  the  kidney 


196  PERCUSSION. 

(see  below).     Palpation  is,  however,  far  more  important  than  percussion 
in  this  instance,  as  in  the  diagnosis  of  all  other  abdominal  tumors. 

TOPOGRAPHIC  PERCUSSION  OF  AIR-CONTAINING  ABDOMINAL 

VISCERA. 

(See  also  section  upon  Examination  of  the  Stomach.)  Percussion  is 
of  no  value  for  distinguishing  one  of  these  organs  from  the  other,  except 
under  certain  quite  well-recognized  conditions — viz.,  where  the  stomach 
or  separate  sections  of  the  intestines  are  filled  with  air,  fluid  or  solid 
contents.  And  then  only  superficial  boundaries  (i.  e.,  with  light  per- 
cussion) can  be  accurately  estimated,  because  stronger  percussion  trans- 
mits the  vibrations  unexpectedly  in  all  directions.  Even  superficial 
percussion  is  quite  untrustworthy,  because  physiologically  the  position 
of  the  stomach  and  intestines  varies  considerably ;  because  their  super- 
ficial boundaries  are  rarely  sharp ;  and  because  although  at  different 
portions  of  the  intestines  the  tympanitic  tone  varies  in  intensity  and 
pitch  it  is  impossible  to  differentiate  one  region  from  the  other.  We  can 
usually  distinguish  the  swollen  stomach  or  the  distended  colon  from  the 
small  intestines  by  ordinary  percussion.  If  this  is  not  possible,  the 
stick-pleximeter  percussion  or  the  auscultatory  percussion  (see  p.  158) 
will  differentiate  them,  provided  there  is  increased  tension  enough  to 
produce  a  metallic  resonance  over  the  air-containing  intestines.  Both 
these  methods  of  examination  elicit- either  a  sharp  rise  in  the  tone  height 
of  the  metallic  resonance  or  a  sudden  cessation  of  the  resonance  at  the 
edges  of  the  organs.  However,  every  spot  over  a  hollow  organ  does 
not  necessarily  give  the  same  pitch  of  metallic  resonance.  Metallic 
resonance  over  an  air  cavity  may  be  present  or  lacking ;  and,  again, 
its  pitch  may  differ  over  different  places  of  the  organ,  especially  if 
it  is  large.  If  we  trace  the  course  of  the  colon  distended  with  gas, 
by  means  of  the  stick-pleximeter  percussion,  we  often  can  appreciate 
entire  scales  of  metallic  resonance.  Different  pitches  may  be  present 
even  over  the  stomach.  Hence,  the  value  of  this  examination  method 
must  be  limited,  although  we  may  make  it  easier  by  dilating  the  stomach 
or  colon  with  air.  (See  Palpation  of  the  Abdomen  and  Examination 
of  the  Stomach.) 

The  demonstration  by  percussion  of  the  tympanitic  colon  anterior  to 
a  kidney  tumor  is  very  valuable  for  diagnosis  (Fig.  109).  It  is  safer  to 
percuss  both  before  and  after  distending  the  colon  with  water  and  then 
with  air. 

Inspection  and  -palpation  generally  furnish  better  evidence  of  the 
extent,  position,  and  peculiarity  of  the  stomach  and  intestines  than 
percussion.      (See  here  special  section,  Examination  of  the  Stomach.) 

TOPOGRAPHIC    PERCUSSION    OF  THE    BLADDER    AND    OF  THE 

UTERUS. 

The  bladder  when  empty  lies  well  hidden  behind  the  symphysis 
pubis.      When   filled   it   ascends,   even    reaching    in    cases  of   urinary 


COMPARATIVE  PERCUSSION.  197 

retention  above  the  navel.  As  it  rises  it  pushes  the  intestines  aside  and 
lies  against  the  abdominal  wall  in  the  form  of  a  vertically  placed  oval 
tumor,  furnishing  an  intense  dulness  to  faint  percussion,  which  corre- 
sponds pretty  accurately  to  its  extent  and  shape.  If  not  very  markedly 
distended  and  if  some  loops  of  intestines  lie  between  it  and  the  abdomi- 
nal wall,  part  of  the  dulness  may  be  deep  (plainer  to  strong  percussion), 
or  there  may  even  be  no  dulness  present. 

According  to  Miiller's  investigations,  a  bladder  must  contain  between 
500  and  600  c.c.  before  it  will  produce  an  appreciable  dulness  in  nor- 
mally developed  women,  and  360  to  500  c.c.  in  men.'  If  the  rectum 
is  distended,  the  bladder  dulness  projects  somewhat  more  to  the  right. 
In  lateral  positions  it  is  depressed  to  the  deeper  side,  sinking  at  the 
same  time  somewhat  into  the  depth  of  the  pelvis,  and  so  appearing 
smaller. 

The  condition  of  the  bladder  can  be  determined  more  accurately  by 
palpation  than  by  percussion  unless  the  tension  is  very  great  or  the 
abdominal  walls  very  thick. 

The  pregnant  or  pathologically  enlarged  uterus  acts  like  the  bladder 
to  percussion,  and  can  be  distinguished  from  it  only  by  careful  atten- 
tion to  other  clinical  relations,  by  determination  of  the  consistence,  by 
means  of  palpation,  by  vaginal  examination,  and  by  catheterization. 

COMPARATIVE  PERCUSSION. 

Comparative  percussion  is  concerned  with  the  qualitative  changes  of 
the  percussion  tone  over  one  and  the  same  organ,  and  the  conclusions 
to  be  drawn  from  such  changes  in  regard  to  the  peculiarity  of  the  organ 
and  its  surroundings.  Topographic  percussion,  as  we  have  seen,  fur- 
nishes us  with  conclusions  as  to  borders — i.  e.,  as  to  the  size  and  posi- 
tion of  organs.  In  comparative  percussion  we  compare  the  tone  over 
a  certain  spot  of  the  body  with  the  normal  tone  over  this  spot,  or  with 
the  tone  over  adjacent  parts  of  similar  organs  which  are  normal.  In 
the  case  of  solid  organs  percussion,  of  course,  can  only  bound  them — 
i.  e.,  determine  their  size,  not  their  structure — and  for  this  purpose 
topographic  percussion  is  all  that  is  essential.  But  with  the  air-con- 
taining organs  of  the  abdomen,  and  especially  those  of  the  thorax — the 
lungs — we  may  determine  countless  quantitative  and  qualitative  modi- 
fications of  the  percussion  note  which  will  furnish  us  most  important 
information  about  pathologic  changes  at  their  surface  or  in  their  interior. 

COMPARATIVE  PERCUSSION  OF  THE  THORAX. 

The  ordinary  lung  tone  is  resonant,  loud,  not  tympanitic.  The 
resonance  or  loudness  varies  with  the  thickness  of  the  covering,  and  is 
also  influenced  by  the  adjacent  organs  (heart,  liver,  etc.).  Beneath 
thick  muscles  or  fat — e.  g.,  over  the  scapula  and  over  the  female  breast^ — 
the  percussion  tone  is  less  resonant  than  at  other  places.  The  intense 
dulness  of  the  pulmonary  tone  in  such  spots  can  be  modified  only  by 
1  Berlin,  kiln.  Woch.,  1895,  No.  13,  p.  278. 


198  PEECUSSIOK 

very  vigorous  percussion.  Again,  the  pulmonary  tone  is  necessarily 
less  resonant  (see  pp.  190  et  seq.,  pp.  162,  178)  over  areas  where  the 
pulmonary  tissue  is  thin — e.  g.,  the  tone  over  the  normal  apices  is  faint 
compared  with  the  loud  tone  over  more  voluminous  portions  of  the 
lung.  The  examiner's  ear  gradually  accustoms  itself  to  these  physio- 
logic diiferences,  so  that  they  are  no  longer  heeded.  Marked  convexity 
of  the  thoracic  wall  will  cause  a  certain  dulness — e.  g.,  in  kyphotic  and 
scoliotic  patients.  If  we  percuss  upon  a  markedly  convex  spot  of  the 
thorax,  a  part  of  the  percussion  force  is  lost,  because  such  places  yield 
so  little ;  whereas  a  flat  section  of  a  rib  oscillates  to  percussion  in  the 
direction  of  its  greatest  elasticity.  So  we  must  be  careful  in  drawing 
conclusions  from  the  tones  obtained  over  kyphoscoliotic  chests  and  over 
physiologically  altered  thoraces. 

Every  structural  change  of  the  lung  itself  has  an  important  influ- 
ence upon  the  character  of  the  pulmonary  tone,  which  may  become 
abnormally  resonant,  tympanitic,  or  more  or  less  dulled.  The  change 
can  be  appreciated  by  comparing  the  tone  with  that  over  either  sym- 
metric or  neighboring  areas.  Wherever  the  changes  in  the  tone  include 
an  entire  lung,  the  beginner  must  compare  the  tone  with  that  of  a 
healthy  person.  To  the  skilled  these  variations  from  the  normal  are 
easily  appreciated  without  such  comparison. 

APPEARANCE  OF  A  DULLED  NOTE  WITHIN  THE  LUNG  BOUNDARIES. 

In  order  not  to  overlook  slight  dulnesses,  it  is  always  a  good  rule 
to  utilize  percussion  of  varying  strengths.  To  make  clear  the  im- 
portance of  this  precaution,  it  is  necessary  to  enumerate  the  different 
anatomic  possibilities  which  can  produce  a  dulness  in  the  lung  tone. 

"Whenever  the  acoustic  range  of  the  percussion  blow  includes  a 
smaller  amount  of  air-containing  lung  tissue,  or  an  area  containing  less 
air  than  normally,  the  tone  will  be  dulled  (p.  162  et  seq.).  This  may 
be  caused : 

1.  By  the  interposition  of  airless  material  between  the  lung  and  the 
thoracic  wall :  exudations,  adhesions,  tumors  (Fig.  94,  I.). 

2.  By  diminution  or  absence  of  air  in  the  lung  parenchyma  itself 
— e.  g.,  in  atelectasis  (collapse  of  the  alveoli),  from  compression  or  from 
closure  of  the  bronchi  with  consequent  resorption  of  the  air ;  in  pneu- 
monia, from  the  filling  of  the  alveoli  with  an  airless  inflammatory  exu- 
date ;  in  carcinoma,  from  the  newly  formed  tumor  tissue  taking  the 
place  of  the  lung  tissue.  These  changes  may  occur  in  large  areas  which 
reach  the  surface  of  the  lung  (Fig.  94,  II.) ;  iu  small  scattered  areas 
(lobular),  partly  at  the  surface,  partly  separated  from  it  by  lung  tissue 
still  containing  air  (Fig.  94,  TIL)  ;  or,  finally,  in  still  larger  areas 
situated  iu  the  depths  of  the  lung  (Fig.  94,  IV.).  Each  of  these  cases 
will  furnish  diiferent  percussion  results. 

If  we  percuss  vigorously  at  6  (Fig.  94,  I.),  provided  the  exudate  is 
not  too  thick,  the  lung  can  be  so  strongly  vibrated  that  the  dulness  Avill 
be  completely  overlooked.  To  differentiate  such  a  dulness  as  sharply 
as  possible  from  the  surroundings  we  should  here  percuss  as  lightly  as 


COMPARATIVE  PERCUSSION. 


199 


possible.  The  same  holds  good  for  the  condition  represented  in  Fig. 
94,  II.  The  duluess  is  superficial  in  both  instances,  and  can  be  best 
attained  by  carefully  regulating  the  acoustic  range  of  the  percussion 


Thoracic 
wall 


I.  Pleural  exudation:  ^,  Acoustic  sphere  of 
action  of  light  percussion  ;  B,  compressed  lung ; 
C,  pleural  exudation. 


Diaphragm 


II.  Superficial  infiltration  area :  A, 
Acoustic  sphere  of  action  of  light  per- 
cussion ;  B,  B,  air-containing  lung 
tissue ;  C,  infiltrated  lung  tissue. 


s.Diaphragm 
III.  Disseminated  small  areas  of  consoli- 
dation :  a,  Sphere  of  action  of  strong,  b,  of 
weak,  percussion  ;  A,  A,  air-containing  lung 
tissue ;  B,  small  infiltration  area. 


Thoracic 
wall 


"Diaphragm 

IV.  Larger  areas  of  consolidation  lying 
deeper:  a,  Sphere  of  action  of  weak,  b, 
of  strong,  percussion;  ^,  ^,  air-contain- 
ing lung  tissue  ;  B,  infiltrated  lung  tissue. 


Fig.  94.— The  different  varieties  (L  e.,  methods  of  origin)  of  dulling  the  lung  tone.  Diagram- 
matic frontal  section  through  the  thorax :  I.,  Pleural  exudation ;  II.,  III.,  IV.,  pulmonary  infil- 
tration. 

blow  so  that  its  longest  diameter  will  not  overstep  the  solid  portion,  as 
in  Fig.  94,  II. 

In  Fig.  94,  III.,  no  very  marked  dulness  can  be  evoked  either  by 
light  (6)  or  by  strong  («)  percussion  ;  both  types  will  furnish  only  a 
slight  dulness,  because  air-containing  tissue  will  still  be  vibrated.  The 
results  of  light  or  strong  percussion  will  vary  with  the  position  of  the 
infiltrated   area,  whether  it  is  near  the  surface  or  not.     If  the  solid 


200  PEECZTSSION. 

area  as  a  whole  is  not  very  extensive,  light  percussion  will  bring  out  the 
dulness  more  plainly,  because  less  air-containing  tissue  in  the  interior 
will  be  set  in  vibration. 

Light  percussion  (acoustic  range  a)  will  demonstrate  nothing  with 
a  larger,  deeply  placed  area,  as  in  Fig.  94,  IV.  ;  but  strong  percussion 
(acoustic  range  b)  will  demonstrate  a  relative  dulness.^ 

Of  course,  we  do  not  know  beforehand  whether  there  is  any  dul- 
ness, or  if  so  what  kind  of  dulness ;  therefore  it  is  always  advisable  to 
employ  different  strengths  of  percussion  in  succession.  Then  we  can 
draw  conclusions  as  to  the  cause  and  position — deep  or  superficial — of 
the  dulness. 

It  is  not  to  be  expected  that  percussion  can  demonstrate  every  small 
area  of  consolidation.  In  fact,  experience  teaches  us  that  isolated 
areas  of  consolidation,  even  though  superficially  located,  to  be  appre- 
ciated must  have  a  flattened  extent  of  at  least  afeic  square  centimeters. 
If  they  lie  deeper,  they  must  naturally  be  larger.  But  there  are  no 
generally  applicable  rules.  For  instance,  multiple  areas,  if  scattered 
thickly  enough,  need  not  be  nearly  so  large  as  single  areas  to  cause 
a  diminution  of  the  resonance — e.g.,  a  lung  richly  sprinkled  with 
miliary  tubercles  will  sometimes  give  a  relatively  dulled  tone.  On  the 
contrary,  even  very  thickly  spread  small  areas  at  other  times  will  cause 
no  dulness.  The  writer  has  watched  cases  where  the  pulmonary  reso- 
nance was  absolutely  normal  during  life,  and  yet  the  autopsies  showed 
that  the  lungs  were  completely  infiltrated  with  sarcomatous  nodules  the 
size  of  nuts.  There  are  many  other  important  factors  in  this  connec- 
tion besides  the  amount  of  air  contained  in  the  lungs.  For  example,  a 
relaxation  of  the  lung  tissue  adjacent  to  solid  areas  will  make  the  tone 
more  resonant  than  normal  (see  p.  210),  and  this  hyperresonance  of  the 
tone  may  offset  the  dulness  from  disseminated  tumor  nodules  or  inflam- 
matory infiltrations. 

In  most  cases  other  methods  of  examination  must  be  resorted  to  in 
order  to  appreciate  the  causes  of  dulness.  The  most  important  charac- 
teristics of  the  different  kinds  of  dulness  of  the  lung  tone  will  be  men- 
tioned in  the  following  sections  : 

Pleuritic  Dulness. 

Early  in  its  formation  a  pleuritic  effusion  furnishes  a  dulness  in  the 
lower  posterior  part  of  the  thorax.  This  gradually  rises  higher,  and 
pushes  further  forward,  the  boundary  line  running  downward  and  for- 
ward (Figs.  95,  97,  I.,  II.).  If  the  effusion  increases  still  farther  the 
dulness  increases  forward,  until  finally  the  greater  part  of  that  side  of 
the  thorax  is  dull,  except  that  a  slightly  resonant  tone  can  be  elicited  in 
the  upper  portions.  Exceptionally  the  dulness  may  run  circularly 
around  the  thorax  instead  of  bowing  down  toward  the  front. 

^  [Forcible  percussion  over  the  lung  area,  although  sometimes  necessary,  on  account 
either  of  muscular  development  or  an  excess  of  fat,  is  generally  inaccuj-ate.  Even  in 
mapping  out  the  area  of  deep  cardiac  dulness,  light  percussion  is  usually  preferable. — Ed.] 


COMPARATIVE  PERCUSSION.  201 

Why  this  dulness,  which  represents  the  position  of  the  border  of  the 
exudate,  forms  such  an  oblique  line  has  been  a  mooted  question.  The 
ordinary  supposition  is  that  the  force  of  gravity  determines  the  position 
of  the  exudate,  and  that  its  peculiar  obliquity  is  essentially  produced 
by  the  patient's  position  during  the  development  of  the  exudation, 
and  then  fixed  by  encapsulation.  If,  then,  a  patient  during  the 
entire  course  of  a  slowly  developing  exudation  be  walking  about,  we 
should  naturally  suppose  that  the  law  of  gravity  would  produce  a  hori- 
zontal position  for  the  fluid.  As  in  most  cases,  however,  patients  remain 
in  bed  in  the  slightly  raised  position,  the  line  running  downward  and 
forward  would  correspond  to  a  horizontal  one  for  them.  But  this  theory 
will  not  hold,  for  even  if  patients  do  walk  about  during  the  formation 
of  an  exudation,  the  same  curved  line  is  almost  always  seen.  Therefore 
another  explanation  of  this  appearance  must  be  assumed.  Probably 
the  following  supposition  is  correct.  Normally  the  surface  of  the  lungs 
is  kept  applied  to  the  costal  pleura  by  the  difference  between  the  air 
pressure  and  the  power  of  retraction  or  elasticity  of  the  lungs.  Now, 
it  is  physically  impossible  that  the  elasticity  in  so  irregularly  shaped  an 
organ  as  the  lung  should  be  at  all  points  of  the  surface  equal.  And 
wherever  the  retraction  power  of  the  lung  is  stronger,  there  it  is  that 
more  of  the  intrabronchial  air  pressure  will  be  borne,  because  less  physi- 
cal resistance  prevents  a  mechanical  separation  of  the  pleura  pulmonis 
from  the  pleura  costalis.  The  posterior  more  voluminous  parts  of  the 
lungs  undoubtedly  possess  the  strongest  retraction  power,  so  that  the 
exudation  behind  finds  the  least  resistance  to  its  formation  and  accumu- 
lation. Thus,  the  boundary  line  bends  downward  and  forward.^  In 
favor  of  this  supposition  is  the  fact  that  the  exudation  is  not  only  higher 
but  also  thicker  behind. 

[Hills'  I/ine. — In  America  the  line  of  pleuritic  dulness  was  first 
described  by  Calvin  Ellis,  at  the  March  meeting,  1873,  of  the  Boston 
Society  for  Medical  Improvement.^  He  said  :  "  When  a  pleural  effu- 
sion is  small  it  may  occupy  a  conical  portion  of  the  pleural  cavity  in 
the  subaxillary  region,  where  respiration  and  resonance  may  be  wanting. 
But  in  a  certain  number  of  cases,  when  the  effusion  is  quite  large,  if  an 
accurate  line  be  drawn  the  flatness  will  be  found  to  describe  a  curve^ 
gradually  approaching  the  spine  toward  the  base  of  the  chest,  leaving 
a  space  from  1  to  3  in.  broad  between  the  spine  and  the  line  of  flatness. 
In  this  space  resonance  will  still  be  detected  and  respiration  heard." 

In  a  letter  to  the  editors  of  the  Boston  Medical  and  Surgical  Journal, 
January  23,  1874,  Dr.  George  W.  Garland  reported  a  series  of  experi- 
ments on  lungs  of  animals,  in  which  he  claims  to  have  explained  the 
curved  line  of  dulness  described  by  Ellis. 

In  a  manual  entitled  Pneumo- Dynamics,  by  G.  W.  Garland,  January 
7,  1877,  p.  6,  the  author  says  that  this  line  was  first  described  by 
Damoiseau,  of  Paris,  and  redescribed  by  Ellis,  of  Boston.  The  latter 
was  the  first  to  trace  its  true  shape. — Ed.] 

1  Ellis's  or  Garland's  line  is  the  term  generally  used  in  America. 
"^Boston  Med.  and  Surg.  Jour.,  Jan.  1,  1873. 


202 


PERCUSSION. 


In  dropsical  effusions,  hydrothorax  (see  p.  205  et  seq.),  the  level  of 
the  fluid,  to  be  sure,  sometimes  becomes  horizontal,  accurately  corre- 
sponding to  the  position  of  the  patient ;  but,  of  course,  the  influence  of 
gravity  must  be  remarkably  strong  upon  a  large  dropsical  effusion.  In 
an  early  case  of  hydrothorax,  where  there  is  only  a  slight  amount  of 
fluid,  the  line  of  dulness  follows  practically  the  same  curve  as  in  an 
exudation.  Since  there  are  no  adhesions,  and  since  the  fluid  is  free  and 
movable,  we  should  suppose  that  it  would  follow  the  law  of  gravity. 
The  reason  why  it  does  not  must  depend  upon  the  force  with  which  the 
border  of  the  lungs  is  pressed  against  the  thorax.     Even  a  large  exudate 


Fig.  95. — Shape  of  dulness  in  a  fresh  pleural  effusion.    Ellis's  or  Garland's  line  :  a,  a,  represents 
the  upper  border  of  dulness  in  a  small  effusion;  6,  b,  the  border  in  a  larger  effusion. 


usually  persists  in  showing  this  curved  line  of  dulness,  probably  because 
adhesions  of  the  pleural  surfaces  are  formed  almost  immediately,  and 
these  adhesions  are  only  very  slowly  dissolved  by  the  increasing  exu- 
date ;  whereas  in  a  hydrothorax  without  adhesions  the  fluid  meets  with 
no  marked  resistance,  and  so  follows  the  laM^s  of  gravity  more  com- 
pletely. Moreover,  in  moderate-sized  hydrothorax  we  can  often  enough 
prove  that  the  change  of  level  due  to  gravity  only  very  gradually  fol- 
lows, showing  that  the  anterior  portion  of  the  lung  still  opposes  a  cer- 
tain resistance  to  the  dislocation  of  the  fluid.  The  cases  where  the  level 
of  dulness  is  horizontal  are  but  rarely  due  to  pleurisy,  nor  are  they 


COMPARATIVE  PERCUSSION. 


203 


limited  to  patients  who  go  about  during  the  formation  of  the  exudation. 
In  such  instances  some  abnormal  resistances  behind — e.  g.,  old  adhesions 
or  pulmonary  changes — probably  oppose  the  collection  of  the  exudation. 
All  possible  anomalies  in  the  form  of  the  dulness  may  be  thus  explained. 

Besides  the  peculiarity  of  the  boundary  line,  large  pleuritic  exuda- 
tions are  characterized  by  the  marked  intensity  of  the  dulness  (flatness). 
We  seldom  meet  so  intense  a  dulness  (the  peculiar  thigh  tone)  in  con- 
solidation of  the  lungs,  because  ordinarily  in  the  latter  case  the  bronchi 
still  contain  air  and  percussion  still  produces  a  certain  amount  of 
resonance. 

Of  still  more  importance,  however,  in  distinguishing  pleural  exuda- 
tions from  pneumonia  is  the  demonstration  of  a  dislocation  of  the  heart 
and  liver  (see  pp.  188  et  seq.,  and  192),  and,  in  marked  cases,  of  a  decided 
enlargement  of  the  affected  side  of  the  thorax  (see  p.  33  et  seq.). 


Fig.  96.— Dulness  in  left-sided  pleural  exudation.    Diminution  of  Traube's  space. 

Corresponding  to  the  position  of  the  complementary  pleural  sinus 
(Figs.  74,  75,  pp.  165  and  166  et  seg.)  the  dulness  in  left-sided  effusions 
reaches  lower  than  the  left  pulmonary  edge.  The  position  of  the  latter 
can  be  determined  from  the  position  of  the  lung-liver  boundary.  Traube's 
space,  the  half-moon  space  (Figs.  79  and  80)  between  the  spleen,  lung, 
and  liver,  will  then  be  encroached  upon  by  a  dulness  from  above  (see 
Figs.  96  and  97,  I.).  Such  a  dulness  can  be  very  easily  demonstrated, 
and  when  present  is  diagnostic  of  a  left-sided  pleural  effusion  ;  but 
according  to  the  writer's  experience  left-sided  exudations  do  not  always 
produce  this  sign,  because  the  complementary  pleural  sinus  is  often 
obliterated  by  early  formed  firm  adhesions,  so  that  the  exudate  does  not 


204  PERCUSSION. 

push  into  the  sinus.  Very  large  pleuritic,  effusions  may  force  the  dia- 
phragm downward,  so  that  the  dulness  which  corresponds  to  the  convex 
bowing  of  the  diaphragm  below  may  oftentimes  project  beyond  the  rib 
border  as  a  narrow  strip  parallel  to  the  costal  margin  (Fig.  97,  I.). 
This  is  rarely  observed,  because  the  intestines  overlap  the  projection  of 
the  diaphragm. 

Pleural  effusions  are  rarely,  if  ever,  freely  movable  with  the  change 
of  the  patient's  position  ;  this  can  be  conceived  of  only  if  there  are  no 
inflammatory  adhesions  at  the  borders  of  the  exudation.  Such  exuda- 
tions, more  frequently  serous  than  purulent,  would  furnish  the  same 
percussion  results  as  a  transudation  (hydrothorax). 

A  pleural  exudate,  even  if  limited  by  adhesions,  may  be  slightly 
mobile.  This  will  be  shown  by  the  fluids  moving  from  behind  forward 
inside  of  the  encapsulated  space  during  the  upright  position  of  the 
patient.  Sitting  or  standing  increases  the  intensity  of  the  dulness 
anteriorly  and  diminishes  it  posteriorly  without  altering  its  boundaries. 
The  fluid  presumably  flows  between  the  base  of  the  lung  and  the 
diaphragm.  This  latter  peculiarity  has  some  diagnostic  importance, 
because  it  explains  how  small  exudates  can  be  plainly  demonstrated 
behind  immediately  after  the  sitting  posture  is  assumed,  while  later  on 
the  dulness  seems  to  disappear,  or,  at  least,  to  be  diminished  in  height 
and  intensity. 

Light  percussion  is  best  suited  to  determine  the  boundaries  of 
pleuritic  exudations,  since  the  dulness  is  superficial.  Fig.  94, 1.,  shows 
a  frontal  section  of  a  pleuritic  exudation.  It  narrows  like  a  wedge  at 
the  top  and  at  the  bottom,  so  that  at  the  top  and  in  Traube's  space  only 
a  very  light  percussion  could  correctly  determine  the  boundary. 

If  a  pleuritic  exudation  becomes  still  larger,  it  compresses  not  only 
the  part  of  the  lung  internal  to  the  fluid  (Fig.  94,  I.),  but  the  entire 
lung,  the  pressure  spreading  in  the  direction  from  the  base  of  the  lung 
to  the  apex  ;  hence,  the  lung  tissue  above  the  exudation  is  under  in- 
creased tension,  and  furnishes  at  first  a  hyperresonant  and  tympanitic 
note  (p.  156),  which  soon,  in  consequence  of  diminished  air  content, 
becomes  more  and  more  dulled  (p.  155).  The  tone  over  a  pleural 
exudate  is  therefore  at  first  contrasted  with  the  normal  lung  tone,  later 
with  a  hyperresonant,  tympanitic  tone,  and  finally  with  a  relatively 
dulled  tone.  In  the  last  instance  differentiation  is  often  very  difficult 
but  generally  possible,  because  the  tone  over  compressed  lung  tissue 
whose  bronchi  still  contain  air  sounds  less  intensely  dulled  than  that 
over  the  exudate,  and  frequently  possesses  some  tympanitic  quality. 
The  Williams's,  tracheal  tone  (see  p.  214)  can  sometimes  be  obtained 
when  the  pulmonary  compression  is  very  marked.  (See  Fig.  97  and  the 
following  pages  for  the  percussion  relations  and  for  the  signs  of  dislo- 
cation in  large  pleuritic  effusions.) 

If  a  pleuritic  exudation  becomes  absorbed  except  for  the  fibrinous 
coating  left  behind,  dulness  may  still  persist.  To  distinguish  such  a 
condition  from  a  fluid  exudation  necessitates  a  very  careful  attention  to 
other  symptoms  and  to  other  examination  methods. 


COMPARATIVE  PERCUSSION.  205 

As  a  rule,  fibrinous  thickenings  produce  intense  dulness  only  when  they  are 
associated  with  signs  of  thoracic  contraction.  In  such  an  event  the  atelectasis  of 
the  lungs  usually  adds  its  share  to  the  dulness.  We  have  no  right  to  argue  against 
a  fluid  effusion  because  the  signs  remain  stationary,  as  exploratory  puncture  has 
frequently  convinced  the  writer  of  the  presence  of  fluid  in  cases  where  the  dul- 
ness which  persisted  long  after  the  beginning  of  the  pleurisy  had  been  attributed 
to  fibrinous  thickening.  Tapping  such  a  chest  usually  causes  a  severe  pain, 
because  the  compressed  lung  cannot  expand ;  hence,  interference  is  contra-in- 
dicated, and  one  should  allow  it  to  remain  as  a  filled  cavity.  The  writer  knows 
a  patient  with  such  an  exudate  who  is  undertaking  high  mountain  climbing. 

The  height  of  the  exudation  will  not  always  determine  its  amount.  If  an  exu- 
date is  well  encapsulated,  increase  or  decrease  of  the  amount  of  the  fluid  is  much 
more  apt  to  produce  an  increase  or  decrease  in  thickness  than  in  height,  changing 
the  intensity  of  the  dulness  rather  than  its  extent.  As  mentioned  above,  abnormal 
relations  of  retraction  or  of  elasticity  are  responsible  for  abnormal  positions  of 
exudates — e.  g,,  a  marked  collection  beneath  or  to  the  median  side  of  the  lung. 
In  such  a  case  neither  the  intensity  nor  the  extent  of  the  dulness  affords  a  clue  to 
the  real  condition,  but  only  a  careful  study  of  the  other  appearances,  such  as 
dyspnea,  dislocation  of  the  organs,  widening  of  the  thorax,  etc.  These  are  all 
very  important  in  localizing  the  point  for  tapping  a  pleuritic  effusion. 

Ferber  has  plainly  demonstrated  a  dulness  after  injecting  120  c.c.  of  fluid  into 
the  cadaver  of  a  four-year-old  child,  and  after  400  c.c.  into  an  adult.  But  in  the 
living,  as  shown  in  the  results  of  tapping,  much  smaller  quantities  of  fluid  are 
often  demonstrable  by  light  percussion. 

Dulness  of  Hydrothorax. 

In  general  dropsy  the  dulness  due  to  the  transudation  of  serum  in 
the  thoracic  cavity  corresponds  to  that  of  a  pleural  exudation.  Here, 
too,  with  small  transudations,  the  boundary  line  tends  to  curve  down- 
ward and  forward  (see  p.  201).  But  as  soon  as  the  fluid  has  reached  a 
certain  amount  it  becomes  more  or  less  movable,  and  the  upper  border 
of  dulness  then  assumes  a  horizontal  level  in  every  position  of  the  body, 
although  at  first  it  may  change  its  position  only  very  slowly  (p.  201). 
This  is  an  important  point  in  making  a  diflPerential  diagnosis  between 
hydrothorax  and  pleurisy.  Hydrothorax  is  for  the  most  part  bilateral, 
but  frequently  more  marked  upon  one  than  upon  the  other  side.  If 
patients  have  maintained  a  constrained  position  upon  one  side,  the  hy- 
drothorax is  ordinarily  more  strongly  developed  upon  the  lower  side, 
or  even  may  be  limited  to  that  side.  Hydrothorax  does  not  often 
produce  any  dislocation,  because  it  is  commonly  bilateral,  and  because 
there  is  ordinarily  an  accumulation  of  fluid  in  the  abdomen  at  the  same 
time.     Traube's  space  is  generally  obliterated. 

Increased  abdominal  contents,  pushing  up  the  diaphragm  and  the  lung  boun- 
daries, often  obscure  the  diagnosis  of  a  coincident  hydrothorax.  If  the  patient 
sits  up  the  anterior  borders  of  the  lungs  will  be  pushed  upward,  but  this  is  of  very 
little  help,  for  the  sitting  posture  compresses  the  abdomen,  and  therefore  also 
elevates  the  diai)hragm.  Hence,  we  must  examine  either  in  the  standing  or  lat- 
eral posture.  To  be  sure,  a  slight  hydrothorax  may  be  hidden  in  the  erect  posture  on 
account  of  the  depression  of  the  diaphragm  (p.  174).  A  moderate  hydrothorax 
in  the  horizontal  lateral  posture  would  furnish  a  strip  of  dulness  running  along 
the  vertebral  column,  which  could  easily  be  determined  by  comparing  it  with  the 
other  side  (see  p.  207  etseq.). 


206  PERCUSSION. 

Dulness  of   a  Pleural   Exudate  when   Combined  with  a  Pneumothorax. 
If  a  pneumothorax  has  persisted  for  some  time,  a  fluid  inflammatory 
pleural  eflusion  commonly  results,  which  may  be  either  purulent  or 

Compressed 
lung. 


Dislocated   . 
mediastinum. 


Boundary  of 
the  exudate 
to  light  per- 
cussion. 


"-i,,  '^-^■^  «^ 


Tic  97  -Results  of  examination  in  a  large  left-sided  pleural  exudate     Pronounced  disloca- 
1  of  "the  heart  of  ?he  mXstinum,  of  thi  left  lobe  of  the  liver,  and  of  the  diaphragm.    (See 


;  et  seq.  for  explanation  of  signs.) 


COMPARATIVE  PERCUSSION. 


207 


serous  (sero-  or  pyopneumothorax).  The  fluid  then  collects  beneath  the 
air  in  the  deepest  portions  of  the  pleural  cavity  and  furnishes  a  dull 
percussion  tone.  Change  of  the  patient's  position  produces  the  most 
decided  mobility  of  this  dulness,  and  such  mobility  is  very  characteris- 
tic of  this  affection.  In  this  condition  pressure  in  the  pleural  cavity  is 
as  a  rule,  strongly  positive,  and  unless  tied  down  by  adhesions  the  entire 
lung  is  separated  from  the  thoracic  wall  by  the  air,  so  that  the  fluid  can 
perfectly  well  follow  the  laws  of  gravity.  The  level  of  dulness  is  there- 
fore exactly  horizontal  in  every  position  of  the  patient.  As  there  is  no 
opposition,  any  change  of  posture  produces  an  instantaneous  change  of 
the  dulness  (a  contrast  to  hydrothorax).  The  fluid  does  not  form  a  wedge, 
as  in  ordinary  pleurisy,  but  all  of  it  is  beneath  the  lung  (Fig.  94, 1.).    The 


Fig.  98.— Dulness  of  hydrothorax  in  right  lateral  posture. 

consequence  of  this  is  that  a  considerable  amount  must  be  present  before 
it  becomes  evident  to  percussion.  In  the  beginning  the  exudations  are 
sometimes  completely  hidden  at  the  bottom  of  the  thorax,  especially  if  left- 
sided.  The  high  pressure  of  the  pneumothorax  depresses  the  diaphragm 
and  makes  it  bulge  out  convexly.  Not  infrequently  we  can  demonstrate 
the  fluid  by  means  of  the  succussion  murmur  (see  p.  240)  before  per- 
cussion will  show  anything.  As  it  increases  in  size  a  narrow  band  of 
dulness  can  be  made  out  at  the  base  of  the  lung,  front  and  back.  We 
are  apt  to  obtain  ])etter  results  from  percussion  if  the  patient  bends  for- 
ward, or  if  he  lies  upon  the  well  side  and  we  percuss  above  the  spinal 
column,  in  the  same  way  as  in  hydrothorax  (Fig.  98).  Figs.  99  and 
134  show  the  results  of  examination  in  sero-  and  pyopneumothorax. 
If  the  lung  of  the  affected  side  is  more  or  less  adherent  at  the  onset 


208  PERCUSSION. 

of  the  pneumothorax,  all  the  relations  will  be  atypical.  Even  a  very- 
small  exudation  may  then  be  appreciated  by  percussion.  Although  the 
relations  of  position  are  atypical,  we  should  still  expect  a  change  of  posi- 
tion in  the  dulness  of  the  fluid. 

Dulness  of  Hemothorax. 

If  blood  is  poured  out  into  the  pleural  cavity  from  traixinatism  or  from  the 
rupture  of  an  aneurism,  the  resulting  dulness  will  ordinarily  correspond  to  that 
of  hydrothorax.  This  dulness  will  usually  shift  with  change  of  the  patient's 
posture  until  some  inflammation  ensues,  when  encapsulation  will  very  soon  fix  it. 
The  blood  coagulates  very  slowly  (after  the  lapse  of  days). 

Dulness  Dae  to  Infiltration  of  the  Lung  (Inflammation;  Tuberculosis;  Infarction). 
An  infiltration  of  the  lungs  presents  a  less  intense  dulness  than  a 
pleural  effusion,  because  the  bronchi  ordinarily  remain  full  of  air,  and 
so  aid  in  producing  a  partially  resonant  tone.  The  shape  of  the  dul- 
ness is  generally  different.  It  is  less  sharply  bounded,  because  the  infil- 
tration gradually  projects  into  healthy  lung  tissue.  In  the  neighborhood 
of  infiltrations  we  frequently  obtain  a  tympanitic  or  hyperresonant  note, 
so  that  the  dulness  is  often  so-called  dull  tympany  (see  p.  209  et  seq.). 

In  croupous  pneumonia  the  dulness  is  more  apt  to  be  located  behind  and  below. 
Frequently  enough  it  is  found  at  the  borders  of  the  lobes  of  the  lung ;  it  may, 
however,  overlap  these  borders  in  an  irregular  way  (see  Figs.  74,  75,  and  76). 

In  bronchopneumonic  infiltrations  the  dulness  is  situated  either  behind  and  below 
or  at  the  sharp  anterior  and  lateral  lung  edges,  or  else  in  a  narrow  strip  along 
both  sides  of  the  spine. 

In  tubercular  infiltrations  the  dulness  is  most  frequently  localized  at  the  apices 
and  at  the  sharp  pulmonary  edges,  especially  at  the  ' '  lingula "  which  bounds 
the  superficial  cardiac  dulness  on  the  left.  Miliary  tuberculosis  generally  causes 
no  dulness,  but  rather  a  hyperresonant  tone  (p.  210,  3).  Very  thickly  studded 
miliary  tubercles  may,  however,  produce  a  diffiise  dulness  simulating  a  catarrhal 
pneumonia  (p.  200). 

Pulmonary  infarctions,  if  large  enough  to  cause  physical  signs,  commonly  occa- 
sion a  less  intense  dulness,  and  generally  over  the  lower  posterior  portions  of  the 
lung. 

Dulness  from  Tumors  of  the  Lungs,  of  the  Pleura,  and  of  the  Mediastinum. 

There  is  little  characteristic  about  the  dulness  of  tumors  of  the  lungs  and 
pleura,  and  this  corresponds  to  their  atypical  topography.  They  furnish  a  marked 
dulness  only  when  they  have  reached  a  considerable  size,  and  then  it  is  apt  to 
be  more  intense  than  the  dulness  of  inflammatory  infiltrations,  because  the  tumor 
tissue  contains  no  bronchi  filled  with  air.  The  more  common  varieties  of  intra- 
thoracic tumors  arise  from  the  mediastinum.  They  furnish  a  somewhat  character- 
istic dulness  over  the  upper  end  of  the  sternum  ;  it  projects  fi'om  there  laterally 
into  the  territory  of  the  lung,  where  it  is  generally  more  or  less  distinctly  separated 
from  the  cardiac  dulness  in  the  shape  of  an  hour-glass.  If  these  tumors  involve 
the  pleura,  they  are  frequently  accompanied  by  pleuritic  exudations,  with  the 
corresponding  physical  signs. 

Dulness  of  Pulmonary  Cavities. 

Tubercular  and  bronchiectatic  cavities  of  the  lung  furnish  a  dull  note  if  the 
cavity  is  filled  with  secretion  instead  of  with  air.  It  is  quite  characteristic  for 
such  a  dulness  to  change  into  a  tympanitic  note  after  copious  expectoration.  But 
the  dulness  generally  disappears  only  in  part,  because  the  thickening  of  the 
pulmonary  tissue  in  the  neighborhood  persists. 


COMPARATIVE  PERCUSSION.  209 

Dulness  from  Pulmonary  Edema. 

It  is  ordinarily  assumed  that  pulmonary  edema  gives  rise  to  a  hyperresonant  note 
(see  the  following  page),  yet  a  series  of  autopsies  has  convinced  the  writer  that 
if  a  pulmonary  edema  is  of  long  duration,  the  air  in  the  area  infiltrated  with  fluid 
becomes  absorbed  and  a  very  intense  dulness  results,  especially  in  the  postero- 
inferior  portions  of  the  lung.  This  dulness  can  be  diflferentiated  from  the  dulness 
of  infiltration  by  its  rapid  alteration  and  by  the  absence  of  bronchial  breathing, 
because  the  bronchi,  too,  are  mostly  filled  with  fluid.  Here  it  is  really  a  sort  of 
fluid  or  serous  infiltration. 

Dulness  of  Atelectasis  of  the  Lungs. 

This  is  in  general  like  the  dulness  of  infiltration.  Obstruction  atelectasis — i.  e., 
one  due  to  a  catarrh  and  plugging  of  the  bronchus,  with  subsequent  resorption  of  air 
from  the  alveoli — ordinarily  tarnishes  a  dulness  like  that  of  small  areas  of  infiltration 
(see  above).  Later  on  the  atelectasis  is  commonly  transformed  into  an  infiltration. 
Compression  atelectasis,  from  dislocation  or  enlargement  of  the  heart  or  from  the 
crowding  of  the  diaphragm  upward  and  the  consequent  compression  of  the  sharp 
pulmonary  edge,  also  furnishes  a  dull  tone.  This  occurs  upon  a  larger  scale  from 
fluid  accumulations  in  the  pleura,  where  the  part  of  the  lung  covered  by  the  fluid, 
and  later  that  lying  above  the  fluid,  is  robbed  of  its  air  content  (see  p.  204). 
Marked  cardiac  enlargement  compresses  the  lung  and  often  causes  a  very  exten- 
sive dulness  of  the  left  posterior  and  inferior  portions  of  the  lung.  It  is  fre- 
quently wrongly  diagnosed  as  a  pleural  effusion  or  pulmonary  infiltration. 

During  the  formation  of  all  kinds  of  atelectasis  the  tissue  is  relaxed,  so  that 
the  normal  tone  is  first  transformed  into  a  hyperresonant  or  tympanitic  tone,  and 
finallv,  on  account  of  the  diminution  of  the  air  content,  into  a  dulled  tone  (see  p. 
155).' 

Dulness  of  Pulmonary  Retraction. 

By  pulmonary  retraction  is  understood  that  chronic  change  of  the  lung  which 
results  from  indurative  (shrinking)  infiltration  and  atelectasis.  The  result  of  per- 
cussion in  the  retraction  associated  with  pulmonary  tuberculosis  corresponds  essen- 
tially to  that  in  tubercular  consolidations. .  The  retraction  resulting  from  a  pleurisy 
causes  a  localized  dulness  corresponding  in  shape  and  extent  to  the  antecedent 
exudation.  If  the  whole  lung  was  compressed,  a  diffuse  relative  dulness  of  the 
entire  lung  will  persist.  Thick  pleuritic  adhesions  or  exudations  which  remain 
stationary  frequently  increase  the  intensity  of  the  dulness  in  these  conditions  of 
pleuritic  shrinking. 

Dulness  from  Diverticulum  of  the  Esophagus. 
(See  later,  Examination  of  the  Esophagus.) 

ABNORMALLY  LOUD   (HYPERRESONANT)  AND  TYMPANITIC  TONES  "WITHIN 
THE  PULMONARY  BORDERS. 

We  have  already  described  upon  pp.  157  and  158  the  conditions 
which  may  give  rise  to  a  hyperresonant  or  to  a  tympanitic  note  over  an 
area  characterized  normally  by  a  non-tympanitic  note. 

Hyperresonant  or  tympanitic  notes  within  the  pulmonary  borders 
occur  as  follows : 

1.  In  pulmonary  emphysema  diffused  over  the  entire  lung.  The  very 
typical  percussion  note  of  emphysematous  lungs  is  called  a  "box  tone." 
The  name  is  sufficiently  descriptive.  Some  authors  consider  it  merely 
an  abnormally  resonant  pulmonary  note ;  others,  a  low  tympanitic  note. 

2.  In  relaxation  of  the  pulmonary  tissue  from  retraction  due  to  a 

u 


210 


PERCUSSION. 


limitation  of  space  in  the  thorax.  This  occurs  in  dislocation  upward  of 
the  diaphragm,  in  intrathoracic  and  intrapulmonary  tumors,  in  pleural 
effusions,  in  cardiac  enlargements,  and  in  pericardial  effusions.  When 
the  diaphragm  is  pushed  upward  the  tone  may  be  abnormally  loud,  and 
equally  so  over  both  lungs.  If  the  relaxation  of  the  pulmonary  tissue 
be  localized,  as  in  the  other  cases  mentioned  above,  the  abnormally  loud 
tone  will  be  especially  noticeable  near  the  cause  of  the  limitation  of 
space.  Thus,  above  the  pleuritic  dulness  the  retracted  lung  gives  an 
abnormally  loud  or  tympanitic  note.  In  all  these  conditions  the  more 
marked  the  relaxation  of  the  lung,  the  more  nearly  tympanitic  this 
abnormally  loud  pulmonary  tone  becomes.     If  the  limitation  of  space 


Upper  borders 
of  the  exu- 
dates, dulness 
in  the  sitting 
posture. 


Fig.  99.— Results  of  percussion  in  a  right  pneumothorax— dorsal  decubitus  (the  exudation  is 
therefore  not  demonstrable  above) :  Loud  tone  overstepping  the  territory  of  the  lung;  dislocation 
of  the  liver,  heart,  and  mediastinum  ;  superficial  cardiac  dulness  restricted  at  the  right. 


proceeds  still  farther,  so  that  the  lung  is  compressed,  the  tone  becomes 
dull. 

3.  In  relaxation  of  the  'pulmonary  tissues  from  structural  changes. 
To  this  type  belong  diffuse  pulmonary  edema  and  the  localized  inflam- 
matory edema  Avhich  appears  nearby,  both  as  a  precursor  and  as  a  re- 
siduum of  the  inflammatory  processes.  Here,  too,  the  normal  pulmonary 
tone  becomes  fir.st  abnormally  loud,  next  hyperresonant,  then  tympanitic, 
and  finally  dull  (see  above).  The  relaxation  of  the  pulmonary  tissue  in 
beginning  obstruction  atelectasis,  due  to  the  plugging  of  a  bronchus  by 
secretion  or  by  a  foreign  body,  also  belongs  to  this  category.  Another 
transition  occurs  here  as  well  from  the  hyperresonant  to  the  tympanitic 


COMPARATIVE  PERCUSSION.  211 

tone,  and  finally,  when  the  atelectasis  becomes   complete  or  leads   to 
infiltration,  to  a  dulness. 

4.  In  pneumothorax  (Fig.  99).  In  most  cases  the  percussion 
tone  becomes  abnormally  loud,  but  only  rarely  tympanitic.  The  so- 
called  valve  pneumothorax  is  the  most  frequent  type,  and  then  the  air  is 
under  such  marked  pressure  that  the  tone  is  mostly  non-tympanitic 
(p.  156).  It  is,  however,  generally  tympanitic  in  open  pneumothorax, 
where  the  air  exists  only  under  the  atmospheric  pressure  (operative 
empyema).  Another  difference  between  the  normal  lung  tone  and  the 
loud  tone  of  a  pneumothorax  is  that  the  latter  projects  noticeably  beyond 
the  normal  lung  boundaries,  because  the  diffuse  air  accumulation  pene- 
trates to  the  complementary  pleural  sinus.  In  right  pneumothorax  the 
liver  dulness  is  diminished  from  above,  the  cardiac  dulness  from  the 
right  (see  p.  180  and  Fig.  99).  In  left-sided  pneumothorax  the  splenic 
dulness  disappears  and  the  cardiac  dulness  is  either  diminished  or,  more 
commonly,  also  disappears  (p.  180).  Very  frequently  distinct  dislocation 
can  be  observed.  Sometimes,  though  not  constantly,  the  loud  tone  over 
a  pneumothorax  presents  a  metallic  character,  which  can  be  appreciated 
with  the  stick-pleximeter  method  of  percussion  (see  p.  157).  Again,  it 
may  exhibit  all  sorts  of  variations  in  the  pitch  (see  following  pages). 
If  the  pneumothorax  is  combined  with  an  inflammatory  fluid  effusion, 
and  this  is  the  rule  when  it  has  persisted  for  any  length  of  time,  the 
fluid  shifts  completely  with  change  of  the  patient's  position,  and  very 
much  more  rapidly  than  in  hydrothorax.  In  every  position  of  the 
patient  we  find,  then,  that  the  lower  part  of  the  thorax  is  dull  ;  and 
that  above  the  dulness,  separated  from  it  by  an  exactly  horizontal  line, 
is  the  hyperresonant  tone  of  the  pneumothorax  (p.  207  and  Fig.  99). 

5.  In  cavities  of  the  lungs  (tubercular,  bronchiectatic,  and  abscess  cav- 
ities). As  a  rule,  the  cavities  are  at  least  partly  filled  with  secretion, 
and  they  are  surrounded  by  tubercular  or  inflammatory  infiltrated  solid 
tissue,  so  that  percussion  over  them  ordinarily  elicits  a  dull  tone  (see 
p.  208).  Stronger  percussion,  especially  after  expectoration  of  the 
secretion,  transforms  the  dulness  into  a  tympanitic  tone.  A  very  large 
cavity  containing  a  great  deal  of  air,  or  one  located  very  superficially 
and  only  surrounded  by  a  thin  layer  of  infiltrated  pulmonary  tissue, 
will  furnish  an  abnormally  loud  tone,  and  even  with  weak  percussion  a 
tympanitic  tone.  Smaller  cavities  (up  to  the  size  of  several  cubic  cen- 
timeters), and  even  very  large  cavities  when  situated  deeply,  generally 
escape  demonstration  by  percussion.  The  stick-pleximeter  percussion 
method  will  sometimes,  though  not  often,  demonstrate  metallic  resonance 
and  change  of  tone  height  over  cavities  (see  pp.  157  and  158  et  seq.). 

6.  Diaphragmatic  hernias  in  the  region  of  the  lung,  containing  intestines,  will 
cause  a  loud  tympanitic  tone.  They  can  be  distinguished,  especially  fi-om 
pneumothorax,  by  their  irregular  shape  and  by  the  intestinal  borborygmus,  mostly 
of  metallic  character. 

7.  See  p.  691,  under  Examination  of  the  Esophagus,  in  regard  to  the  tym- 
panitic note  of  esophageal  diverticula. 


212  PERCUSSION. 

PECULIAR  PERCUSSION  PHENOMENA  OVER  THE  THORAX. 
Metallic  Resonance  Over  the  Thorax. 

See  p.  157  in  regard  to  the  origin  and  peculiarity  of  metallic  reso- 
nance. 

Metallic  resonance  is  most  frequently  observed  in  pneumothorax  (see 
the  foregoing  pages).  It  is  favored  by  the  size  of  the  air  space  and  by 
the  smoothness  of  the  walls,  and  is  most  readily  demonstrated  by  the 
stick-pleximeter  method  of  percussion  combined  with  auscultation. 
Metallic  resonance  is,  however,  not  a  constant  sign  of  pneumothorax^ 
because  it  requires  a  peculiarity  in  the  shape  of  the  air  space  and  a  cer- 
tain degree  of  tension  of  the  enclosed  air.  If  the  air  exists  under  too 
slight  or  even  under  too  high  a  pressure,  the  metallic  resonance  dis- 
appears. It  often  requires  a  certain  strength  of  percussion  to  make  it 
audible,  and  not  infrequently  it  can  only  be  appreciated  at  certain  places. 
In  most  cases  the  metallic  tone  is  too  weak  to  be  appreciated  at  a  dis- 
tance— i.  e.,  without  coincident  auscultation. 

The  metallic  resonance  of  a  pneumothorax  frequently  disappears  after  aspira- 
tion ;  or,  in  case  it  was  not  present  beforehand,  aspu-ation  may  bring  it  out.  This 
is  due  to  the  influence  of  the  tension  of  the  enclosed  air. 

The  metallic  resonance  of  a  pneumothorax  frequently  exhibits  distinct 
variations  in  pitch,  depending  upon  whether  we  percuss  the  patient  in 
the  sitting  or  recumbent  posture.  This  is  plainly  due  to  the  mobility 
of  the  fluid  in  the  pleural  cavity  with  change  of  the  patient's  posture. 
A  deepening  of  the  tone  in  the  sitting,  and  an  elevation  in  the  recum- 
bent, posture  is  more  frequently  noted  than  the  reverse  (the  so-called 
Biermer  tone  change).  The  height  of  the  metallic  resonance  varies 
inversely  with  the  greatest  diameter  of  the  air  space  (see  p.  207) ; 
therefore  we  assume  that  in  the  former  case  the  diaphragm,  under  the 
weight  of  the  exudation  in  the  sitting  posture,  drops  downward.  When 
the  tone  becomes  higher  in  sitting  up,  we  assume  that  it  is  due  to  the 
resulting  shortening  of  the  air  space  by  the  rise  of  the  exudation  in  the 
sitting  posture.  The  pitch  of  the  metallic  resonance  varies  in  different 
places  ;  hence,  in  such  an  examination  we  should  always  percuss  the 
same  spot. 

In  pneumopericardium  an  abnormally  loud  tympanitic  or  non-tym- 
panitic  note  takes  the  place  of  the  cardiac  dulness,  sometimes  modified 
by  a  dulness  from  the  exudation  and  sometimes  not  (see  p.  180).  A 
metallic  resonance  can  at  times  be  demonstrated  similar  to  that  of  pneumo- 
thorax. The  patient's  posture  may  also  influence  the  loudness  and  the 
pitch  of  this  metallic  resonance  (change  of  tension  of  the  air,  disloca- 
tion of  the  heart  and  of  the  exudation). 

Pulmonary  cavities  only  rarely  furnish  metallic  resonance,  because 
they  do  not  often  fulfil  the  conditions  for  its  establishment  (see  p.  158). 
They  are  either  too  small,  have  too  irregular  or  too  thick  walls,  or  are 
situated  too  deeply.  If  a  metallic  resonance  is  obtained  over  a  pul- 
monary cavity,  similar  alterations  in  pitch  may  be  brought  out ;  concern- 
ing which  see  pp.  214  and  21b  et  seq. 


COMPARATIVE  PERCUSSION.  213 

Diaphragmatic  hernias  within  the  tliorax  may  also  give  rise  to  a 
metallic  resonance. 

CRACKED-POT   RESONANCE   OVER  THE    THORAX   (CHINK   OF  COINS; 
SPINNING-TOP  MURMUR). 

(See  p.  158  as  to  its  origin.)  Cracked-pot  resonance  may  be  produced 
while  percussing  a  normal  thorax  under  entirely  physiologic  conditions 
— e.g.,  over  the  lungs  of  a  crying  child,  or,  provided  the  thorax  is 
yielding,  over  an  adult's  luugs  while  he  is  talking,  or  during  forced 
expiration  with  half-open  vocal  cords.  Vigorous  percussion,  proximity 
to  the  trachea,  and  open  mouth  all  favor  the  production  of  this  reso- 
nance. The  noise,  under  physiologic  circumstances,  is  assumed  to  arise 
at  the  narrowed  glottis,  because  the  percussion  blow  causes  the  sudden 
escape  of  air  (see  p.  158). 

It  can  also  be  noted  over  relaxed  or  partly  infiltrated  pulmonary 
tissue  under  all  those  conditions  which  furnish  abnormally  loud  or  tym- 
panitic pulmonary  tones — e.  g.,  at  the  borders  of  pleuritic  exudations 
and  in  the  neighborhood  of  infiltrations.  Its  explanation  under  these 
circumstances  is  not  yet  entirely  clear,  whether  here,  too,  it  is  due  to  a 
stenotic  murmur  (p.  158)  arising,  as  in  the  crying  child,  at  the  glottis, 
or  in  loco.  If  the  conditions  which  give  rise  to  the  noise  even  in 
healthy  persons  are  absent — e.  g.,  speaking,  pressure  of  the  half-open 
glottis,  etc. — the  writer's  experience  has  convinced  him  that  cracked-pot 
resonance  rarely  results  from  the  above-mentioned  pathologic  conditions 
(relaxation,  infiltration).  Cracked-pot  resonance  has  a  certain  signifi- 
cance in  the  diagnosis  of  pulmonary  cavities.  It  is  very  common,  for 
example,  over  small  superficial  cavities  (a  few  centimeters)  which  com- 
municate with  a  bronchus,  especially  upon  rather  vigorous  percussion. 
It  is  probably  due  here  to  the  production  of  a  stenotic  murmur  at  the 
opening  of  the  bronchus  into  the  cavity.  Marked  emaciation  will  favor 
the  production  of  the  murmur.  We  are  inclined  to  attribute  consider- 
able importance  to  this  phenomenon  in  the  diagnosis  of  pulmonary 
cavities. 

CHANGE  IN  THE  PITCH  OF  THE  PERCUSSION  NOTE   OVER  THE  THORAX. 

Wintrich's  Phenomenon  and  Williams'  Tracheal  Tone. 

— If  the  patient  opens  his  mouth  during  percussion  the  pitch  of  a  tym- 
panitic pulmonary  note,  or  of  a  metallic  resonance  over  pulmonary 
cavities,  will  be  raised,  while  if  the  mouth  is  closed  the  pitch  will  be 
deepened.  This  is  Wintric/i's  phenoniienon.  The  patient  should  breathe 
naturally,  and  the  note  should,  of  course,  be  compared  during  the  same 
phase  of  respiration,  because  its  pitch  also  varies  with  the  phase  of  res- 
piration. (See  p.  215,  Friedreich's  Tone  Change.)  It  is  a  sign  of  a 
cavity,  and  arises  if  the  cavity  communicates  with  the  bronchus  and 
transmits  the  resonance  into  the  trachea,  and  from  there  into  the  mouth. 
The  pitch  in  the  mouth  must  vary  Nvith  its  being  ojion  or  shut,  according 
to  the  laws  of  open  and  closed  pipes.  If  we  approach  the  ear  to  the 
patient's  mouth  we  can  readily  be  convinced  that  the  notes'  change  of 


214  PERCUSSION. 

pitch  in  reality  depends  upon  an  admixture  of  the  percussion  tone  with  the 
individual  tone  of  the  mouth.  Hence,  Wintrich's  change  of  tone  is  not 
absolutely  pathognomonic  of  a  cavity.  As  a  matter  of  fact,  we  do  observe 
this  same  sort  of  tone  change  in  percussing  over  the  supra-  and  infra- 
clavicular fossae  from  infiltration  or  contraction  of  the  upper  part  of  the 
lung  or  from  marked  compression  by  pleuritic  exudation,  because  vigor- 
ous percussion  will  readily  transmit  the  vibration  through  the  thickened 
tissue  to  the  main  bronchus  and  to  the  trachea.  The  note  which  sounds 
dull  to  light  percussion  then  becomes  tympanitic,  and  opening  and  shut- 
ting the  mouth  will  evoke  the  same  Wintrich  tone  change.  The  name 
Williams'  tracheal  tone  has  been  given  to  this  phenomenon  when  due  to 
infiltrated  or  contracted  areas  of  lung  without  cavities.  If  AVintrich's 
change  of  tone  appears  and  disappears,  depending  upon  the  body  post- 
ure, we  speak  of  it  as  the  interimpted  Wintrich  tone  change,  as  contrasted 
with  the  simple  Wintrich  tone  change.  Secretion  closes  the  communication 
between  the  cavity  and  the  bronchus,  and  so  the  sound  is  not  transmitted. 
This  peculiarity  will  sometimes  aid  in  differentiating  the  Wintrich  phe- 
nomena from  the  Williams'  tracheal  tone. 

Gerliardt  Tone  Change  (Gerhardt's  Phenomenon). — If 

W' — > 


6 
Fig.  100.— Gerhardt's  phenomenon. 

the  pitch  of  a  tympanitic  note  or  of  the  metallic  resonance  over  a  pul- 
monary cavity  changes  with  the  patient's  position,  we  speak  of  this 
change  as  Gerhardt's  phenomenon.      Fig.  100,  a  and  6,  explains  this. 

A  cavity  contains  both  air  and  fluid.  The  fluid  is  freely  movable. 
The  diameter  of  the  part  of  the  cavity  containing  air  is  longer  in  the 
recumbent  than  in  the  erect  posture,  or  vice  versa.  Hence,  percussion 
will  produce  a  note  of  deeper  or  higher  pitch  according  to  the  patient's 
position.  This  would  naturally  lead  us  to  believe  that  Gerhardt's  phe- 
nomenon not  only  demonstrates  the  presence  of  a  cavity,  but  also  the 
direction  of  its  longer  axis ;  in  other  words,  tells  us  about  its  shape. 
From  a  practical  standpoint,  however,  we  should  remember  that  a  dis- 
tinct Gerhardt's  phenomenon  is  rare  ;  that  other  methods  of  examination, 
such  as  auscultation,  are  quite  as  diagnostic ;  and  besides,  that  slight 
differences  of  percussion  notes  with  change  of  position  may  be,  within 
physiologic  limits,  due  simply  to  alteration  in  the  tension  of  the  thoracic 
wall  without  any  cavity  within  the  chest.  As  simple  a  condition  as  is 
represented  in  Fig.  100  is  rarely  observed  upon  the  autopsy  table.    The 


COMPARATIVE  PERCUSSION.  215 

cavities  have  more  jagged  shape,  so  that  there  is  more  than  one  long 
axis  to  influence  the  pitch  ;  and  besides,  the  variation  of  the  tension  with 
change  of  position  plays  a  very  important  part,  because  the  walls  of 
many  cavities  adhere  to  the  costal  pleura. 

Wherever  Gerhardt's  tone  change  could  be  demonstrated  exactly  as 
is  explained  above,  the  secretion  flowing  forward  in  the  sitting  posture 
should  furnish  a  dulness  at  the  lower  border  of  the  tympany  and  so 
clinch  the  diagnosis, 

Friedreich's  Phenomenon,  or  the  Respiratory  Tone 
Change. — Inspiration  raises  the  pitch  of  the  tympanitic  or  metallic 
note  over  a  cavity  and  expiration  deepens  it.  This  is  Friedreich's 
phenomenon.  However,  respiration  slightly  alters  the  pitch  of  the  note 
over  a  perfectly  normal  lung,  so  that  this  phenomenon  is  not  diagnostic 
of  cavities  unless  it  is  very  marked  and  perceived  at  a  circumscribed 
and  perhaps  suspicious  spot.  The  phenomenon  depends  upon  the  vari- 
able tension  of  the  lungs  in  the  normal  case,  and  of  the  cavity-wall  in 
the  pathologic  case. 

Biermer's  Phenomenon. — The  pitch  of  the  metallic  resonance 
over  a  sero-  and  pyopneumothorax  is  deepened  in  the  erect  and  raised  in 
the  recumbent  posture  (see  p.  212).  Biermer's  change  of  tone  is  in  a 
way  identical  with  Gerhardt's,  except  that  tlie  former  author  limited  his 
description  to  the  metallic  resonance  over  pneumothorax,  and  Gerhardt, 
to  the  tympanitic  note  over  pulmonary  cavities. 

COMPARATIVE  PERCUSSION  OF  THE  ABDOMEN. 

The  percussion  note  over  the  abdomen  becomes  more  resonant,  or 
louder  : 

1.  From  distention  of  the  intestines  with  gas  {meteorism).  The  ten- 
sion of  the  intestinal  coils  is  increased  and  so  dulls  the  tone,  but  the 
increased  volume  of  gas  seems  to  overpower  the  dulness ;  therefore,  the 
note  becomes  higher,  sometimes  deeper,  according  as  the  influence  of  the 
increase  of  volume  or  the  increase  of  tension  predominates.  The  in- 
crease of  volume  tends  to  deepen  the  pitch  ;  the  increase  of  tension,  to 
raise  it.  The  more  the  tension  increases,  the  less  tympanitic  tiie  note, 
until  eventually  it  will  resemble  a  hyper-resonant  lung  tone. 

2.  From  an  accumulation  of  air  within  the  peritoneal  cavity,  pneumo- 
peritoneum (perforation  of  stomach  or  intestine).  Here  the  influence 
of  the  volume  of  air  and  of  tlie  tension  acts  precisely  as  in  meteorism. 
If  the  air  accumulation  is  freely  movable  it  naturally  occupies  the 
highest  point  of  the  peritoneal  cavity  and  overlaps  the  liver,  sometimes 
enough  to  obliterate  the  liver  dulness.  If,  as  commonly  happens,  an 
exudation  is  associated  with  the  accumulation  of  air  in  the  peritoneal 
cavity,  the  inferior  portions  become  dull.  This  dulness  shifts  exactly 
as  in  pyopneumothorax,  and  so  always  presents  a  horizontal  level.  The 
stick-pleximeter  method  of  percussion  ordinarily  brings  out  or  empha- 
sizes the  metallic  resonance  over  an  air  accumulation  in  the  abdominal 
cavity. 


216  PEBCUSSION. 

The  abdominal  note  becomes  dulled  : 

1.  In  a  diffuse  way,  from  diminution  of  the  gaseous  contents  of  the 
intestines  (starvation,  hunger,  scaphoid  belly  of  meningitis  tuberculosa). 

2.  In  a  circumscribed  way,  from  solid  or  fluid  material  filling  the 
intestinal  coils. 

3.  From  tumors  which  are  situated  in  the  intestines,  which  lie  between 
the  intestine  and  the  abdominal  walls,  or  which,  arising  from  the  depths, 
push  the  intestines  aside.  Palpation  bounds  these  much  more  accurately, 
so  that  the  only  value  of  percussion  is  to  determine  whether  the  intestine 
or  stomach  lies  in  front  of  the  tumor  or  not,  by  the  presence  or  absence 
of  a  superficial  dulness  over  the  palpable  resistance.  For  this  purpose 
it  goes  without  saying  that  we  must  employ  as  light  a  percussion  as 
possible,  in  order  to  avoid  vibrating  neighboring  or  deeper-lying  intestinal 
coils.  It  is  difficult  to  determine  deep  dulness  over  the  abdomen,  so 
that  percussion  has  very  little  value  in  localizing  deep-lying  tumors  (see 
p.  196). 

4.  From  a  large  number  of  perfectly  empty  and  contracted  intestinal 
coils.^     These  may  produce  quite  an  intense  localized  dulness. 

5.  From  inflammatory  infiltrations  of  the  intestinal  walls  or  of  the 
peritoneum.  Palpation  also  appreciates  them  as  resistances  resembling 
tumors.  To  this  group  belong  the  dulness  noted  in  the  right  iliac  fossa 
in  perityphlitis  and  that  of  chronic  inflammatory  and  tubercular  adhe- 
sions. The  dulness  can  sometimes  be  sharply  defined,  sometimes  not. 
Light  percussion  is  necessary.  Palpation  again  generally  furnishes  more 
accurate  data. 

6.  From  fluid  effusions  between  the  intestines  ■  and  the  abdominal 
wall.  At  a  moderately  acute  stage  inflammatory  effusions  are  frequently 
encapsulated  by  adhesions,  and  then  furnish  a  circumscribed,  irregularly 
shaped  dulness.  Inflammatory  serous  effusions  which  are  chronic  in 
their  development — e.g.,  tubercular  peritonitis,  and  even  acute  purulent 
effusions — are  not  necessarily  encapsulated.  We  shall  obtain  from 
them  a  more  or  less  intense  dulness  in  the  dependent  portions  of  the 
abdomen,  shifting  with  the  movements  and  forming  an  approximately 
liorizontal  level  in  every  position.  This  horizontal  level  of  dulness  may, 
however,  frequently  be  interrupted  at  one  or  two  places,  where  separate 
intestinal  loops  are  adherent  or  where  marked  tympanites  may  press 
them  against  the  abdominal  wall.  This  change  in  the  position  of  the 
dulness  need  not  appear  instantly  in  every  case,  even  though  adhesions 
be  absent,  because  the  distended  intestines  are  likely  to  oppose  some 
obstacle  to  the  movement.  Ascites  or  dropsical  effusions  in  the  abdomen 
(general  dropsy,  portal  stasis)  furnish  similar  percussion  results.  The 
<3ulness  is  always  superficial,  so  that  percussion  must  be  light  in  order 
to  bound  the  fluid  dulness. 

A  free  fluid  effusion  in  the  abdomen  must  attain  considerable  dimensions  before 
it  produces  distinct  dulness.  F.  Miiller  ^  found  in  experimenting  upon  the  cadaver 
that  in  children  one  year  old  100  c.c.  could  not  be  demonstrated;  that  150  c.c. 
gave  a  relative  dulness;  and  that  200  c.c.  give  an  absolute  dulness,  shifting  with 

iR  Miiller,  Berlin,  klin.  Woch.,  1895,  No.  13,  p.  278.  -^  Loc.  cit. 


AUSCULTATION.  217 

change  of  position.  In  grown  people  1000  c.c.  furnished  no  distinct  dulness  ;  but 
with  1500  c.c.  a  dulness  was  perceptible  in  the  dependent  portions  (lumbar  regions)  ; 
while  with  2000  c.c.  the  dulness  reached  a  hand's  breadth  and  became  absolute.  He 
rightly  emphasized  the  greater  accuracy  of  percussion  of  the  living  body;  and  this  is 
in  accordance  with  countless  clinical  and  pathologico-anatomic  experiences.  The 
more  favorable  results  in  percussing  the  living  depend,  the  writer  believes,  on  the 
one  hand,  upon  the  greater  elasticity  of  the  living  abdominal  walls,  which,  there- 
fore, furnish  a  better  localization  of  the  percussion  blow ;  and,  on  the  other  hand, 
upon  the  fact  that  during  life  the  movements;  of  the  intestines  prevent  the  loss  of 
any  fluid  between  separate  coils  of  intestines. 

Very  large  fluid  effusions  furnish  a  dull  note  over  the  greater  part  of  the  abdo- 
men. But  even  then  a  rounded  tympanitic  area  very  characteristically  persists  at 
the  highest  point  of  the  abdomen — i.  e.,  the  epigastrium — corresponding  to  the 
top  of  the  intestinal  coils  floating  in  the  fluid.  Free  fluid  effusion  in  the  abdominal 
cavity  can  thus  be  differentiated  from  the  equally  marked  abdominal  distention  due 
to  cystic  tumors.  In  women  such  cysts  frequently  originate  in  the  ovaries  ;  in  men, 
very  rarely  in  the  pancreas.  With  these  cysts  the  dulness  is  most  marked  in  the 
middle  of  the  abdomen,  because  they  quickly  grow  in  the  middle  line,  the  direction 
of  least  resistance,  and  crowd  the  intestines  backward. 

(See  the  next  paragraph  in  regard  to  the  demonstration  of  free  fluid  effusions 
in  the  abdomen,  with  coincident  edema  of  the  abdominal  walls.) 

7.  From  thickening  of  the  abdominal  walls,  whether  on  account  of 
fat-accumulation  or  of  edema.  The  edema  is  ordinarily  localized  in  the 
dependent  portions,  so  that  percussion  may  confuse  it  with  ascites. 
Palpation  of  the  abdominal  walls,  and  the  fact  that  the  dulness  does 
not  shift  with  the  changing  of  the  patient's  position,  will  generally  pre- 
vent a  mistake.  If  the  edema  is  combined  with  ascites,  the  movable 
fluid  can  sometimes  be  demonstrated  only  in  the  knee-chest  position, 
because  the  edematous  lateral  walls  of  the  abdomen  furnish  so  much 
dulness. 


AUSCULTATION. 
AUSCULTATION  IN  GENERAL;  INSTRUMENTS, 

Auscultation,  in  its  broadest  sense,  means  the  examination  of  the 
body  by  the  sense  of  hearing.  It  should  include  the  appreciation  of 
any  sounds  the  body  may  furnish,  whether  heard  nearby,  at  a  distance, 
or  with  the  aid  of  instruments — e.  g.,  the  cough,  the  voice,  etc.  In  the 
narrow  and  more  usual  sense,  auscultation  includes  only  the  diagnostic 
method  of  listening  to  the  body  by  means  of  some  specially  constructed 
sound-conducting  apparatus  or  by  means  of  the  ear  directly  applied. 

A  few  experiments  and  essays  antedated  the  practical  listening  to  the 
interior  of  the  body.  Auscultation  Avas,  however,  first  })ractically  em- 
ployed by  Laennec.  His  work  upon  auscultation  was  published  in  the 
year  1819.  In  it  he  not  only  instituted  these  methods  of  examination, 
but  ventured  definite  conclusions  which  were  based  upon  several  years' 
study.  He  also  invented  the  stethoscope.  A  great  number  of  learned 
authors  have  since  then  developed  the  scope  of  auscultation ;  among 


218  AUSCULTATION. 

them  notably  Skoda,  Wintrich,  Zamminer,  Traube,  Bamberger,  A.  Geigel, 
Th.  Weber,  and  Gerhardt. 

In  regard  to  method,  we  distinguish  between  an  immediate  or  direct 
and  a  mediate  or  indirect  auscultation.  In  the  former  the  examiner's 
ear  is  applied  directly  to  the  patient's  body  ;  in  the  latter  we  listen  with 
the  aid  of  an  instrument  called  the  stethoscope. 

According  to  tlie  writer's  opinion,  the  essential  for  a  good  stethoscope  is  not, 
as  was  contended  by  Laennec,  and  since  his  time  by  many  others,  its  capability 
of  intensifying  the  tone  vibrations.  Unless  an  examiner  is  hard  of  hearing, 
stethoscopes  which  transmit  to  the  ear  vibrations  intensified  by  resonance  are 
by  no  means  the  best,  because  they  are  bound  to  alter  the  tone  to  some  degree. 
Examples  of  this  type  are  the  instruments  of  Voltolini,  Hiiter,  and  Konig.  In 
that  of  Hiiter,  the  opening  of  the  sound  funnel  is  closed  by  a  simple  rubber  mem- 
brane ;  in  that  of  Konig,  by  two  rubber  membranes  with  an  air-tight  space  between, 
whose  form  can  be  changed  by  blowing  upon  it  into  a  lens-shaped  resonating  cham- 
ber. The  microphone,  devised  to  intensify  the  sounds,  has  not  thus  far  proved 
practical. '  The  requisite,  then,  for  a  good  stethoscoiae  is  not  so  much  the  capacity 
to  magnify  as  the  capacity  to  transmit  the  tones  to  the  ear  at  least  not  markedly 
weakened.  This  essential  is  fulfilled  by  practically  all  the  countless  stethoscopes 
met  with  in  practice,  in  the  use  of  which  we  are  sure  that  we  hear  only  what  is 
appreciated  by  the  ear.  The  stethoscope  might  therefore  be  considered  superfluous, 
and  only  immediate  auscultation  practised.  But  it  has  certain  advantages,  the- 
most  important  of  which  is  that  it  enables  us  to  auscultate  an  exactly  circum- 
scribed spot  to  the  exclusion  of  the  neighborhood  ;  in  other  words,  to  exclude  the- 
sounds  of  adjacent  body  parts.  In  cardiac  diagnosis  this  is  absolutely  necessary. 
On  the  other  hand,  immediate  auscultation  offers  certain  disadvantages  in  the- 
direction  of  convenience  and  cleanliness ;  besides,  in  the  supraclavicular  it  is  impos- 
sible, in  the  infraclavicular  region  very  difficult,  to  apply  the  ear  directly.  Direct 
contact  can,  of  course,  be  avoided  by  interposing  a  soft  towel  between  the  patient's. 
body  and  the  examiner's  ear. 

Stethoscopes  have  been  made  in  the  most  varied  forms  and  out  of  the  most 
varied  materials.  They  ordinarily  consist  of  a  hollow  stem  of  wood,  hard  rubber 
or  metal,  with  an  enlarged  tip  slightly  funnel-shaped  at  one  end,  and  an  ear  plate, 
with  a  hole  in  the  middle,  fastened  perpendicularly  to  the  other  end  of  the  stem. 

^  The  so-called  phonendoscope,  recently  so  extensively  advertised  and  discussed,  is  in. 
reality  nothing  more  than  the  old  resonance  stethoscope,  which  long  ago  fell  into  disuse 
on  account  of  the  alteration  of  the  tone.  Its  popularity  is  probably  due  to  the  name 
and  to  the  appearance  of  the  instrument.  Like  the  microphone,  its  principle  of  con- 
sti'uction  is  based  upon  the  false  assumption  that  the  main  trouble  in  auscultation  consists 
in  the  difficuhy  of  appreciating  the  sounds.  Anyone  who  has  had  much  experience 
will  complain  rather  of  an  embarrassment  of  riches  in  auscultation.  The  real  difficulty 
lies  in  judging  the  significance  of  the  sounds,  and  this  difficulty  will  not  be  made  any 
less  by  using  an  instrument  which  magnifies  unimportant  or  artificial  overtones.- 

^  [Despite  Prof.  Sahli's  objections  to  the  resonating  stethoscope,  its  use  in  America 
is  so  universal  that  we  believe  a  word  in  its  support  might  be  in  place  here.  The 
choice  of  a  stethoscope  is,  after  all,  quite  a  matter  of  custom  and  convenience.  Many 
good  stethoscopes  are  made  in  America,  especially  the  Tiemann  and  Ford  models,  the 
favorites  in  New  York  City,  and  the  Gannett  model,  so  often  selected  by  clinicians  in 
Boston  and  Baltimore.  The  resonance  is  decided  with  any  of  these  instruments,  but  we 
have  not  found  that  it  seriously  detracts  from  their  practicability.  The  Bowles'  model, 
a  type  of  phonendoscope,  is  warmly  ]-ecommended  by  many  of  the  younger  clinicians. 
In  our  opinion  it  has  many  advantages,  although  we  still  depend  upon  the  other 
models  for  most  purposes.  One  especial  advantage  is  that  it  can  often  be  used  when 
another  type  of  instrument  fails — e.  9.,  when  a  patient  is  recumbent  and  too  sick 
to  be  moved.  Then,  by  slipping  it  under  the  patient's  back,  we  can  often  obtain 
an  approximately  accurate  idea  of  the  breathing  over  the  bases  of  the  lungs  behind. 
—Ed.] 


AUSCULTATION  OF  THE  RESPIRATORY  ORGANS.  219 

The  fiinnel-shaped  end  is  placed  against  the  skin  of  the  patient,  and  the  ear  of  the 
examiner  is  applied  to  the  ear  plate  as  smoothly  as  possible.  The  ear  plate  is  in  some 
instruments  concave,  in  others  convex.  For  most  observers  the  former  shape  seems 
to  adapt  itself  better  to  the  ear.  To  carry  the  instrument  conveniently  in  the 
pocket,  it  is  desirable  to  be  able  to  separate  the  ear  plate  from  the  tube  by  unscrew- 
ing or  in  some  other  way.  There  is  no  advantage  in  substituting  for  the  ear  plate 
an  olive-shaped  peg  adapted  to  fit  into  the  external  canal  of  the  ear.  Experiments 
have  shown  that  the  canal  which  is  bored  through  the  tube  in  the  axis  of  the  steth- 
oscope should  have  about  the  same  diameter  as  the  entrance  of  the  external  ear.  In 
order  not  to  cause  the  patient  pain,  the  edge  of  the  funnel  end  must  be  well  rounded. 
The  width  of  the  funnel  varies  with  different  instruments.  A  wide  fiinnel  has  the 
advantage  of  receiving  sound  waves  over  a  large  area,  and  therefore,  in  general,  of 
transmitting  the  sounds  more  powerfully  to  the  ear.  On  the  other  hand,  a  narrow 
funnel  has  the  advantage  of  better  isolating  the  sounds  and  of  modifying  them 
less  by  resonance.  It  is  of  some  advantage,  therefore,  to  possess  a  stethoscope  with 
a  wide  funnel  at  one  end  and  a  narrow  one  at  the  other,  in  either  of  which  the 
ear  plate  can  be  inserted  by  means  of  a  conical  peg.  The  funnel  should  not  be  too 
long.  The  long  bell-shaped  funnel  ends  of  many  hard-rubber  stethoscopes  really 
confuse  the  respiratory  murmurs,  and  often  in  a  very  marked  way,  by  resonance. 
The  length  of  the  cylindric  part  of  the  instrument  is  of  minor  importance. 

Flexible  stethoscopes  transmit  the  sound  from  a  funnel  through  a  tube  or 
tubes  to  the  ear  of  the  observer.  This  is  the  principle  of  most  of  the  above- 
mentioned  resonance  stethoscopes.  They  are  very  convenient,  especially  the  biau- 
ricular, and  furnish  a  very  loud  tone  ;  but  the  resonance  is  confusing,  and  the 
slightest  movement  in  handling  gives  rise  to  perplexing  murmurs.  The  same  dif- 
ficulty occurs  even  in  the  double-eared  Camman'  s  stethoscope  (recently  devised  and 
warmly  recommended  by  Piel)  and  in  similar  instruments  in  which  accompanying 
noises  are  hindered  by  making  the  sound-conducting  tube  partly  quite  firm,  partly 
of  very  dense  tubing.  After  many  attempts  with  all  these  instruments,  the  writer 
must  recommend  for  practice  the  ordinary  single-barrel  stethoscope,  for  he  is  con- 
vinced that  in  a  method  of  examination  which  is  already  difficult  itself,  it  is  not 
advisable  to  complicate  the  affair  for  the  sake  of  external  convenience  and  to  use 
instruments  which  possess  such  essential  faults.  Flexible  stethoscojDCs  are  abso- 
lutely necessary  only  for  auscultating  one's  own  body. 

The  Technic  of  Auscultation. — The  stethoscope  should  be  applied  very  carefully, 
so  that  the  edge  of  the  funnel  makes  an  air-tight  connection  with  the  skin  ;  the  ear 
should  be  lightly  applied  to  the  ear  plate  without  leaning  or  propping  the  head 
upon  it.  Tilting  the  stethoscope  should  be  avoided,  because  it  is  very  painful  for 
the  patient  and  prevents  correct  auscultation.  The  best  way  is  to  hold  the  stem 
with  the  thumb  and  forefinger  lightly  applied  near  the  funnel  end,  so  that  the 
slightest  movement  can  be  readily  felt  and  corrected. 

AUSCULTATION  OF  THE  RESPIRATORY  ORGANS. 

The  immediate,  as  well  as  the  mediate,  method  should  be  used  in 
auscultating  the  lungs,  for  some  sounds,  such  as  faint  bronchial  breath- 
ing, are  better  appreciated  by  applying  the  ear  directly  to  the  chest,  and 
an  exact  localizatioii  is  of  less  value  than  in  cardiac  diagnosis. 

It  is  exactly  in  these  cases  (in  general  rare)  where  the  tones  are  so  weak  as  to 
be  doubtful  that  the  tone-increasing  or  resonating  stethoscope  is  useless,  for  it 
makes  the  doubt  still  greater  by  its  modifications  of  the  sounds.  We  will  mention 
in  a  special  section  the  sources  of  error  which  may  arise  from  involuntarily  moving 
the  stethoscope  while  auscultating  the  lungs. 

It  is  advisable  to  auscult  during  normal,  and  then  during  exaggerated, 
respiration,  and  over  any  suspicions  places  both  during  and  after  cough, 
as  well  as  to  listen  in  such  places  to  the  loud  and  the  whispered  voice. 


220  A  USOULTA  TION. 

THE  NORMAL  VESICULAR  RESPIRATORY  MURMUR. 

A  characteristic  sighing  or  sipping  noise,  perhaps  resembling  a  very 
soft  "f,"  is  heard  over  a  healthy  lung  throughout  inspiration  ;  during 
expiration  there  is  either  no  sound,  or  at  the  beginning  a  very  short, 
faint  noise.  The  latter  is  rather  difficult  to  describe ;  it  is  apt  to  be 
lower  pitched  than  the  murmur  during  inspiration,  and  is  slightly 
rustling,  or  over  certain  places  slightly  blowing,  in  character.  Its  dura- 
tion corresponds  normally  to  less  than  a  fifth  of  that  of  the  inspiratory 
murmur.  These  two  sounds  constitute  the  normal  breathing  murmur, 
the  so-called  vesicular  breathing.  Its  presence  shows  us  that  the  lung 
parenchyma  at  the  spot  of  auscultation  not  only  contains  air,  but  also 
breathes — that  is,  during  inspiration  air  enters  the  alveoli.  The  inspira- 
tory murmur  is  evidently  the  essential  characteristic  of  vesicular  breathing. 

jS^umerous  theories  have  been  suggested  in  explanation  of  this  vesicu- 
lar breathing,  but  as  yet  there  is  no  one  definitely  accepted.  Laennec, 
the  inventor  of  auscultation,  assumed  that  vesicular  breathing  was  caused 
by  the  rubbing  of  the  inspiratory  air  stream  against  the  walls  of  the  fine 
bronchi  or  infundibula.  But  if  friction  exists  it  must  act,  not  between 
the  walls  and  the  air,  but  between  the  outer  layer  of  air,  which  rests 
nearly  motionless  against  the  walls,  and  the  more  central  actively  moving 
current.  Laennec's  theory,  however,  did  not  lay  any  emphasis  upon 
the  frictions  taking  place  at  the  outer  boundary  of  the  air  stream,  and 
might  be  stated  to-day  by  saying  that  vesicular  breathing  is  the  acoustic 
expression  of  the  friction  caused  by  the  entry  of  air  into  the  pulmonary 
parenchyma.  It  has  also  been  objected  that  the  current  of  air  entering 
the  bronchi  during  inspiration  is  not  rapid  enough  to  cause  friction 
noises. 

Baas  has  advanced  a  more  recent  theory,  which  many  authors  believe 
disproves  Laennec's.  Vesicular  breathing  he  regards  as  a  modification 
of  the  blowing  noise  arising  in  the  larynx  and  trachea  during  respira- 
tion, transmitted  through  the  bronchi  to  the  interior  of  the  lungs,  and 
thence  through  the  air-containing  lung  to  the  observer's  ear.  The 
following  experiment  was  made  in  proof:  An  inflated  lung  was  placed 
upon  the  larynx  of  a  living  man,  the  laryngotracheal  murmur  was  aus- 
cultated through  this  lung,  and  it  was  expected  that  the  blowing  mur- 
mur would  be  transformed  into  a  sipping  vesicular  breathing  by  the  air- 
containing  lung.  The  author  has  never  heard  anything  but  a  weakened 
blowing  tracheal  murmur  in  performing  this  experiment.  It  is,  in  fact, 
difficult  to  imagine  how  the  tracheal  murmur,  with  an  expiratory  portion 
the  equal  of  or  stronger  than  the  inspiratory  portion,  could  be  both  quali- 
tatively and  quantitatively  modified  by  the  interposition  of  an  air-contain- 
ing lung.  Nor  does  clinical  evidence  support  Baas'  theory,  for,  as  soon 
as  a  bronchus  is  plugged  by  secretion  or  by  a  foreign  body,  no  vesicular 
breathing  can  be  heard  over  the  pulmonar}^  area  supplied  by  that  bronchus 
until  the  bronchus  becomes  free  again.  This  surely  proves  that  in- 
spiratory filling  of  the  lung  with  air  is  necessaiy  to  produce  vesicular 
breathing.  The  pathologic  modifications  of  vesicular  breathing  sim- 
ilarly disprove  the  Baas  theory — e.  g.,  we  hear  an  intensified  vesicular 


AUSCULTATION  OF  THE  RESPIRATORY  ORGANS.  221 

breathing  over  circumscribed  areas  of  lung  when  for  some  reason  the 
breathing  is  more  vigorous  (vicarious) ;  and,  on  the  contrary,  a  localized 
diminished  breathing  wherever  for  any  reason  the  corresponding  lung 
area  is  limited  in  its  movement  (through  lack  of  room  or  adhesions). 
Again,  despite  the  increase  of  the  laryngeal  breathing  noise  in  laryngeal 
stenosis,  diminished  vesicular  breathing  is  heard  over  the  lung.  Fur- 
ther, the  thicker  the  layer  of  lung,  the  more  intense  is  the  vesicular 
breathing,  although  according  to  this  theory  it  should  be  diminished. 
Finally,  systolic  vesicular  breathing,  a  respiratory  murmur  synchronous 
with  the  cardiac  systole  and  not  in  the  least  dependent  upon  a  laryngo- 
tracheal breathing  murmur,  speaks  with  certainty  against  the  Baas  theory, 
and  decidedly  favors  the  idea  that  vesicular  breathing  depends  upon  the 
pulmonary  excursion.  The  writer  considers  these  arguments  sufficient 
to  discountenance  Baas'  theory. 

Now,  after  all  this  critical  discussion,  what  is  the  real  explanation  of 
vesicular  breathing  ?  In  the  writer's  work  upon  the  origin  of  vesicular 
breathing  he  demonstrated  upon  a  man  with  congenital  fissure  of  the 
sternum  ^  that  vesicular  breathing  arises  from  inflation  of  the  lung  tis- 
sue, even  with  the  exclusion  of  every  laryngotracheal  murmur.  This 
man  had  a  hernia  of  the  lung  in  the  region  of  the  sternal  fissure  which 
protruded  externally  to  a  marked  degree  when  the  patient  strained — i.  e., 
increased  his  intra-abdominal  tension.  When  this  pulmonary  hernia 
was  auscultated  at  the  same  time  that  the  patient  strained,  the  most 
distinct  vesicular  breathing  was  heard,  which  was  due  to  an  expiratory 
filling  of  the  pulmonary  alveoli,  and,  since  the  laryngotracheal  murmur 
was  excluded  by  the  closure  of  the  glottis,  we  obtained  a  certain  proof 
that  the  murmur  of  vesicular  breathing  is  due  to  the  local  inspiratory 
movements  of  the  pulmonary  parenchyma.  The  writer  has  recently  had 
an  opportunity  to  make  a  similar  examination  of  the  pulmonary  apices 
of  an  emphysematous  subject,  which  became  inflated  like  balloons  when 
the  patient  strained,  and  over  which  could  be  heard  distinct  vesicular 
breathing.  In  these  examinations  he  could  not  determine  whether  the 
vesicular  murmur  was  produced  by  the  distention  of  the  pulmonary 
tissue  or  by  the  friction  in  the  interior  of  the  inspiratory  air  stream  in 
the  smallest  bronchi  and  alveoli.  That  is  a  fine  point  of  no  great  sig- 
nificance. Stretching  of  the  lung  tissue  may  cause  the  murmur.  The 
distention  of  separate  lung  alveoli  doubtless  does  not  happen  at  the 
same  instant,  and  may  produce  a  series  of  vibrations  lasting  over  the 
entire  inspiratory  period,  which  together  may  cause  the  vesicular  murmur. 

To  explain  the  normal  brief  expiratory  murmur  we  must  assume 
either  that  the  weak  remnant  of  the  laryngotracheal  breathing  murmur 
is  transmitted  from  the  bronchi,  or  else  that  the  expiratory  murmur 
arises  like  the  vesicular  inspiration,  locally,  through  movements  in  the 
lung.  If  the  expiratory  murmur  has  a  plain  blowing  character  like  that 
of  the  laryngotracheal  murmur,  the  former  hypothesis  may  be  enter- 
tained. It  should  then  be  classed  under  the  so-called  physiologic  bron- 
chial breathing  (see  p.  222  et  seq.).  If  this  blowing  character  is 
'  Corresfpondenzhlatt  fixr  Schweizer  Aertze,  1892. 


222  A  USCULTA  TION. 

lacking,  the  expiratory  murmur  probably  comes  from  within  the  lung, 
especially  because  expiration,  just  as  inspiration,  may  be  modified  by 
local  lung  changes.  The  prolonged  expiration  in  catarrh  (see  p.  225 
€t  seq.)  can  be  explained  only  by  assuming  such  a  localized  origin.  The 
elastic  retraction  of  the  lung  in  the  beginning  of  expiration  must  be 
strongest  and  quickest ;  hence,  the  expiratory  murmm-  is  normally  to 
be  heard  only  at  the  very  beginning  of  expiration. 

Systolic  vesicular  breathing  (mentioned  above)  is  occasionally  to  be  found  both 
in  healthy  and  in  diseased  individuals.  Its  origin  is  unknown  ;  it  has  no  patho- 
logic significance,  is  heard  only  in  the  neighborhood  of  the  heart,  in  slightly  marked 
instances  merely  as  a  systolic  accentuation  of  regular  vesicular  breathing.  It  cer- 
tainly depends  upon  variations  of  the  intrathoracic  negative  pressure  connected 
with  the  systolic  diminution  in  the  size  of  the  heart  (meiocardia).  Many  so-called 
accidental  heart  murmurs  (see  later)  are  nothing  more  than  systolic  vesicular 
breathing. 

PHYSIOLOGIC  BRONCHIAL   (MIXED)  BREATHING  MURMUR. 

Over  certain  areas  of  the  normal  lungs  the  respiratory  murmur  sounds 
bronchial.  Such  a  murmur  corresponds  in  most  essentials  to  the  laryn- 
gotracheal breathing  heard  over  the  larynx  (p.  220).  In  contrast  to 
the  vesicular,  bronchial  breathing  presents  a  blowing  character  and 
approaches  to  a  definite  pitch.  We  can  reproduce  the  sound  quite 
perfectly  by  vigorously  inspiring  and  expiring  with  the  mouth  fixed 
as  if  about  to  pronounce  the  syllable  "  ha."  We  can  simulate  different 
pitch  by  changing  the  position  of  the  mouth.  In  physiologic  bronchial 
breathing  expiration  lasts  longer  and  is  more  strongly  accentuated  than 
inspiration,  exactly  the  reverse  of  the  relation  between  them  in  vesicular 
breathing.  The  rima  glottidis  is  narrowed  during  expiration,  and  that 
is  a  sufficient  cause  for  an  expiratory  stenotic  murmur  or  for  an  accen- 
tuation, as  well  as  for  its  prolonged  duration. 

Physiologic  bronchial  breathing  is  nothing  more  than  the  laryngo- 
tracheal murmur  which  originates  at  the  upper  air  passages  and  is 
transmitted  through  the  bronchi  to  certain  areas  over  the  lungs.  Its 
intensity  varies  considerably  in  accordance  with  the  individual  peculiar- 
ities of  acoustic  transmission.  In  many  men  the  laryngotracheal 
murmur  is  audible  only  over  the  neck,  while  all  over  the  lung  pure 
vesicular  breathing  can  be  heard.  Physiologic  bronchial  breathing  is 
most  frequently  audible  anteriorly  over  the  superior  portions  of  the 
lungs,  and  posteriorly  in  the  interscapular  space.  This  is  due  to  the 
location  of  the  trachea  and  great  bronchi.  The  right  bronchus  is  wider 
and  a  more  direct  continuation  of  the  trachea  than  the  left ;  hence  this 
breathing  is  naturally  more  evident  upon  the  right  side  and  sometimes 
also  over  the  upper  part  of  the  sternum.  Vesicular  breathing  is  almost 
always  to  be  heard  at  the  same  time  with  the  physiologic  bronchial 
breathing ;  but  if  the  respiration  is  especially  faint,  then  the  physiologic 
bronchial  breathing  will  alone  be  heard — e.  g.,  a  thick  thoracic  wall  ren- 
ders the  appreciation  of  the  vesicular  breathing  difficult.  A  so-called 
mixed  breathing  is,  however,  the  general  rule — i.  e.,  during  inspiration 


AUSCULTATION  OF  THE  RESPIRATORY  ORGANS.  223 

the  vesicular,  and  during  expiration  the  bronchial,  character  predomi- 
nates. Forced  breathing,  dyspnea,  thinness  of  the  thorax,  any  changes 
in  the  larynx  and  trachea  which  favor  the  production  of  a  strong  stenotic 
murmur  (compression  of  the  trachea  from  the  side  by  a  goiter,^  and  the 
like) — all  these  will  intensify  physiologic  bronchial  breathing.  A  sus- 
picion of  physiologic  bronchial  breathing  may  very  rarely  be  heard  all 
over  the  lung,  but  more  frequently  along  the  spine  and  over  most  of 
the  sternum. 

Physiologic  bronchial  breathing  may  depend  in  some  persons  upon 
certain  peculiar  positions  of  the  mouth.  It  may  be  considerably  in- 
fluenced, intensified,  diminished,  or  even  caused  to  disappear  by  alter- 
ing the  position  of  the  mouth. 

ALTERATIONS    OF  VESICULAR    BREATHING   UNDER   PHYSIOLOGIC 
AND    PATHOLOGIC  CONDITIONS. 

INCREASED  (PUERILE)  AND  WEAKENED  VESICULAR  BREATHING. 

The  intensity  of  the  vesicular  breathing  varies  with  the  depth  of  the 
respiration  and  with  the  spot  auscultated.  It  is  weaker  at  the  apices 
and  borders,  where  the  pulmonary  layer  is  thin,  than  over  the  thick 
parts  of  the  lung.  Thick  thoracic  walls  also  weaken  it.  Children 
present  an  exceptionally  loud  and  strong  vesicular,  so-called  puerile 
breathing,  with  which  physiologic  bronchial  breathing  is  often  espe- 
cially plainly  mixed.  Beginners  are  apt  to  mistake  it  for  a  pathologic 
phenomenon. 

Pathologic  increased  vesicular  breathing  is  best  designated  as  sharp  or 
increased  vesicular  breathing.  The  writer  emphasizes  these  two  ad- 
jectives because  the  expressions  sharp  or  increased  vesicular  breathing 
and  rough  vesicular  breathing,  though  fundamentally  different,  are  often 
used  synonymously.  If  ordinary  vesicular  breathing  is  represented  by 
the  sound  of  a  soft  /,  increased  vesicular  breathing  roughly  corresponds 
to  the  consonants  ff.  The  physiologic  increased  breathing  (mentioned 
above)  must  first  be  taken  into  account  before  we  decide  that  increased 
vesicular  breathing  is  pathologic. 

Pathologically  increased  vesicular  breathing  depends  most  frequently 
upon  a  catarrh  of  the  finer  bronchial  tubes.  The  latter  are  narrowed 
by  the  swollen  mucous  membrane,  and  this  stenosis  presumably  causes 
the  increased  breathing.  This  explanation  would  naturally  support  the 
friction  theory  of  vesicular  breathing. 

Another  cause  for  pathologically  increased  vesicular  breathing  is  the 
more  active  breathing  of  a  certain  portion  of  the  lung.  This  happens 
wherever  a  lung  part  is  retracted  or  relaxed,  and  is  generally  accom- 
panied by  an  abnormally  loud  or  tympanitic  percussion  note  (see  p.  210). 
Thus,  we  frequently  hear  increased  vesicular  breathing  in  the  first  stage 
of  croupous  pneumonia,  in  the  neighborhood  of  infiltrations,  or  in  the 
neighborhood  of  affections   of  the  thoracic  cavity  which  limit  the  space, 

'In  such  a  case  the  expression  "physiologic  bronchial  breathing"  signifies  merely 
that  the  phenomenon  does  not  depend  upon  any  pathologic  changes  in  the  lung. 


224  A  USCULTA  TION. . 

etc.  In  pleurisy  with  effusion  and  in  pneumothorax  the  respiratory 
murmur  is  diminished  or  absent  over  one-half  of  the  thorax,  despite  the 
pronounced  retraction  of  the  lung.  But  over  the  other  chest-half  the 
breathing  is  increased  vicariously.  The  same  condition  is  often  noted 
in  pneumonia  and  in  pulmonary  tumors. 

Increased  vesicular  breathing  is  of  special  importance  in  demonstra- 
ting multiple  small  infiltration  areas  which  furnish  no  other  auscultatory 
or  percussion  signs.  The  increase  depends  partly  upon  the  retraction 
and  relaxation  of  the  neighboring  pulmonary  tissue,  partly  upon  the 
accompanying  localized  catarrh.  For  this  reason  increased  vesicular 
breathing  localized  over  one  apex  is  an  important  sign  for  recognizing 
incipient  tuberculosis,  and  especially  so  because  at  the  apex,  where 
tuberculosis  most  frequently  makes  its  first  appearance,  vesicular  breath- 
ing is  normally  weak. 

Weakness,  diminution  or  absence  of  vesicular  hi^eathing  is  observed 
under  manifold  conditions.  Careful  attention  should  be  given  to  the 
physiologic  variations  before  we  can  assume  any  pathologic  processes. 
Any  cause  which  limits  the  inspiratory  distention  of  the  pulmonary 
parenchyma  will  diminish  and  finally  abolish  the  vesicular  breathing — 
e.  g.,  any  obstacle  to  respiration  situated  in  the  larger  air  passages.  If 
the  obstacle  is  located  in  the  larynx  or  trachea,  the  respiratory  murmur 
will"  be  diminished  over  both  lungs.  If  located  in  one  bronchus,  it  will 
be  diminished  over  the  entire  pulmonary  territory  supplied  by  that  bron- 
chus. This  furnishes  us  with  a  means  of  estimating  the  degree  of 
laryngeal  stenosis  in  croup  and  of  determining  any  extension  of  the 
croupous  process  down  into  one  or  the  other  bronchus.  A  localized 
diminution  or  abolition  of  the  vesicular  breathing  is  important  for  esti- 
mating the  position  of  a  foreign  body  in  the  bronchus.^  The  respiratory 
murmur  is  diminished  in  certain  forms  of  catarrh  which  cause  an  ex- 
ceptionally marked  stenosis  of  the  affected  bronchi.  The  murmur  is 
abolished  in  obturation  atelectasis. 

Even  if  the  air  passages  are  free,  diminished  breathing  will  be 
observed  when  any  sort  of  mechanical  obstruction  prevents  the  normal 
alveolar  distention — e.  g.,  firm  pleural  adhesions  which  limit  the  lung 
excursions.  Multiple  small  infiltrations  often  diminish  or  abolish  the 
vesicular  breathing  because,  to  a  certain  extent,  they  make  the  pul- 
monary area  between  them,  which  is  still  pervious  to  air,  stiff  and  non- 
.  expansive.  Increased  vesicular  breathing  is,  however,  more  commonly 
heard  over  multiple  small  infiltrations. 

Such  a  localized  diminution  of  the  respiratory  murmur,  whether 
depending  upon  a  circumscribed  catarrh  stenosing  the  bronchi,  or  upon 
fixation  of  the  lung  by  small  areas  of  infiltration,  or  by  pleural  adhe- 
sions, is  very  important  in  diagnosing  circumscribed  tubercular  areas. 
Sometimes,  though  rarely,  even  extensive  tubercular  infiltration  does 
not  show  the  expected  bronchial  breathing,  but  diminished  vesicular 
breathing.  This  peculiarity  of  many  tubercular  infiltrations,  as  con- 
trasted with  other  kinds  of  pulmonary  consolidation,  can  be  explained 
^  [The  x-ray  will  often  aid  here. — Ed.] 


AUSCULTATION  OF  THE  RESPIRATORY  ORGANS.  225 

by  the  frequent  narrowing  or  contraction  of  the  bronchial  lumen  in 
tuberculosis. 

Diminished  breathing  is  observed  in  pleurisy  over  the  affected  side 
even  at  the  places  where  the  lung  lies  against  the  thoracic  wall,  because 
either  the  exudation  or  the  pain  limits  the  excursions  of  that  side. 

An  emphysematous  lung  makes  very  slight  excursions,  on  account 
of  its  permanent  inspiratory  position ;  hence  the  respiratory  murmur 
is  frequently  diminished.  But  a  coincident  catarrh  of  the  bronchi 
would  tend  to  intensify  the  respiratory  murmur,  and  so  the  final  result 
will  naturally  depend  upon  which  factor  is  in  excess.  Diminished 
breathing  is  one  of  the  cardinal  symptoms  of  pkurisy,  pneumothorax, 
and  pulmonary  tumors,  for  two  reasons  :  In  the  first  place  the  excursion  of 
the  aifected  side  is  limited ;  and  in  the  second  place  the  transmission 
of  the  breathing  to  the  examiner's  ear  is  impaired  by  the  interposition  of 
fluid  or  solid  tissue. 

VESICULAR  BREATHING  "WITH  A  PROLONGED  EXPIRATION. 

Normally  we  hear  only  a  faint  murmur  or  none  at  all  over  the  lung 
during  expiration.  But  under  some  circumstances  the  expiratory  murmur 
may  be  prolonged  until  it  lasts  even  longer  than  inspiration. 

Prolonged  expiration  is  a  frequent,  though  not  constant,  accompani- 
ment of  increased  vesicular  breathing.  It  occurs  in  bronchitis,  probably 
because  the  swollen  mucous  membrane  opposes  an  obstacle  to  the  res- 
piratory current,  and  produces  a  stenotic  murmur  with  expiration.  Expi- 
ration, as  is  well  known,  is  less  powerful  and  slower  than  inspiration, 
and  the  stenosis  slows  it  still  more.  If  the  catarrh  is  localized  at 
certain  places,  the  prolonged  expiration  will  also  be  a  local  phenomenon. 
The  prolonged  expiratory  murmur  in  the  catarrh  of  emphysema  and  in 
asthmatic  attacks  is  much  more  extensive,  being  diifused  over  the  entire 
lung.  In  such  cases  the  entire  expiratory  movements  of  the  thorax  are 
slowed  (p.  90  et  seq.).  Prolonged  expiration  is  therefore  a  symptom  of 
catarrh.  If  it  is  localized,  it  has  the  same  significance  in  the  diagnosis 
of  diseased  areas  (infiltration,  tuberculosis)  as  has  increased  or  diminished 
vesicular  breathing  (pp.  223  and  224). 

ROUGH  OR  IMPURE  AND  COG  "WHEEL  VESICULAR  BREATHING. 

Rough  vesieular  breathing  is  an  impure,  slightly  uneven  murmur 
heard  during  inspiration,  as  if  strange  accompanying  noises  were  ad- 
mixed with  the  normal  vesicular  murmur.  In  order  to  prevent 
confusion  with  sharp  or  increased  vesicular  breathing  (p.  223),  the  term 
impure  breathing  is  more  fitting.  Increased  breathing  is  exquisitely 
pure  and  generally  very  intense,  whereas  rough  breathing  is  more  fre- 
quently weak  and  faint. 

Impure  as  well  as  increased  breathing  is  a  sign  of  bronchial 
catarrh,  and  may  or  may  not  be  accompanied  by  })rolonged  expiration. 
Either  the  partial  impermeability  of  the  bronchi  produces  unequal  res- 
piratory excursions  of  the  lung  area  in  question  or  else  accomj^anying 
noises  derived  from  the  presence  of  secretion  complicate  the  pure  vesicular 

15 


226  AUSCULTATION. 

murmur.  If  these  accompanying  noises  can  be  plainly  isolated,  we  call 
them  rales  (see  p.  232),  but  if  they  remain  indistinct  and  blended,  the 
vesicular  breathing  becomes  impure  or  rough. 

The  so-called  cog-wheel  respiration  is  somewhat  like  impure  breathing, 
but  is  characterized  by  jerky  intermittent  pauses  in  the  inspiratory  mur- 
mur or  by  accompanying  noises  which  plainly  separate  the  individual 
portions  of  the  murmur  from  each  other.  In  contrast  to  impure  breath- 
ing, these  individual  portions  retain  their  smooth  sighing  or  sipping 
character.  The  acoustic  peculiarities  of  cog-wheel  respiration  convince 
us  that  it  is  caused  by  the  air  current  being  forced  into  the  alveoli  with 
effort  and  intermittently  overcoming  some  obstacles.  Cog-wheel  respi- 
ration localized  over  a  definite  area  of  the  lung  is  also  a  sign  of  catarrh, 
and  so  it  is  natural  to  suppose  that  in  this  case  this  intermittent 
obstruction  to  the  respiration  is  due  either  to  valve-like  swellings  of  the 
mucous  membrane  or  to  accumulations  of  secretion  which  must  be  pushed 
aside  by  the  air  current.  Hence  its  relationship  to  impure  or  rough 
breathing.  Naturally  cog-wheel  inspiration  may  be  an  increased  or 
diminished  breathing  and  may  be  associated  with  prolonged  expiration. 
Sometimes  the  expiration  is  also  cog-wheel  in  type. 

Hensen  ^  has  called  attention  to  the  fact  that  in  many  cases  of  cog- 
wheel breathing  the  intermissions  are  synchronous  with  the  pulse.  He 
explains  this  phenomenon  by  the  supposition  that  hyperemia  of  the  lung 
is  responsible  for  this  form  of  cog-wheel  breathing.  This  pulsating 
character,  however,  may  be  explained  equally  well  by  the  previous 
statements  if  M'e  bear  in  mind  that  every  systole  of  the  heart  produces 
a  negative  variation  of  the  intrathoracic  pressure  and,  consequently, 
accelerates  the  inspiratory  air  current. 

There  is  another  kind  of  cog-wheel  respiration  not  at  all  dependent 
upon  the  pulmonary  or  bronchial  condition,  but  upon  uneven  or  inter- 
mittent action  of  the  inspiratory  muscles.  This  occurs  by  no  means 
rarely  in  partial  paralyses  and  in  fatigued  conditions  of  the  respiratory 
muscles.  It  can  be  distinguished  from  the  form  described  above  by  its 
more  even  distribution  over  the  entire  lung. 

PATHOLOGIC  BRONCHIAL  BREATHING. 

Pathologic  bronchial  breathing  is  a  blowing  murmur  heard  over  mor- 
bid areas,  and  is  practically  identical  with  the  sound  we  have  already 
described  under  the  term  physiologic  bronchial  breathing — i.  e.,  with 
a  laryngotracheal  murmur  resembling  the  syllable  "  ha."  From  experi- 
ence we  have  learned  that  it  is  to  be  heard  wherever  the  pulmonary 
parenchyma  is  airless  (whether  on  account  of  external  compression  or 
on  account  of  infiltration),  wherever  there  are  pathologic  pulmonary 
cavities  which  freely  communicate  with  the  bronchus,  and  wherever  the 
bronchi  themselves  are  dilated,  either  diffusely  or  in  the  form  of  a  sac. 

One  of  the  oldest  explanations  of  the  origin  of  bronchial  breathing 
over  solid  portions  of  the  lung  assumed  that  the  vesicular  breathing 
disappeared  and  that  the  laryngotracheal  murmur  was  transmitted  more 
1  Arch.  f.  klin.  Med.,  1902,  vol.  Ixxiv.,  p.  237. 


AUSCULTATION  OF  THE  RESPIRATORY  ORGANS. 


227 


plainly  to  the  surface  of  the  thorax  through  the  thickened  lung  par- 
enchyma than  through  the  air-containing  tissue.  But  this  explanation 
is  not  tenable,  because  we  can  prove  that  a  solid  organ  does  not  transmit 
this  murmur  as  well  as  does  the  air-containing  lung.  However,  although 
the  hepatized  tissue  itself  does  not  transmit  the  laryngeal  murmur 
better  than  the  normal  lung,  nevertheless  the  air-containing  bronchi 
incased  in  a  solid  tissue  are  better  conductors  than  when  incased  in 
air-containing  tissue. 

This  modified  explanation  is  generally  accepted  as  correct,  but  it  will 
not  hold  good  in  every  case,  for  in  pneumonia  bronchial  breathing  is 
heard  not  only  over  the  infiltrated  area,  but  also  in  its  vicinity  and  upon 
the  opposite  (healthy)  side  in  the  neighborhood  of  the  spinal  column. 
Witli  such  a  result  we  sometimes  erroneously  diagnose  a  double  pneu- 
monia, and  learn  at  the  autopsy  that  the  bronchial  breathing  must  have 
been  transmitted  from  the  affected  side.  This  transmission  of  bronchial 
breathing  shows  how  imperfect  the  preceding  theory  is,  since  it  shows. 


Lung  tissue 
containing  air. 


Solidified  lung  tissue 
(not  containing  air). 


Fig.  101.       ' 


that  bronchial  breathing  can  be  well  transmitted  in  air-containing 
tissue.  Then,  if  the  bronchial  breathing  is  really  as  intense  in  the 
normal  bronchi  as  in  the  infiltrated  tissue,  how  can  we  explain 
why  in  sound  lungs  it  should  not  be  able  to  reach  the  examiner's 
ear?  The  vesicular  breathing  certainly  does  not  conceal  the  bron- 
chial breathing,  because  both  in  transmitted  bronchial  breathing  and 
also  under  other  circumstances  (mixed  breathing,  see  p.  231)  we  can 
appreciate  at  the  same  time  both  a  bronchial  and  a  vesicular  murmur. 
Personally  the  writer  can  explain  transmitted  bronchial  breathing  only 
by  assuming  that  the  infiltrated  lung  not  only  transmits  the  laryngeal 
murmur  to  the  surface  through  the  bronchi,  but  magnifies  it.  It  is 
evident  that  such  an  increase  in  a  portion  of  the  lung  immovable  on 
account  of  the  infiltration  would  be  produced  best  by  resonation  or 
consonation  (Skoda).  The  variations  observed  in  the  pitch  of  bronchial 
breathing  (p.  229)  show  that  real  resonating  phenomena  can  appear  in 
the  bronchi  of  infiltrated  portions  of  Inng.  This  question  of  resonance 
will  be  discus.sed  under  Consonating  Rales. 


228  A  USCUL  TA  TION. 

Fig.  101  explains  another  cause  of  the  increase  of  bronchial  breath- 
ing over  infiltrated  areas.  Here  a,  b,  c,  d  represents  an  infiltrated, 
a,  f,  e,  d  a  non-infiltrated,  bronchial  area  with  the  tributary  bronchi  g,  h 
and  g,  i.  As  a  consequence  of  the  infiltration  the  air  current  between  h 
and  g  ceases,  whereas  that  from  g  to  i  persists,  so  that  at  the  point  g  the 
current  conditions  are  decidedly  altered.  The  current  of  a.ir  i,  g  blows 
over  a  quiet  column  of  air  and  might  very  likely  produce  bronchial 
breathing  similarly  to  the  noise  made  by  blowing  over  the  opening  of  a 
key. 

Pathologic  bronchial  breathing  is  sometimes,  although  rarely,  heard 
louder  during  inspiration,  and  not,  as  is  the  laryngeal  murmur,  during 
expiration.  This  fact,  it  seems  to  the  writer,  argues  in  favor  of  the 
latter  theory  of  the  origin  or  increase  of  bronchial  breathing,  and 
cannot  be  explained  by  mere  conduction  and  resonation. 

The  result  of  this  discussion  should  lead  us  to  conclude  that  better 
transmission  of  the  laryngotracheal  murmur  is  not  sufficient  to  explain 
the  presence  of  pathologic  bronchial  breathing  over  pulmonary  con- 
solidation, but  rather  that  the  laryngotracheal  murmur  comes  much 
better  to  the  surface  in  solid  tissue  with  open  bronchi,  and  that  in  the 
thickest  portions  it  is  even  intensified. 

There  is  no  appreciable  acoustic  difference  in  the  bronchial  breathing 
whether  the  pulmonary  consolidation  consists  in  an  infiltration  of  the 
alveoli  with  inflammation  products,  or  in  an  atelectasis  from  compression 
of  a  pleuritic  exudation,  pneumothorax,  hydrothorax,  or  pericardial 
exudation.  Naturally  this  compression  of  the  lungs  must  be  limited  to 
the  alveoli  alone  and  not  involve  bronchi,  at  least  those  of  any  size.  For 
as  soon  as  an  effusion  increases  enough  to  compress  the  larger  bronchi, 
the  bronchial  breathing,  which  is  frequently  heard  with  difficulty  on 
account  of  the  interposition  of  the  effusion,  becomes  weaker  and  weaker 
and  finally  disappears. 

Obturcdion  atelectasis,  due  to  the  plugging  of  a  bronchus  and  a  con- 
sequent resorption  of  air  from  the  alveoli,  prevents  the  production  of 
bronchial  breathing,  and  in  spite  of  the  thickness  of  the  pulmonary 
tissue  and  of  the  consequent  dulness  no  respiratory  murmur  can  be 
heard  unless  transmitted  from  the  neighborhood. 

Even  very  tiny  areas  of  consolidation  too  small  to  dull  the  percussion 
tone  may  cause  bronchial  breathing.  This  shows  how  valuable  a  sign 
it  is  in  diagnosis,  and  is  also  another  argument  against  the  decided  value 
of  the  transmission  theory  of  bronchial  breathing. 

Bronchial  breathing  is  also  heard  over  air-containing  cavities  which 
communicate  with  the  bronchi,  and  over  dilatations  of  the  bronchi  them- 
.selves.  Here  it  is  probably  due  to  a  better  transmission  of  the  laryngeal 
murmur,  especially  if  the  cavity  or  the  bronchiectasy  lies  superficially. 
Besides,  such  cavities  are  almost  always  surrounded  by  infiltrated  tissue, 
so  that  resonance  contributes  considerably  to  the  increase  of  the  laryngeal 
murmur.  Finally,  we  must  not  forget  that  under  some  circumstances  a 
cavity  itself  breathes — i.  e.,  a  respiratory  current  of  air  streams  through 


AUSCULTATION  OF  THE  RESPIRATORY  ORGANS.  229 

the  entrance  of  the  cavity  into  the  bronchus  and  back  again.     And  this 
would  cause  a  blowing  respiratory  murmur  just  as  in  the  larynx. 

Sometimes  it  requires  very  deep  respirations  to  make  the  bronchial 
breathing  audible.  Again,  closure  of  the  bronchus — e.  y.,  by  secretion — 
will  interrupt  the  bronchial  breathing.  Hence,  sometimes  after  coughing 
the  bronchial  breathing  will  reappear.  A  good  device  for  bringing  out 
faint  bronchial  breathing,  if  a  patient  cannot  be  persuaded  to  breathe 
deeply,  consists  in  having  the  patient  count  aloud  as  long  as  possible 
during  one  respiration,  while  the  examiner  auscultates.  The  next 
inspiration  will  be  a  maximum.  This  method  has  also  the  advantage  of 
demonstrating  bronchophony  (see  p.  241).  The  ear  applied  directly  to 
the  chest  will  sometimes  appreciate  weak  bronchial  breathing  better  than 
with  the  interposition  of  the  stethoscope  (p.  219). 

DIFFERENT    KINDS    OF    PATHOLOGIC    BRONCHIAL   BREATHING. 

Bronchial,  far  more  than  vesicular,  breathing  has  a  definite  pitch 
(p.  222),  which  may  vary  quite  decidedly.  These  variations  can  easily 
be  reproduced  by  fixing  the  mouth  in  the  position  for  saying  the  syllables 
"  ha,"  "  he,"  "  hi,"  "  ho,"  "  hu,"  and  then  inspiring  and  expiring. 

The  pitch  of  bronchial  breathing  depends  in  certain  cases  upon  the 
conditions  of  resonation,  and  with  them  upon  the  width  of  the  bronchi 
or  of  the  cavities.  But  up  to  the  present  time,  except  perhaps  in 
distinguishing  so-called  amphoric  breathing,  the  pitch  has  not  occupied 
an  important  place  in  diagnosis.  By  amphoric  or  cavernous  breathing 
we  mean  a  very  deep  and  soft  and  generally  not  very  loud  bronchial 
breathing,  heard  especially  over  large  cavities  (lung  cavities  and  pneumo- 
thorax). Besides  its  low  pitch  it  has  a  very  characteristic  metallic 
resonance,  apparently  due  to  the  overtones  from  the  resonance  in  the 
cavity.  Amphoric  breathing  is,  therefore,  sometimes  associated  with  a 
metallic  percussion  tone.  We  may  reproduce  it  by  whispering  the 
syllable  "  hu "  or  by  blowing  over  an  empty  jar ;  whence  the  name. 
Provided  that  we  do  not  call  any  deep  bronchial  breathing  amphoric  (a 
frequent  mistake),  amphoric  breathing  is  a  pretty  safe  sign  of  a  cavity. 
The  metallic  resonance  accompanying  it  is  the  essential  guide.  Like 
metallic  percussion,  amphoric  breathing  arises  for  the  most  part  only 
over  cavities  which  are  at  least  6  cm.  in  diameter  (according  to  the 
ordinary  estimate) ;  but  it  is  sometimes  found  over  smaller  cavities. 

The  pitch  of  amphoric  breathing — i.  e.,  of  its  metallic  resonance — 
may  vary  in  accordance  with  laws  similar  to  those  governing  the  metallic 
percussion  resonance.  (See  the  paragraphs  upon  the  Percussion  Tone 
Change,  p.  213  et  seq.) 

Metallic  breathing  can  sometimes  be  distinguished  from  amphoric 
breathing.  It  is  a  murmur  with  high  metallic  overtones  and  without 
the  deep  basal  tones.  It  has  no  especial  significance  different  from  that 
of  amphoric  respiration. 

Amphoric  or  metallic  respiration  may  rarely  be  heard  over  pulmonary 
consoliclation,  even  without  the  formation  of  a  cavity.  We  do  not  know 
the  explanation. 


230  AUSCULTATION. 

The  respiratory  murmur  may  in  rare  cases  assume  an  amphoric  or 
metallic  character  on  account  of  the  resonation  set  up  in  neighboring 
physiologic  air-containing  cavities,  such  as  the  stomach  or  the  distended 
intestines. 

Amphoric  respiration  may  be  heard  over  a  pneumothorax  from  reso- 
nation if,  as  is  most  common,  it  is  a  closed,  or  valve,  pneumothorax. 

In  marked  dyspnea  certain  positions  of  the  mouth  may  add  an  amphoric  reso- 
nance to  pathologic  or  physiologic  bronchial  breathing.  But  such  amphoric  breath- 
ing can  be  appreciated  at  a  distance,  and,  besides,  is  distributed  exactly  like  physio- 
logic bronchial  breathing,  so  no  confusion  need  result. 

METAMORPHOSED    BREATHING    MURMUR. 

Metamorphosed  breathing  is  essentially  bronchial  in  type.  In  the 
more  common  form  inspiration  begins  sharp,  blowing  and  bronchial, 
gradually  becoming  much  softer,  and  sometimes  ending  in  amphoric 
breathing.  In  another  variety  the  pitch  of  the  bronchial  element 
changes  during  inspiration  or  during  expiration  or  during  both.  Either 
type,  if  heard  continuously,  is  a  practically  safe  sign  of  a  cavity. 
Probably  after  the  inspiration  has  lasted  for  a  certain  time  it  distends 
the  cavity  and  its  orifice  enough  to  modify  the  pitch  of  the  respiratory 
murmur.  A  similar  metamorphosed  breathing  murmur  might  arise  if 
the  inspiratory  current  pushed  aside  the  secretion  of  a  partially  occluded 
bronchus.  Laennec's  ^'  souffle  voile  "  is  another  variety.  It  begins  as 
vesicular  and  then  changes  into  bronchial  or  mixed  •breathing  (see  p.  231). 
The  vesicular  element  in  this  case  is  probably  transmitted.  It  occurs 
principally  over  tuberculous  infiltrations. 

The  writer  once  succeeded  in  demonstrating  two  different  metamor- 
phosed breathing  murmurs  over  adjacent  areas  (one  higher  during 
inspiration,  the  other  deeper),  and  in  making  a  diagnosis,  which  was 
later  confirmed  by  autopsy,  of  two  small  abscess  cavities  situated  near 
together. 

INDEFINITE  BREATHING  MURMUR. 

This  is  neither  vesicular  nor  bronchial,  but  sounds  like  the  expiratory 
portion  of  normal  breathing.  The  term  indefinite  is  applied  also  to 
breathing  which  is  very  faint  and  difficult  to  hear.  Both  bronchial  and 
vesicular  breathing  may  be  diminished  enough  by  a  pleural  exudation 
to  become  transformed  into  indefinite.  Sometimes  the  breathing  becomes 
indefinite  because  it  is  masked  by  other  louder  noises  (rales  or  friction 
sounds).  The  true  nature  of  indefinite  breathing  can  often  be  brought 
out  after  the  patient  breathes  deeply.  Loud,  distinct  breathing  is  never 
indefinite,  nor  is  the  mixed  murmur  (to  be  described  below).  The  only 
diagnostic  significance  of  indefinite  breathing  is  that  of  a  very  weakened 
murmur  whose  vesicular,  bronchial,  or  mixed  origin  cannot  be  deter- 
mined. 


AUSCULTATION  OF  THE  RESPIRATORY  ORGANS.  231 

MIXED  BREATHING  MURMURS   (BRONCHOVESICULAR 
BREATHING). 

There  are  two  main  types  of  bronchovesicular  breatbing : 

1.  Vesicular  inspiration  with  bronchial  expiration. 

2.  Mixed  inspiration — i.  e.,  inspiration  which  is  both  vesicular  and 
bronchial — with  bronchial  expiration. 

The  conditions  of  origin  of  bronchial  and  of  vesicular  breathing 
differ  so  manifestly  that  at  first  sight  it  would  seem  difficult  to 
explain  these  mixed  murmurs.  Practically,  however,  the  vesicular 
and  bronchial  elements  never  arise  from  one  spot,  but  each  is  trans- 
mitted from  some  distance  and  heard  in  combination  with  the  other ; 
and  so  a  mixed  murmur  entitles  us  to  assume  that  there  exists  in 
close  proximity  both  normal  pulmonary  tissue  and  tissue  so  altered  as 
to  produce  bronchial  breathing.  Thus,  bronchovesicular  breathing  is  to 
be  heard  :  (a)  over  portions  of  the  lung  containing  scattered  small  in- 
filtrations ;  {!))  over  normal  pulmonary  tissue  near  large  infiltrations ; 
(c)  in  the  neighborhood  of  the  upper  boundaries  of  dulness  of  a  pleural 
effusion  which  compresses  the  inferior  while  permitting  free  breathing  of 
the  superior  portion  of  the  lung;  {d)  over  cavities  surrounded  by  healthy 
lung  tissue,  etc.  The  importance  of  bronchovesicular  breathing  in  dis- 
closing small  areas  of  consolidation  is  evident,  because  such  areas  need 
not  produce  any  dulness. 

Physiologic  bronchial  breathing  is  almost  always  combined  with 
vesicular  breathing.  This  is  important  in  differentiating  physiologic 
from  pathologic  bronchial  breathing.  But  the  latter  may  also  be  mixed 
with  vesicular  breathing,  and  the  distinction  between  physiologic  and 
pathologic  mixed  breathing  is  as  difficult  as  it  is  important.  Physiologic 
mixed  breathing  is  especially  common  over  certain  areas,  mentioned  above, 
whereas  pathologic  mixed  breathing  may  be  heard  over  any  part  of  the 
lung.  Even  where  physiologic  mixed  breathing  is  diffused  over  a  large 
area,  we  can  easily  determine  that  the  nearer  we  listen  to  the  greater  bronchi 
or  the  roots  of  the  lungs  the  stronger  the  bronchial  element  becomes  ;  and, 
conversely,  the  farther  from  them,  the  weaker.  If  the  bronchial  element 
increases  with  the  distance  from  the  lung  roots,  we  may  infer  that  it  is 
pathologic  mixed  breathing.  Physiologic  mixed  breathing  is  much  more 
affected  by  the  intensity  of  the  laryngeal  murmur  and  l)y  the  position 
of  the  mouth  than  is  pathologic.  The  character  of  bronchovesicular 
breathing  often  varies  at  different  examinations,  at  the  one  time  plainly 
vesicular,  at  another  bronchial.  This  is  supposed  to  be  due  to  secretion 
plugging  a  bronchus,  at  one  time  in  the  infiltrated  area,  at  another  in 
the  normal  area.  In  the  former  case  the  bronchial,  in  the  latter  the 
vesicular,  component  is  weakened  or  disappears. 

There  is  still  another  type  of  mixed  breathing  which  is  of  diagnostic 
importance.  Mixed  breathing  is  sometimes  heard  over  a  considerable 
area  of  the  lung,  loudest  near  the  hilus  (physiologic  type) ;  or,  conversely, 
near  the  pulmonary  edges.  If  accompanied  by  a  chronic  cough,  but  with 
no  other  evidence  of  pulmonary  infiltration  or  tuberculosis,  it  would  argue 
very  strongly  for  a  bronchiectasis. 


232  A  USCUL  TA  TION. 

The  device  for  recognizing  weak  bronchial  breathing  (p.  229  et  seq.) 
also  aids  in  differentiating  mixed  from  pure  vesicular  breathing. 

RALES  (RhoncW). 
Under  this  term  are  included  all  sounds  which  are  caused  by  the 
motion  in  the  bronchi,  not  only  of  air,  but  of  secretions  or  of  other  fluid, 
semifluid  or  solid  materials.  Moist  rales  depend  upon  fluid,  dry  upon 
solid,  material  within  the  bronchi.  To  determine  rales  exactly  and  care- 
fully analyze  them  we  must  auscultate  the  patient  while  breathing  deeply 
as  well  as  while  breathing  quietly,  and  also  during  and  following  a  cough. 
No  other  auscultatory  phenomena  are  so  markedly  altered  by  such  a  vari- 
ation in  the  type  of  examination.  Coughing,  for  instance,  will  oftentimes 
cause  rales  either  to  appear  or  disappear.  If  a  patient  is  difficult  to  exam- 
ine, if  he  cannot  be  persuaded  to  breathe  properly,  tell  him  to  count  aloud 
as  long  as  possible,  and  the  next  inspiration  will  naturally  be  full  and 
deep.  We  can  often  bring  out  a  very  few  rales,  the  demonstration  of 
which  over  the  pulmonary  apices  is  very  essential  in  the  diagnosis  of 
pulmonary  tuberculosis,  by  auscultating  the  patient  early  in  the  morning, 
before  he  has  expectorated  the  secretion  accumulated  during  the  night. 
Rales  can  often  be  felt  by  the  hand  placed  upon  the  chest. 

Transmission  of  S.ales. — Rales  can  also  be  heard  by  transmission  at  a  certain 
distance  from  their  place  of  origin.  But  their  intensity  ordinarily  decreases  so 
quickly  that  the  determination  of  their  origin  rarely  offers  difficulty. 

Oral  Hales. — It  frequently  happens  that  rales  may  be  heard  at  some  distance 
when  the  patient  breathes  with  his  mouth  open.  As  a  general  rule  these  are  large 
rales,  and  can  also  be  heard  at  some  distance  proceeding  from  the  thorax  even  when 
the  mouth  is  closed.  This  transmission  of  rales  through  the  mouth  is  particularly 
marked  in  the  tracheal  and  pharyngeal  rales  of  moribund  patients.  These  rales 
owe  their  origin  to  the  flooding  of  the  trachea  and  pharynx  by  the  fluid  of  the 
pulmonary  edema,  but  may  also  be  caused  by  failure  to  swallow  the  pharyngeal 
mucus.  By  auscultating  the  trachea  and  the  larynx,  it  may  be  determined  whether 
the  rales  arise  here  or  in  the  depths  of  the  lung.  It  occasionally  happens  that  a 
deep  area  in  the  center  of  the  lung  produces  oral  rales  which  are  not  transmitted 
to  the  surface  of  the  thorax.     This  symptom  has  a  certain  diagnostic  significance. 

MOIST    OR    BUBBLING    RALES. 

The  sound  of  moist  or  bubbling  rales  can  be  imitated  by  blowing 
through  a  glass  tube  into  a  vessel  of  water.  The  expansion  of  air  into 
bubbles  causes  a  characteristic  crackling  noise,  which  will  vary  with  the 
caliber  of  the  tube  and  with  the  strength  of  the  bubble.  A  wide  tube 
will  produce  large  bubbles,  with  a  sound  resembling  the  so-called  large 
or  coar.se  bubbling  rales ;  a  narrow  tube  causes  fine  bubbles,  the  sound 
resembling  the  small  or  fine  bubbling  rales. 

It  is  much  easier  to  appreciate  by  the  ear  the  difference  between  the 
fine  and  the  coarse  bubbling  rales  than  it  is  to  define  it  scientifically. 
Coarse  bubbling  rales  are  fewer  in  number,  more  intense,  and  of  a  lower 
pitch.  Fine  bubbling  rales  are  more  numerous,  less  intense,  and  of  a 
higher  pitch.  This  distinction  does  not,  however,  entirely  fulfil  the 
conditions,  because  accelerating  the  air  current  will  increase  the  number 
of  the  bubbles  without  altering  their  character.     On  the  other  hand, 


AUSCULTATION  OF  THE  RESPIRATORY  ORGANS.  233 

approaching  the  ear  close  to  or  distant  from  the  tube  will  increase  or 
diminish  their  intensity  also  without  altering  their  character.  Neither 
does  the  essential  distinction  depend  upon  the  pitch,  for  in  many  cases 
no  distinct  pitch  can  be  recognized.  Therefore,  some  other  difference 
between  coarse  and  fine  bubbling  rales  must  exist.  The  writer  imagines 
some  difference  depends  upon  the  size  of  the  mass  set  in  motion — /.  e., 
in  coarse  bubbling  rales  the  energy  of  the  vibration  is  greater  than  in 
fine  bubbling  rales,  because  the  moving  mass  is  larger.  And  this  influ- 
ences not  only  the  intensity  of  the  vibrations,  but,  in  consequence  of  the 
law  of  inertia,  the  duration  of  the  tone  itself.  The  coarse  rales  last 
longer.  (See  Duration  of  the  Percussion  Tone.)  If  this  explanation  is 
correct,  rales  may  be  few  in  number,  and,  when  they  arise  close  to  the 
ear,  intense  ;  and  yet  retain  their  fine  bubbling  character. 

The  term  "  bubbling  "  was  employed  because  it  was  formerly  sup- 
posed that  moist  rales  arose  from  the  bursting  of  air-bubbles  in  fluid 
secretion.  Of  course,  we  know  now  that  the  contents  of  the  bronchi 
are  not  sufficiently  fluid  for  such  an  explanation  ;  and  so  we  suppose 
that  the  rales  arise  from  membranes  of  secretions  being  formed  in 
the  bronchial  lumen,  and  then  torn  apart  again,  partly  by  the  move- 
ment of  the  air  and  partly  by  the  movement  of  the  lungs.  The 
coarse  bubbling  rales  would  therefore  correspond  to  the  thicker,  and  the 
fine  to  the  thinner,  layers  of  secretion.  We  always  auscultate  over  a 
more  or  less  extensive  bronchial  area ;  hence  many  different  individual 
noises  may  give  rise  to  the  resultant  "much  bubbling"  noise.  Moving 
or  bursting  of  real  bubbles  probably  occurs  only  in  quite  isolated 
cases,  and  then  really  only  when  the  lung  is  saturated  with  thin  fluid — 
e.  g.,  in  pulmonary  hemorrhage,  pulmonary  edema,  or  drowning. 

Moist  rales  may  be  heard  during  expiration  as  well  as  during  inspi- 
ration, although  during  inspiration  they  are  almost  always  much  plainer, 
possibly  because  the  movement  of  the  lung  is  quicker. 

Very  fine  bubbling  or  moist  rales  are  also  named  crackling  or  sub- 
crepitant  rales,  the  latter  from  a  certain  similarity  to  crepitant  rales  (pp. 
237  and  238). 

A  complete  series  of  transitions  exists  between  the  coarse  bubbling 
rales  as  one  extreme  and  the  fine  moist  rales  as  the  other.  The  rattling 
tracheal  or  pharyngeal  rale,  generally  heard  in  the  moribund,  even  at  a 
distance,  belongs  to  the  former  variety.  Fine  moist  rales  more  com- 
monly originate  in  the  fine  tubes  ;  coarse,  in  the  larger  tubes  or  in 
pathologic  cavities.  The  former  are  generally  more  numerous  because 
there  are  more  fine  tubes. 

Moist  rales  arise  only  when  the  bronchi  contain  fluid  or  semi-fluid 
material ;  in  most  cases,  therefore,  they  signify  a  bronchial  catarrh,  to 
be  located  in  the  large  or  small  bronchi,  according  to  the  size  of  the 
rales.  Fine  moist  rales  have  in  general  a  more  serious  import,  be- 
cause a  catarrh  of  the  finer  bronchi  often  leads  to  bronchopneumonia, 
and  because  such  a  catarrh  frequently  depends  upon  local  changes  of 
the  pulmonary  parenchyma  (such  as  inflammatory  infiltration,  tubercu- 
losis or  infarction).     This  is  especially  true  if  the  fine  moist  rales  are 


234  A  USCULTA  TION. 

heard  localized  over  a  definite  area  of  the  lung.  The  obstinate  per- 
sistence of  such  localized  rales  over  the  same  area  while  the  rest  of  the 
lung  is  permanently  free,  even  without  any  other  signs,  justifies  the 
diagnosis  of  a  serious  process,  either  a  tubercular  or  a  lobular  pneumonic 
infiltration  or  an  infarction.  On  the  contrary,  an  ordinary  innocent 
catarrh  is  much  more  diffused,  because  an  otherwise  healthy  mucous 
membrane  presents  practically  the  same  fostering  soil  throughout  its 
entire  extent.  Coarse  bubbling  rales  heard  over  areas  where  no  large 
bronchi  are  to  be  found  signify  an  especially  serious  aifection,  because 
they  must  arise  either  from  pathologically  dilated  bronchi  or  from  cavi- 
ties. When  heard  over  the  apices,  they  are  thus  important  signs  of 
tubercular  cavities  ;  when  heard  over  the  postero-inferior  portions  of 
the  lungs,  they  more  frequently  depend  upon  bronchiectasis.  Coarse 
moist  rales  are,  however,  frequently  transmitted  to  quite  a  distance,  a 
possibility  which  must  be  kept  in  mind  when  they  are  heard  over  areas 
somewhat  remote  from  the  roots  of  the  lungs.  Such  a  possibility  may, 
however,  be  excluded  if  at  the  same  time  no  coarse  rales  are  heard  over 
the  larger  bronchi.  Moist  rales  of  any  size,  when  obstinately  localized 
over  a  circumscribed  area,  point  to  a  serious  focal  lesion  of  the  lungs. 

Mixed  bubbling  rales  arise  when  the  small  as  well  as  the  large 
bronchi  are  aft'ected.  They  also  arise  from  the  larger  bronchi  and 
from  pulmonary  cavities. 

Pulmonary'  hemorrhage  and  pulmonar^'  edema,  unless  the  larger 
bronchi  are  also  flooded  with  fluid,  present  quite  uniformly  fine  bubbling 
rales,  which  are  frequently  heard  both  with  inspiration  and  expiration 
(continuous  rales).  The  expectoration  in  these  cases  is  ordinarily  very 
foamy. 

The  sticky  mucous  secretion  of  an  ordinary  catarrhal  bronchitis 
generally  produces  dry  rales.  Moist  rales  have  a  more  serious  signifi- 
cance ;  their  appearance  is  associated  with  a  fluid  secretion  deficient 
in  mucus — e.  g.,  they  are  especially  common  in  intense  inflammatory 
processes  of  the  mucous  membrane  or  of  the  pulmonary  tissue,  in 
edema,  stasis,  and  hypostasis.  IVIoist  rales  constantly  present  over  the 
apices  of  the  lungs  almost  always  mean  tuberculosis.  In  such  a  case 
a  thin  fluid  secretion,  such  as  the  moist  rales  suggest,  signifies  a  marked 
purulent  and  destructive  process. 

DRY  RALES  (CRACKLING  OR  SNAPPING  AND   MUSICAL  RALES). 

Dry  rales  are  produced  by  the  movement  of  a  viscid  secretion. 
They  have  a  more  manifold  character  than  moist  rales.  The  latter  are 
always  composed  of  a  more  or  less  regular  succession  of  separated 
noises.  The  former  present  either  a  quite  isolated  sound,  a  crackling 
which  resembles  to  some  extent  a  moist  rale,  or  a  prolonged,  distinctly 
musical  sound  (the  humming,  whistling,  sonorous  or  sibilant  rale).  The 
difficulty  in  moving  the  tenacious  secretion  probably  accounts  for  the 
lack  of  regularity  in  the  succession  of  the  dry  rales. 

To  explain  the  origin  of  the  crackling  dry  rale,  we  should  remember 
that  the  secretion  of  the  mucous  membrane  of  the  bronchi  is  stretched 


AUSCULTATION  OF  THE  RESPIRATORY  ORGANS.  235 

out  in  the  form  of  threads  or  membranes,  is  torn  loose  either  by  the  air 
current  or  by  the  movement  of  the  lungs,  and  later,  by  virtue  of  its 
tenacity,  again  sticks  fast  to  another  portion  of  the  bronchial  wall  with- 
out necessarily  giving  rise  to  another  series  of  noises.  Thus,  they 
differ  very  slightly  in  their  origin  from  the  moist  rale,  except  that  on 
account  of  its  viscidity  the  secretion  is  probably  only  seldom  stretched 
and  then  torn  loose  from  the  mucous  membrane,  whereas  in  moist 
rales  this  process  is  constantly  repeated.  Such  a  conception  practically 
tabulates  the  dry  crackling  rales  as  a  subdivision  of  the  moist  rale. 

Very  possibly  certain  forms  of  crackling  rales  are  not  real  rales — i.  e. ,  they  do 
not  dei^end  upon  the  movement  of  secretion,  but  upon  a  jerky  current  of  air  over 
a  surface  roughened  and  irregular  from  infiltration  in  the  neighborhood — e.  g.,  in 
tubercular  apices. 

Musical  dry  rales  arise  from  the  vibration  of  threads  or  membranes 
which  are  drawn  out  across  the  bronchial  lumen.  They  are  set  in  vibra- 
tion (but  not  torn  away  by  the  air  current)  just  like  the  strings  of  a 
fiddle  or  the  tongues  of  a  pipe.  Again,  some  of  the  walls  of  the  finer 
tubes  may  be  so  swollen  by  inflammation  as  to  be  almost  occluded,  and 
form  a  sort  of  whistle.  Finally,  the  swelling  of  the  mucous  membrane 
may  be  situated  at  the  angle  between  two  communicating  bronchi,  thus 
acting  like  the  tongue  of  a  pipe.  These  various  causes  explain  the 
diversity  of  musical  rales,  which  sometimes  resemble  the  purring  of  a 
cat,  sometimes  the  tone  of  a  violin,  a  harp,  or  a  bass  viol,  sometimes  the 
snoring  of  a  sleeper,  sometimes  a  shrill  whistle.  The  deeper  sonorous 
rales  generally  arise  in  the  larger  bronchi ;  the  higher,  whistling  or 
sibilant  rales,  in  the  smaller. 

The  names  crackling,  sonorous,  or  sibilant  rales — more  briefl}^, 
crackles,  snores,  or  whistles — are  well  used  to  characterize  the  sounds. 

When  dry  rales  are  obstinately  localized  at  one  spot  they  have  the 
same  serious  significance  as  moist  rales,  even  without  other  auscultatory 
or  percussion  phenomena  (see  pp.  233  and  234).  Pulmonary  tuberculosis 
for  a  long  time  may  be  evidenced  only  by  the  sounds  of  a  dry  catarrh 
at  one  apex. 

Dry  rales  are  often  transmitted  to  a  considerable  distance.  Sonorous 
rales  are  often  appreciated  by  the  palpating  hand,  and  resemble  a 
pleuritic  friction  (see  p.  239). 

RESONANT    (Consonating)    AND    NON-RESONANT    (Non-consonating)    RALES. 

Rales  which  arise  in  bronchi  surrounded  by  solid — /.  e.,  airless  tissue 
(infiltration,  atelectasis) — are  transmitted,  intensified  or  modified  by  res- 
onance, exactly  as  is  pathologic  bronchial  breathing  (see  p.  226  et  seq.). 
They  then  become  exceptionally  sharp  and  distinct,  and  are  called  res- 
onant  or  consonating  rdles,  in  distinction  to  the  non-resonant  rales  heard 
over  normal  pulmonary  parenchyma.  The  terminology  is  here  some- 
what confusing,  for  a  dry  musical  rale  must  naturally  be  resonant,  but 
is  not  modified  by  a  resonance  in  the  sense  mentioned  above.  To  avoid 
this  confusion  it  would  be  advisable  to  return  to  Skoda's  terminology, 
consonating  rdles. 


236  AUSCULTATION. 

Dry  musical  rales  (sonorous  and  sibilant),  even  when  they  arise  in 
aerated  pulmonary  tissue,  have  so  distinct  and  well  recognized  a  musical 
character  that  conditions  of  resonance  or  consonance  cannot  alter  them 
to  any  extent,  and  only  a  very  skilled  ear  can  distinguish  any  differ- 
ence between  consonating  and  non-consonating  musical  rales.  On 
account  of  the  marked  preponderance  of  a  ground-tone,  consonance 
in  such  rales  is  evidenced  more  by  an  increased  intensity  than  by 
any  qualitative  modification  of  the  timbre.  Merely  from  the  increase 
in  intensity  we  can  draw  no  further  conclusions.  But  moist  and  also 
crackling  rales  are  very  plainly  affected  by  consonation.  The  entire 
effect  is  increased  in  intensity,  and  certain  high  partial  tones  are  espe- 
cially intensified  by  resonance.  The  result  is  difficult  to  describe  clearly, 
but  can  easily  be  demonstrated  upon  an  appropriate  patient.  In  the 
discussion  of  bronchial  breathing  we  showed  that  actual  resonating 
phenomena  do  appear  in  the  bronchi,  and  so  there  is  no  reason  to  doubt 
that  a  rale  may  resonate.  But  the  better  conduction  through  infil- 
trated tissue  is  not  alone  sufficient  to  make  the  rales  resonant ;  nor  is 
loudness  of  any  avail — e.  g.,  tracheal  rales  loud  enough  to  be  heard  even 
at  a  distance  show  no  trace  of  resonance.  The  resonating  character 
depends  for  the  most  part  on  an  admixture  of  the  higher  overtones. 
Certain  types  of  stethoscopes  will  add  a  distinct  resonance  to  rales 
(see  p.  244).  A  pulmonary  cavity  which  presents  a  metallic  note  to 
percussion  and  an  amphoric  breathing  to  auscultation  also  furnishes 
consonating  rales,  with  a  metallic  resonance. 

The  so-called  noise  of  falling  drops  (gutta  cadens),  heard  especially 
in  tubercular  destruction  of  the  lung,  is  apparently  nothing  but  a  me- 
tallic consonating  crackling  rale  in  a  cavity  (see,  however,  a  similar  sound 
with  a  different  import,  p.  240  et  seq.).  After  this  discussion  of  its  origin, 
the  diagnostic  significance  of  the  consonating  rale  will  require  fewer 
words,  for  it  should  now  be  clear  that  the  demonstration  of  the  consona- 
tion of  rales  has  exactly  the  same  significance  as  the  demonstration  of 
pathologic  bronchial  breathing.  And  the  writer  would  emphasize  to  the 
beginner  the  importance  of  distinguishing  consonance  and  non-consonance 
of  the  rales  in  the  diagnosis  of  infiltrations.  If  bronchial  breathing,  con- 
sonating rales,  and  dulness  of  the  percussion  tone  were  always  present 
together  over  pulmonary  infiltrations,  the  presence  of  one  or  the  other 
of  these  signs  would  be  sufficient,  and  we  could  then  dispense  with  the 
others.  Unfortunately,  it  is  not  so  simple;  for,  as  we  have  already 
seen,  bronchial  breathing  is  very  often  heard  without  any  dulness,  and 
just  as  frequently  consonating  rales  without  bronchial  breathing.  In 
gross,  the  conditions  essential  for  consonating  rales  and  for  bronchial 
breathing  are  the  same ;  but  either  may  be  present  alone,  because  quite 
distinct  sound  elements  must  be  increased  by  resonation  to  exhibit  the 
consonating  character  in  the  rales,  on  the  one  hand,  and  in  the  respiratory 
murmur  on  the  other. 

From  a  practical  standpoint  tliere  is  one  thing  more  to  empha- 
size. A  rale  must  possess  a  certain  strength  to  be  able  to  consonate 
plainly  ;  hence,  with  very  superficial  breathing  we  frequently  hear  over 


AUSCULTATION  OF  THE  RESPIRATORY  ORGANS.  237 

an  infiltration  or  cavity  non-consonating  rales,  which  with  deeper  breath- 
ing are  transformed  into  consonating  rales.  Lobular  pneumonia  is 
often  very  difficult  to  demonstrate  in  quite  sick  patients,  especially  be- 
cause the  superficial  breathing  characteristic  of  this  disease  is  scarcely 
strong  enough  to  produce  plain  bronchial  breathing.  With  mixed  bub- 
bling rales  certain  ones  may  be  consonating  and  others  non-consonating, 
because  parts  of  the  mixed  breathing  murmur  are  not  strong  enough  to 
brino;  out  the  consonation. 

CREPITANT  RALES  OR  CREPITATION- 

During  the  first  stage  of  pulmonary  infiltration,  when  anatomically 
the  lung  is  in  the  state  of  engorgement,  when  the  pulmonary  tissue  is 
still  full  of  air,  when  percussion  discloses  no  dulness,  and  when  auscul- 
tation shows  no  bronchial  breathing,  there  is  to  be  heard  over  the 
aifected  part  of  the  lung  the  so-called  crepitant  rale,  or  crepitation 
(crepitatio  indux).  A  similar  noise  (crepitatio  redux)  is  to  be  heard 
during  the  resolution  stage  of  pneumonia  when  the  solidified  lung 
again  becomes  aerated.  This  characteristic  sound  is  to  be  heard  both 
in  croupous  and  catarrhal  pulmonary  inflammation,  in  certain  stages  of 
tubercular  infiltration,  and  in  hemorrhagic  infarctions  and  in  beginning 
pulmonary  edema.  In  most  cases  only  audible  during  inspiration, 
crepitation  possesses  a  certain  acoustic  similarity  to  a  very  fine  moist 
rale  (subcrepitant),  and  can  be  very  well  imitated  by  rolling  one's  hair 
between  the  fingers,  near  the  ear. 

Formerly  crepitation  was  considered  to  be  a  true,  very  fine,  moist 
rale,  arising  when  the  air  current  set  into  motion  fluid  secretion  in  the 
finest  bronchi  and  alveoli.  But  this  supposition  has  been  disputed  ;  in 
the  first  place,  because  we  can  reproduce  crepitation  by  blowing  up  or  by 
pressing  between  the  fingers  a  cadaver's  dry  lung ;  and  again  because 
in  perfectly  healthy  individuals  with  no  real  secretion  in  the  alveoli  or 
bronchi,  crepitation  is  sometimes  heard,  especially  at  the  inferior  bound- 
ary of  the  lung,  or  after  they  have  been  breathing  superficially  for  a  long 
time  and  then  take  a  deep  breath.  The  fact  that  it  is  heard  only  with 
inspiration  is  a  further  argument  against  its  origin  from  the  movement 
of  secretion.  It  is  now  apparently  universally  conceded  that  crepitation 
does  not  arise  from  this  cause,  nor,  as  was  earlier  supposed,  as  a  conse- 
quence of  a  great  number  of  microscopic  explosions  of  air  bubbles  in 
the  fluid  contents  of  the  alveoli,  but  from  the  tearing  apart  of  the 
approximated  alveolar  walls  by  the  inspiratory  stream.^  In  pulmonary 
engorgement  related  to  the  first  stage  of  pulmonary  edema  we  can  well 
imagine  that  the  increasing  swelling  and  soaking  of  the  alveolar  walls 
would  approximate  them,  and  the  presence  of  some  fluid  secretion  or 
exudation  in  the  alveoli  would  only  favor  each  expiratory  adhesion. 

^  [Prof.  Sahli  has  entirely  disregarded  one  theory  of  the  origin  of  crepitation — viz., 
that  it  is  in  reality  a  very  fine  pleural  friction  rub  and  does  not  come  from  within  the 
lung.  This  theory  seems  to  us  less  plausible,  but  so  good  an  authority  as  Osier  says, 
"  Whether  this  is  a  fine  pleural  crepitus  or  is  produced  in  the  air  cells  and  finer  bronchi 
is  still  an  open  question." — Ed.] 


238  AUSCULTATION. 

Still,  fluid  plays  here  a  secondary  role.  In  pulmonary  edema,  if  the 
transudation  increases,  genuine  fine  bubbling  rales  become  gradually 
associated  with  crepitation,  and  later  on,  when  the  fluid  reaches  the 
greater  bronchi,  even  coarse  moist  rales  are  developed.  An  excellent 
opportunity  is  thus  afibrded  to  study  the  difference  between  crepitation 
and  the  fine  moist,  or  so-called  subcrepitant,  rales.  They  are  easily 
distinguished  by  remembering  that  the  former  occurs  during  inspiration 
and  possesses  a  resonating  character. 

AVhen  associated  with  bronchial  breathing,  crepitation  points  to  the 
beginning  of  an  infiltration,  and  has,  therefore,  a  serious  significance. 
On  the  contrary,  however,  the  crepitatio  redux  at  the  termination  of  a 
pneumonia  is  a  longed-for  sign  of  beginning  resolution,  and  a  demon- 
stration that  the  alveoli  have  once  more  become  permeable  to  air. 
Crepitation  may  in  certain  cases  be  heard  over  some  spot  or  other  of 
the  chest  during  the  entire  course  of  croupous  pneumonia,  because  this 
disease  almost  never  develops  simultaneously. 

Actual  crepitation  may  exceptionally  be  heard  with  expiration, 
probably  depending  upon  the  fact  that  under  unusual  conditions  some 
of  the  alveoli  become  filled  with  air  during  expiration  instead  of  during 
inspiration.  This  is  simple  enough  to  understand  if  w^e  suppose  that, 
in  consequence  of  adhesions  or  of  partial  rigidity  from  small  areas  of 
infiltration,  one  portion  of  the  lung  does  not  breathe  as  well  as  an  ad- 
joining part,  and  that  the  good  breathing  part,  on  account  of  some 
obstacle  opposing  its  emptying  (secretion  or  swelling  of  the  mucous 
membrane),  sometimes  pumps  the  expirator}^  air  into  the  poor  breathing 
part.  The  latter  will  then  be  distended  while  the  rest  of  the  lung 
expires,  thus  giving  rise  to  a  crepitation  which  is  expiratory  in  relation 
to  the  general  respiration,  but  inspiratory  in  relation  to  the  affected 
part  itself.  In  lobular  infiltrations  at  the  sharp  pulmonary  edges  the 
writer  has  not  infrequently  found  this  expiratory  crepitation. 

CARDIOPNEUMATIC  RALES    (Cardiac  Rales  and  Cardiac  Crepitation). 

Before  concluding  the  discussion  of  the  ordinary  rales  occasioned  by 
respiratory  movements,  we  should  mention  the  fact  that  in  rare  cases 
with  coexistent  catarrh  of  the  bronchi,  rales  may  be  produced  by  the 
movements  of  the  heart  itself  These  are  due  in  part  to  the  direct 
mechanical  vibration  of  the  adjoining  portions  of  the  lung;  in  part, 
however,  to  the  systolic  and  diastolic  variations  of  intrathoracic  pressure 
from  alterations  in  cardiac  volume  (auxo-  and  meiocardia).  Such 
variations  cause  real  respiratory  excursions  of  the  adjoining  pulmonary 
parts.  (Already  noted  under  Systolic  Vesicular  Breathing,  ]5p.  221  and 
222.)  Cardiac  rales  are  most  frequently  systolic  when  the  lung,  partly 
infiltrated  or  filled  with  cavities,  is  adherent  to  the  pleura  near  the 
heart,  and  then  set  into  active  motion  by  the  cardiac  action. 

In  a  similar  way,  provided  the  essential  characteristics  are  present 
in  the  lungs,  crepitation  may  be  occasioned  by  the  heart  action  (cardio- 
systolic  rales. 


AUSCULTATION  OF  THE  RESPIRATORY  ORGANS.  239 


PLEURAL    FRICTION    RUB. 

The  two  pleural  surfaces  move  against  each  other  normally  without 
producing  any  noise ;  but  when  the  surfaces  have  become  roughened,  as 
in  pleurisy,  in  tuberculosis,  in  tumors,  or  with  the  abnormal  pleural  dry- 
ness of  cholera,  a  characteristic  friction  rub  is  developed.  The  area 
over  which  the  friction  rub  is  audible  varies  with  the  extent  of  the 
fibrinous  deposition  or  roughness.  The  excursions  of  the  pleural  sur- 
faces are  more  extensive  at  the  pulmonary  edges ;  therefore,  a  friction 
rub  is  more  often  heard  there  than  at  the  hilus  of  the  lung.  Friction 
rubs  are  rarely  heard  over  the  apices  of  the  lungs,  where  the  movement 
is  more  a  distention  by  centrifugal  inflation  than  a  sliding.  Depending 
upon  the  type  of  the  roughness,  the  rub  will  be  either  inspiratory 
or  expiratory,  or  both.  The  kind  of  noise  produced  is  practically  mani- 
fold. It  may  be  imitated  by  placing  the  flat  of  the  hand  against  the 
ear  and  slowly  rubbing  the  back  of  the  hand  with  the  ball  of  a  finger 
of  the  other  hand.  The  character  of  the  rub  varies  with  the  amount  of 
pressure.  Some,  exceptionally  loud,  simulate  the  creaking  of  new  leather 
or  sonorous  rales,  whereas  others,  much  fainter,  resemble  the  noise  caused 
by  rubbing  two  pieces  of  silk  stuff  together,  and  still  others  resemble 
crepitation,  cog-wheel  breathing,  or  even  faint  bronchial  breathing. 
Another  peculiarity  of  friction  rubs  is  that  they  are  usually  jerky  and 
not  smoothly  spread  over  each  phase  of  the  breathing. 

Though  a  mere  beginner  recognizes  without  difficulty  a  decided  rough 
pleuritic  rub,  yet  even  an  expert  is  oftentimes  in  doubt  over  the  nature  of 
a  sound  which  reseml)les  a  sonorous  or  crackling  rale  as  much  as  it  does 
a  frictioQ  rul).  One  way  of  determining  is  to  try  the  effect  of  cough- 
ing. It  will  often  entirely  change  the  character  of  a  rale,  and  some- 
times even  cause  it  to  disappear,  but  does  not  affect  a  rub.  On  the  other 
hand,  pressure  of  the  stethoscope  or  of  the  flat  hand  intensifies  a  rub,  but 
does  not  affect  a  rale.  A  third  source  of  help  is  palpation,  which  appre- 
ciates a  friction  rub  more  readily  than  a  rale.  The  confusion  between  a 
soft  rub  and  faint  bronchial  or  cog-wheel  breathing  can  be  cleared  up  only 
by  an  expert's  repeated  and  accurate  examinations.  Another  peculiar 
rub,  which  fortunately  is  quite  rare,  can  be  distinguished  from  crepitation 
only  by  the  fact  that  it  can  be  just  as  plainly  heard  during  expiration 
as  during  inspiration,  and  that  it  is  more  jerky  than  the  crepitation. 
Friction  rubs  heard  over  the  precordia,  which  originate  from  the  pleura, 
from  the  pericardium,  or  from  the  sharp  pulmonary  edge  overlapj)ing 
the  lieart,  may  be  synchronous  with  the  cardiac  action  as  well  as  with 
the  breathing.  They  are  called  pleuropericardial,  pseudopericarrJial,  or 
extrapevlcardial  friction  rubs,  and  are  liable  to  be  confused  with  true 
pericardial  rubs.      (See  Pericardial  Friction  Rubs  for  Diagnosis.) 

When  a  fluid  exudation  complicates  pleurisy,  the  friction  rub  dis- 
appears, because  the  layer  of  fluid  prevents  the  two  pleural  surfaces  from 
touching  and  rubbing.  The  rub  may  persist,  however,  along  the  edge 
of  dulness,  rather  more  commonly  in  front  than  behind.  Such  a  per- 
sistence proves  that  the  two  pleural  surfaces  touch  and  rub  against  each 


240  AUSCULTATION. 

other  somewhere  above  or  below  the  adhesions,  encapsulating  the  fluid 
exudation.  The  reappearance  of  a  rub  within  the  boundaries  of  the 
dulness  is  a  favorable  sign,  because  it  shows  that  the  fluid  is  diminishing 
and  the  pleural  surfaces  are  again  in  contact.  The  dulness  may  then  be 
due,  at  least  in  part,  to  thick  layers  of  fibrin.  Loud  friction  rubs  may, 
of  course,  be  transmitted  some  distance  from  their  place  of  origin;  but 
if  they  are  plainly  felt  by  the  palpating  hand  over  the  area  where  they 
are  loudest  heard  it  is  pretty  good  evidence  that  they  arise  very  nearby. 

RESPIRATORY   MURMURS    IN    INTERSTITIAL    PULMONARY 

EMPHYSEMA. 

When  air  from  within  the  lung  is  forced  into  the  interstitial  pulmonary  connec- 
tive tissue  by  the  rupture  of  one  or  more  alveolar  walls,  bubbling  sounds  and 
sometimes  murmurs  are  produced  by  each  respiratory  excursion.  These  sounds 
generally  recall  coarse  or  mixed  moist  rales,  and  for  the  most  part  are  resonant  in 
character.  The  resonance,  which  may  even  take  on  a  metallic  character,  probably 
depends  upon  the  resonation  in  the  cavities  formed  by  the  bubbles.  Sometimes 
these  sounds  simulate  the  familiar  emphysematous  crackling  of  the  skin  (see  p.  52), 
but  they  are  too  coarse  to  be  confused  with  crepitation  (p.  237  et  seq.).  When 
large  emphysematous  bubbles  are  situated  beneath  the  pleura,  they  may  sometimes 
decidedly  weaken  the  respiratory  murmur.  Interstitial  emphysema  may  be  present 
at  any  spot ;  it  may  spread  over  the  entire  lung,  and  from  there  into  the  subcu- 
taneous connective  tissue.  Sometimes  the  diagnosis  of  interstitial  pulmonary  em- 
physema will  be  first  securely  established  and  the  confusion  with  rales  prevented 
by  the  demonstration  of  the  precordial  murmur  of  emphysema,  and  of  the  charac- 
teristic crackling  of  the  skin. 

NOISES    AUDIBLE    IN    PNEUMOTHORAX. 

PLEURAL    SPLASHING     NOISE     (Succassio  Hippocratis). 

Hippocrates  first  described  the  characteristic  splashing  noise  produced 
by  shaking  a  patient  with  sero-  or  pyopneumothorax.  The  noise  is 
similar  to  that  made  by  shaking  a  large  flask  half-filled  with  water, 
and  arises  in  the  same  way.  Sometimes  it  is  audible  at  a  distance ; 
sometimes  only  to  be  heard  when  the  examiner  places  his  ear  against 
the  chest.  The  patient  himself  sometimes  notices  the  noise  during  all 
violent  movements.  The  splashing  sometimes  presents  a  distinctly 
metallic  timbre,  according  to  the  shape  and  size  of  the  pneumothorax 
cavity  and  to  the  tension  of  the  contained  air. 

Similar  succussion  noises  may  evidently  arise  in  any  other  physiologic 
or  pathologic  body  cavity  containing  both  air  and  fluid ;  for  example, 
when  air  is  contained  in  the  pericardium  or  in  the  peritoneum  with  a 
fluid  eifusion.  It  is  also  occasionally  heard  in  a  large  pulmonary  cavity, 
and  quite  frequently  in  perfectly  healthy  people  with  stomachs  distended 
with  large  amounts  of  fluid  and  air.  In  order  to  differentiate  the  Hippo- 
crates succussion  from  these  phenomena,  and  especially  from  the  last-men- 
tioned physiologic  murmur  from  the  stomach  contents,  we  must  utilize 
the  results  of  other  methods  of  examination  and  endeavor  to  localize  the 
origin  of  the  splashing  as  accurately  as  possible  by  the  proximity  of  the 
ear,  and  also  by  carefully  examining  with  a  filled  and  a  fasting  stomach. 
Frequently  the  examiner  can  appreciate,  with  his  hand  applied  to  the 


AUSCULTATION  OF  THE  RESPIRATORY  ORGANS.  241 

thorax  of  the  patient,  a  distinct  blow  of  the  fluid  wave  within  the  pleural 
cavity  at  the  moment  of  the  shaking. 

■WATER-"WHISTLE    NOISE    (Pulmonary  Fistula  Noise). 

This  is  a  characteristic  gurgling  noise  which  often  sounds  metallic  and  reminds 
one  of  a  coarse  bubbling  rale.  It  is  heard  over  a  pneumothorax  occasionally  when 
the  air  or  the  fluid  is  removed  by  aspiration,  and  so  the  atmospheric  pressure  dimin- 
ishes the  pressure  in  the  pleural  cavity.  In  a  valvular  pneumothorax  the  murmur 
will  arise  as  soon  as  the  pressure  within  the  pleural  cavity  is  diminished  to  below 
that  of  the  atmospheric  pressure  ;  then  air  immediately  escapes  from  the  patent  jjul- 
monary  fistula.  If  this  fistulous  opening  is  situated  below  the  level  of  the  fluid, 
the  noise  is  produced  by  the  rising  of  the  air  bubbles.  On  account  of  its  acoustic 
character  and  of  its  mode  of  origin,  Unverricht  called  it  a  water-whistle  noise,  and 
Riegel  called  it  a  pulmonary  fistula  noise.  The  same  noise  will  be  noted  even 
without  aspiration  if  in  a  patient  with  a  pyopneumothorax  perforating  into  the 
lung  air  is  sucked  in  with  inspiration  during  the  expectoration  of  the  exudate, 
•or,  again,  if  with  coughing  air  is  squeezed  out  of  the  lung  by  the  fluid  in  a 
pyopneumothorax  which  opens  through  the  thoracic  wall  and  which  also  has  a 
pulmonary  fistula.  The  sign  is  of  some  diagnostic  value  in  recognizing  the  occur- 
rence of  a  pulmonary  fistula. 

NOISE    OF   FALLING    DROPS    IN    PNEUMOTHORAX. 

In  pulmonary  tuberculosis,  as  we  have  seen  upon  p.  236  et  seq.,  the  so-called 
noise  of  falling  drops  is  always  to  be  considered  as  a  simple  metallic  crackling 
rale ;  but  in  pneumothorax,  on  the  contrary,  it  is  possible  to  hear  actual  falling 
drops.  When  such  a  patient  changes  from  the  recumbent  to  the  sitting  posture,  it 
is  quite  possible  that  the  shaggy  prominences  of  the  pleura  covered  with  fibrin, 
which  were  previously  moistened,  free  themselves  from  fluid  drop  by  drop,  and  in 
this  way  produce  a  metallic  dropping  noise. 

AUSCULTATION  OF  THE  VOICE  SOUNDS  OVER  THE  CHEST 

[Bronchophony]  ♦ 

Transmission  of  the  voice  sounds  from  the  larynx  and  trachea 
through  the  lung  to  the  chest  surface  is  subject  under  normal  conditions 
to  the  laws  which  govern  the  transmission  of  the  laryngotracheal 
respiratory  murmur.  The  voice  sounds  are  therefore  heard  best  over 
the  areas  where  we  hear  physiologic  bronchial  breathing — i.  e.,  near  the 
hilus  of  the  lung  between  the  shoulder  blades,  and  over  the  upper  end 
of  the  sternum.  But  even  in  these  regions  articulation  is  faintly  appre- 
ciated, while  over  the  peripheral  portions  of  the  lung  only  an  indis- 
tinct murmur  can  be  detected.  This  comparatively  distinct  transmis- 
sion of  the  voice  over  the  areas  of  physiologic  bronchial  breathing  is 
known  as  jihysiologic  bronchophony.  At  best  the  voice  cannot  be 
heard  distinctly,  but  sounds  as  if  someone  were  talking  at  some  dis- 
tance in  a  hall  of  poor  acoustic  qualities.  The  whispered  voice  is 
usually  heard  a  little  more  distinctly.  Pronounced  bronchophony  will 
at  least  transnlit  individual  sounds  and  the  rhythm  of  syllables.  Very 
faint  bronchophony  is  known  as  "  bronchial  whispering."  '  Pathologic 
bronchophony  is  due  to  the  same  conditions  and  is  subject  to  the  same 
laws  as  pathologic  bronchial  breathing.      It   is   heard  over  areas  of 

'  [The  term  "  bronchial  whisper  "  should  not  be  confused  with  "  whispered  broncho- 
phony."— Ed.  ] 

16 


242  AUSCULTATION. 

compressed  or  infiltrated  lung  with  patent  bronchi,  over  bronchiectases, 
and  over  pulmonary  cavities.  Bronchophony  may  acquire  a  metallic 
sound  over  cavities.  Pathologic  bronchophony,  like  bronchial  breathing, 
owes  its  origin  partly  to  better  conduction  of  sound  by  bronchi  which 
are  surrounded  by  an  infiltrated  area  and  partly  to  resonance.  Physio- 
logic bronchophony  varies  in  different  individuals ;  hence,  in  order  to 
detect  any  pathologic  change,  it  is  usually  advisable  to  compare  sym- 
metric portions  of  the  chest.  It  should,  however,  be  remembered  that 
physiologic  bronchophony  is  ordinarily  louder  on  the  right  side,  just  as 
is  physiologic  bronchial  breathing.  Both  the  spoken  and  the  whispered 
voice  should  be  tested,  and  the  ear  which  is  not  used  for  auscultation 
should  be  closed,  so  as  to  avoid  any  sound  transmission  through  the  air. 
Pathologic  bronchophony  has  exactly  the  same  diagnostic  significance 
as  consonating  rales  and  pathologic  bronchial  breathing  (see  above). 
All  these  signs,  in  virtue  of  their  common  origin  and  uniform  signifi- 
cance, may  be  included  in  the  term  "consonating  phenomena."  Each 
one  should,  however,  be  looked  for,  because,  in  spite  of  their  uniform 
cause  and  significance,  any  one  of  the  three  may  be  imperfectly  devel- 
oped ;  whispered  bronchophony,  for  instance,  may  be  heard  over  an 
infiltrated  area,  although  bronchial  breathing  is  indistinct.  If  deep 
breathing  is  painful  or  impossible,  the  demonstration  of  bronchophony 
may  be  of  great  value. 

Extreme  bronchophony,  or  pectoriloquy,  and  egophony,  a  form  of 
bronchophony  with  a  peculiar  bleating  sound,  are  sometimes  considered 
as  distinct  and  separate  phenomena  from  bronchophony.  But  the 
writer  does  not  consider  it  justifiable  to  attribute  these  signs  to  different 
conditions,  because  the  various  types  of  bronchophony  blend  in  such  a 
manner  as  to  be  indistinguishable  one  from  the  other.  Neither  does 
he  consider  it  justifiable  to  attribute  any  special  diagnostic  significance 
to  pectoriloquy  as  a  sign  of  cavities,  nor  to  egophony  as  a  sign  of  a 
pulmonary  compression  which  is  sufficient  to  cause  flattening  of  the 
bronchi.  Pectoriloquy  may  be  so  decided  over  an  infiltrated  area  that 
the  examiner  can  appreciate  the  articulation  although  he  cannot  actually 
distinguish  the  word.  Egophony  may  also  be  audible  over  such  an 
area.  All  sorts  of  theories  have  been  suggested  to  explain  the  occur- 
rence of  the  bleating  vsound  in  egophony,  but  none  of  them  has  satis- 
fied the  conditions  from  the  standpoint  of  physics.  In  any  case 
egophony  is  simply  a  quantitative  increase  of  ordinary  bronchophony. 
If  the  breathing  sounds  amphoric  and  if  the  percussion  note  is  metallic, 
the  bronchophony  is  apt  to  be  either  amphoric  or  metallic.  By  ex- 
amining for  bronchophony  with  the  naked  ear  the  degree  of  vocal 
fremitus  can  be  accurately  determined  at  the  same  time.  In  fact,  the 
skin  of  the  ear  can  appreciate  the  vibration  even  more  delicately  than 
can  the  hand. 

VARIOUS  ERRORS  IN  PULMONARY  AUSCULTATION. 
Even  an  expert  finds  auscultation  of  the  lungs  much  more  difficult 
than  auscultation  of  the  heart,  and  to  a  beginner  the  former  is  especially 


AUSCULTATION  OF  THE  RESPIRATORY  ORGANS.  243 

difficult  on  account  of  many  possible  errors.  First  of  all  there  is  the 
so-called  hair  crepitation,  caused  by  the  displacement  of  the  hairs  under 
the  stethoscope  with  respiration.  This  occurs  in  persons  with  even  a 
moderate  growth  of  hair  on  the  chest.  The  crepitations  are  syn- 
chronous with  the  respiratory  movements,  and  an  expert  will  quickly 
notice  that  the  sound  is  just  as  marked  during  inspiration  as  during 
expiration,  and  that  it  is  intensified  by  a  careless  use  of  the  stethoscope. 
This  source  of  error  may  be  so  annoying  that  it  is  necessary  to  wet  the 
hair  thoroughly  with  water  or  oil. 

Muscle  sounds  may  also  lead  to  error.  In  auscultating  the  apices 
the  muscle  sounds  produced  in  the  trapezius  as  it  takes  part  in  the 
respiratory  excursion  may  be  very  disturbing.  They  may  simulate 
rough  breathing  or  even  rales.  It  is  important  to  be  able  to  recognize 
this  condition,  so  as  to  avoid  error.  Muscle  sounds  may  also  be  pro- 
duced by  fibrillary  contraction  of  muscles — e.  g.,  "  shivering  "  due  to 
the  sudden  exposure.  These  sounds  may  be  appreciated  long  before 
shivering  is  apparent  to  the  eye.  Such  sounds  may  be  diiferentiated 
from  the  respiratory  murmur  by  asking  the  patient  to  hold  his  breath  ; 
if  they  persist  they  are  not  respiratory.  Besides  these  active  muscle 
sounds  there  is  a  so-called  "  passive  variety,"  which  may  be  produced 
by  the  displacement  of  bundles  of  muscle  fibers  under  the  edge  of  a 
stethoscope  by  light  movements  of  the  instrument  or  by  the  respiratory 
excursion  of  the  chest  itself.  These  sounds  may  be  recognized  by  inten- 
tionally moving  the  stethoscope,  and  so  reproducing  the  sound  even 
when  the  patient  is  not  breathing.  Again,  such  sounds  will  not  be 
heard  when  examining  with  the  naked  ear  or  when  very  gently  applying 
the  stethoscope.  Other  noises  originate  from  similar  conditions,  as,  for 
instance,  that  produced  by  pressing  the  stethoscope  over  the  lobulated  fat 
in  the  female  breast.  These  sounds  frequently  resemble  rales  very  closely. 
They  disappear  when  the  stethoscope  is  used  properly,  and  reappear  when 
a  little  pressure  is  exerted,  even  when  the  patient  stops  breathing. 

In  auscultating  portions  of  the  body  which  are  difficult  of  access  a 
beginner,  is  often  liable  to  produce  typical  friction  sounds  artificially, 
especially  so  if  he  is  in  an  uncomfortable  position,  so  that  his  stetho- 
scope is  not  accurately  or  firmly  applied,  so  that  the  patient's  skin 
beneath  it  moves  with  respiration.  Hence,  it  is  a  good  plan  for  him  to 
confirm  his  examination  by  listening  with  the  naked  ear  or  by  carefully 
readjusting  his  stethoscope. 

There  are  a  great  many  other  opportunities  for  producing  extraneous 
sounds  and  so  confusing  the  examiner.  We  might  emphasize  the  neces- 
sity of  persuading  patients  that  their  chests  should  be  entirely  uncov- 
ered for  a  proper  examination,  that  they  should  not  scratch  themselves 
during  the  examination,  and  should  remain  absolutely  quiet.  It  is 
perfectly  useless  to  attempt  an  examination,  particularly  of  the  apices 
of  the  lungs,  unless  the  patient's  upper  chest  is  entirely  uncovered. 
A  patient's  false  modesty,  his  fear  of  catching  cold,  or  the  examiner's 
laziness — none  of  these  reasons  can  possibly  excuse  a  careless  exami- 
nation. 


244  A  USOULTA  TION. 

It  is  desirable  for  every  physician  to  accustom  himself  thoroughly  to 
the  use  of  one  form  of  stethoscope.  Even  if  one  is  accustomed  to  a  poor 
instrument,  he  will  make  much  better  use  of  it  than  at  his  first  attempts 
with  a  better  one.  Stethoscopes  differ  decidedly  in  their  reproduction 
of  consonation — i.  e.,  bronchial  phenomena.  The  popular  hard-rubber 
stethoscopes,  for  example,  with  comparatively  long,  open  bells  and 
thin,  smooth  walls  increase  the  resonatiou  very  decidedly.  Mixed 
breathing  through  one  of  these  instruments  sounds  much  more  bron- 
chial than  through  a  cylindric  wooden  stethoscope.  Rales  assume  a 
more  consonating  character  when  heard  through  the  former,  a  fact 
which  the  Avriter  considers  a  practical  proof  that  consonating  rales  are 
produced  by  resonation  and  consonation.^ 

Another  source  of  error  in  auscultating  the  chest  may  be  mentioned. 
If  the  stethoscope  bell  is  carelessly  applied  to  the  chest-wall,  so  that 
part  of  its  edge  does  not  rest  there  firmly,  but  is  slightly  elevated, 
thus  allowing  the  air  free  entrance  to,  and  exit  from,  the  bell,  the 
examiner  will  frequently  hear  a  very  good  imitation  of  bronchial 
breathing.  The  sound  is,  of  course,  due  to  resonation.  Probably  the 
noise  of  the  patient  breathing  through  his  mouth  is  transmitted  and 
exaggerated  by  the  open  bell.  It  is  quite  similar  to  the  sound  we  hear 
when  we  place  a  large  sea  shell  with  its  opening  near  the  ear ;  when 
external  sounds  ordinarily  unnoticeable  are  so  much  exaggerated  by 
resonation,  that  children  frequently  imagine  they  hear  the  roaring  of 
the  sea. 

AUSCULTATION  OF  THE  HEART. 

"We  almost  always  need  a  stethoscope  to  auscultate  the  heart  prop- 
erly, because,  for  the  sake  of  diagnosis,  we  wish  not  only  to  appreciate 
the  sounds,  but  also  to  localize  them  as  accurately  as  possible.  We 
often  need  to  auscultate  the  heart  both  in  the  recumbent  and  in  the 
erect  posture,  and  sometimes  in  other  postures.  Hence,  it  is  a  good 
routine  to  auscultate  every  patient's  heart  both  while  he  is  lying  down 
and  while  he  is  sitting  or  standing  up.  (See  Mitral  Insufficiency  and 
Aortic  Insufficiency.) 

NORMAL  AUSCULTATION  SIGNS  OVER  THE  HEART. 

The  only  sounds  we  hear  over  a  healthy  individual's  heart  are  the 
so-called  '^ heart  tones.'''  The  word  "tone"  is  not  used  here  in  its  strict 
acoustic  sense,  because  the  sounds  heard  are  more  properly  noises,  and 
only  quite  rarely  possess  a  distinctly  recognizable  pitch.  French 
authors  call  normal  heart  tones  "  bruits  normaux  " ;  but  the  Germans 
and  the  English  have  retained  the  term  ''  tone "   despite  its  acoustic 

^  [The  use  of  the  single-barrel  stethoscope  preferred  by  Prof.  Sahli  is  not  common 
among  the  profession  in  America.  Undoubtedly  many  of  his  reasons  for  this  preference 
are  well  founded ;  but  we  think  that  a  good  bi-aural  stethoscope  Avill  transmit  the  sounds 
quite  as  plainly,  always  provided  that  the  examiner  is  thoroughly  accustomed  to  the 
resonation  of  his  own  instrument.  So  many  different  stethoscopes  have  been  advised  by 
different  authorities,  that  it  seems  hardly  fitting  for  us  to  recommend  especially  the  type 
with  which  we  are  personally  more  familiar. — Ed.] 


AUSCULTATION  OF  THE  HEART.  '  245 

inaccuracy,  and  have  reserved  the  word  "  gerausche  "  (noises,  murmurs) 
for  certain  pathologic  sounds  to  be  discussed  later.  (See  p.  260  for  the 
distinction  between  tones  and  murmurs.) 

We  normally  hear  two  heart  tones  over  the  entire  precordia,  and 
with  increased  cardiac  activity  they  may  often  be  heard  at  some  distance 
from  the  cardiac  region.  One  tone  follows  the  other  with  a  definite 
rhythm.  They  can  be  imitated  by  pronouncing  the  syllables  "  lubb- 
dupp,"  or  by  tapping  a  closed  book  quite  lightly  with  the  tips  of  the 
fingers.  A  short  pause  exists  between  the  first  and  the  second  tone, 
and  a  longer  pause  ensues  before  another  first  tone  occurs.  The  first 
tone  (the  so-called  systolic  tone)  is  synchronous  with  the  apex  beat  as 
felt  in  the  fifth  intercostal  space — i.  e.,  the  beginning  of  systole.  The 
second  sound  is  synchronous  with  the  beginning  of  diastole,  and  is 
therefore  called  the  diastolic  tone. 

Physiologists  have  proved  that  each  heart  tone  is  made  up  of  several 
factors,  and  that  the  reason  why  at  any  point  of  the  heart  we  hear  only 
two  tones  is  because  all  cardiac  tones  are  either  systolic  or  diastolic ;  in 
other  words,  all  systolic  tones  are  massed  together,  and  so  are  all 
diastolic  tones.  In  reality,  six  different  tones  arise  over  the  heart — 
four  systolic  and  two  diastolic. 

The  four  systolic  tones  originate  : 

1.  Over  the  left  ventricle,  at  the  mitral  valve. 

2.  Over  the  right  ventricle,  at  the  tricuspid  valve. 

3.  Over  the  beginning  of  the  aorta. 

4.  Over  the  beginning  of  the  pulmonary  artery. 
The  two  diastolic  tones  originate  : 

5.  Over  the  aortic  semilunar  valves. 

6.  Over  the  pulmonary  semilunar  valves. 

Hence,  no  diastolic  tone  originates  over  the  auriculoventricular 
valves — i.  e.,  over  the  ventricles. 

It  has  been  clearly  understood  for  years  that  the  diastolic  tones  could 
be  produced  only  by  diastolic  tension  of  the  semilunar  valves.  The 
origin  of  the  systolic  tones  have,  however,  baffled  investigators  for  some 
time.  Without  going  into  the  historic  presentation  of  this  question,  the 
present  theory,  which  has  apparently  stood  the  test  of  physiologic  and 
clinical  observation,  will  be  briefly  mentioned.  The  systolic  tone,  w^hich 
is  heard  at  the  apex,  originates,  according  to  this  theory,  principally  from 
the  systolic  tension  of  the  auriculoventricular  valves,  which  are  closed 
at  the  end  of  diastole.  This  view  is  supported  by  clinical  observations. 
In  addition,  experiments  upon  the  bloodless  heart  have  proved  that  the 
muscular  sound  of  the  heart  muscle  also  takes  part  in  the  production 
of  this  systolic  tone.  The  expression  "  muscular  sound  "  should  not  be 
construed  in  the  same  way  as  when  that  term  is  applied  to  the  skeletal 
muscles.  The  muscle  sound  of  a  skeletal  muscle  is  one  whose  pitch 
depends  directly  upon  the  number  of  individual  contractures,  which 
together  produce  the  condition  of  tetanus.  The  contraction  of  the  heart 
is,  however,  single  and  not  tetanic ;  hence,  its  muscular  sound  is  verj 
different  from  the  skeletal  muscle  sound.     The  muscular  sound  of  the 


246  AUSCULTATION. 

heart  is  in  reality  a  vibratory  phenomenon  caused  by  the  sudden  sys- 
tolic contraction  of  the  heart — in  other  words,  a  systolic  tension  tone, 
exactly  of  the  same  character  as  and  coincident  in  time  with  the  tones 
produced  at  the  auriculoventricular  valves  and  over  the  large  arteries 
(aorta,  pulmonary  artery).  This  conception  therefore  means  that  all 
systolic  tones  of  the  heart  are  identical  in  character  and  are  due  to  ten- 
sion of  its  walls — L  e.,  including  its  valves.  The  systolic  tones  of  the 
aorta  and  pulmonary  artery  are  referable  to  the  systolic  tension  of  the 
conns  arteriosus  and  the  closed  semilunar  valves.  They  are  produced 
by  the  sudden  increase  in  intracardiac  pressure  at  the  beginning  of 
systole.  It  is  incorrect  to  maintain,  as  has  been  frequently  done,  that 
the  first  tone  is  produced  by  systole  forcing  the  blood  into  the  aorta 
and  into  the  pulmonary  artery,  because  Martins'  experiments  proved 
that  the  first  tone  is  synchronous  with  the  beginning  (closure  or  tension 
time)  of  systole ;  and  because  at  that  moment  the  arterial  openings  are 
still  closed. 

Clinically,  it  has  been  quite  generally  accepted  that  the  systolic  tones  originate 
not  only  at  the  auriculoventricular  valves  and  over  the  ventricles,  but  also  at  the 
great  vessels  (aorta  and  pulmonary  artery).  This  opinion  has  been  attacked  upon 
physiologic  grounds.  Nevertheless,  the  writer  considers  that  the  clinical  view 
is  strongly  supported  by  cases  of  mitral  and  tricuspid  insufficiency  which  furnish 
a  systolic  tone  over  the  auscultation  area  of  the  great  vessels,  while  no  such  tone 
can  be  made  out  over  the  ventricles.     Such  cases  are  not  very  rare. 

Systolic  tones  which  are  heard  over  the  left  ventricle  are.  commonly 
called  "  mitral  tones,"  those  heard  over  the  right  ventricle,  "  tricuspid 
tones."  We  thus  limit  the  tones  to  that  part  of  the  sound  which  origi- 
nates at  the  valves  alone,  in  order  to  interpret  clinically  the  pathologic 
alterations  in  the  systolic  tones.  The  so-called  muscular  tone  has  thus 
far  proved  of  little  diagnostic  significance  because  we  cannot  readily 
distinguish  it  from  the  proper  valvular  tones.  Certain  impurities  in 
the  first  tone,  usually  referable  to  the  auriculoventricular  valv^es,  may, 
however,  be  caused  by  the  muscular  tone.  Perhaps  finer  methods  of 
examination  may  be  devised,  so  that  we  may  be  able  to  utilize  these 
muscular  tones  in  the  diagnosis  of  diseases  of  the  heart  muscle  (see 
p.  254). 

In  order  to  make  an  exact  diagnosis  of  the  condition  of  the  diflPer- 
ent  chambers  of  the  heart  we  should  separate  the  elements  of  the  tones 
and  distinguish  them  individually,  although  the  above-mentioned  six 
tones  of  the  heart  are  so  intimately  merged  into  a  mixed  systolic  and  a 
mixed  diastolic  tone  that  an  inexperienced  ear  can  only  perceive  the 
same  tone  over  the  entire  heart. 

The  fact  that  the  projections  of  the  arterial  openings  and  of  the 
valves  upon  the  chest-wall  are  at  some  distance  from  each  other 
(Fig.  102)  enables  us,  according  to  the  spot  auscultated,  to  appreciate 
at  will  sometimes  one  elementary  tone  of  the  heart  better,  sometimes 
another.  We  do  not,  however,  best  accomplish  such  an  acoustic  sep- 
aration by  auscultating  each  valve  exactly  at  the  point  of  its  j)ro- 
jection  upon  the  chest-wall,  for  these  points  of  projection  are  situated 


AUSCULTATION  OF  THE  HEART. 


247 


rather  near  each  other,  as  is  shown  in  Fig.  102.  Hence,  the  sounds 
at  each  point  are  quite  confused.  In  practice,  except  for  the  pulmonary- 
valve,  which  is  auscultated  exactly  over  its  point  of  projection,  we 
employ  the  following  device :  We  set  the  stethoscope  over  the  valve  to 
be  auscultated,  and  then  move  it  away  from  this  point  of  projection 
until  we  reach  a  spot  where  the  tone  we  wish  to  auscultate  can  still  be 
distinctly  heard,  but  where  the  other  tones,  on  account  of  their  greater 
distance,  are  as  faintly  heard  as  possible  and  so  no  longer  cause  con- 
fusion. This  device  is  founded  upon  the  well-known  law,  that  the 
intensity  of  sound  varies  inversely  with  the  square  of  the  distance  from 
its  point  of  origin.  By  carefully  noting  the  result  of  auscultation  in 
valvular  disease  (including  the  substitution  of  murmurs  for  the  tones  of 


Fig.  102.— Projection  of  the  heart  valves. 

the  affected,  valve)  and  by  comparing  such  results  with  the  changes 
subsequently  found  in  the  valves  at  autopsy,  we  are  able  to  select 
empirically  the  points  at  w^hich  each  valve  tone  can  be  best  auscultated 
separately. 

The  following  relations  between  the  sites  of  the  valves  (Luschka)  and 
their  respective  auscultation  points  have  been  demonstrated  by  extensive 
experience  : 

The  mitral  valve  is  situated  beneath  the  junction  of  the  third  left 
costal  cartilage  with  the  sternum ;  its  tone  is  heard  best  at  the  apex 
beat. 

The  tricuspid  valve  is  situated  halfway  between  the  points  where  the 
left  third  and  right  fifth  costal  cartilages  join  the  sternum.  Its  tone  is 
heard  best  over  the  lower  end  of  the  sternum. 


248  AUSCULTATION. 

The  pulmonary  valves  are  situated  in  the  second  intercostal  space, 
somewhat  to  the  left  of  the  edge  of  the  sternum.  Their  tones  are  best 
heard  at  this  point. 

The  aortic  valves  are  situated  about  the  middle  of  the  sternum,  at  the 
level  of  the  third  costal  cartilage.  Their  tones  are  best  heard  in  the 
right  second  intercostal  space,  near  the  edge  of  the  sternum. 

The  mitral  valve  is  best  heard  at  the  apex  beat,  because  the  valve 
itself  is  overlapped  by  the  lungs  and  by  the  right  ventricle  with  the 
tricuspid  valve,  while  at  the  apex  beat,  the  overlying  lung  tissue  is 
very  thin,  and  the  left  ventricle,  in  which  the  sound  is  produced,  is  not 
covered  there  by  the  right  ventricle,  or,  at  least,  to  a  less  degree  than 
farther  above.  Further,  eccentric  situation  of  the  apex  prevents  the 
other  heart  tones  from  being  so  readily  transmitted  there. 

The  above  statements  explain  why  the  rhythm  of  the  heart  tones 
differs  at  different  points  over  the  heart.  The  writer  will  state  the 
facts,  and  then  attempt  to  explain  them.  Over  the  auscultation  points 
for  the  aorta  and  pulmonary  artery  and  in  the  vicinity  the  heart  tones 
exhibit  an  iambic  rhythm  (lubb-diipp,  lubb-dtipp) 

Over  the  lower  part  of  the  sternum,  however,  and  as  far  as  the  apex 
beat — i.  e.,  over  the  auscultation  points  for  the  auriculoventricular 
valves  (the  ventricles) — the  heart  tones  produce  a  trochee  (liibb-dupp, 
liibb-dupp) 

This  may  be  explained  as  follows  :  No  diastolic  tone  is  produced  at 
the  auscultation  points  for  the  auriculoventricular  valves.  The  second 
tone  is  heard  only  by  transmission  from  the  aorta  and  pulmonary 
artery ;  consequently,  it  is  proportionately  diminished.  Hence,  the 
accent  upon  the  first  tone  (trochee).  The  conditions  are  different  over 
the  great  vessels,  where  both  a  first  and  a  second  tone  are  produced. 
Naturally,  the  first  tone  is  relatively  weak  because  it  is  produced  by  a 
moderate  increase  in  pressure  upon  the  arterial  semilunar  valves  acting 
against  considerable  arterial  pressure  at  the  beginning  or  closure  time 
of  systole.  On  the  other  hand,  the  second  tone  is  much  stronger  and 
accentuated  because  it  is  produced  by  the  rapid  and  forcible  closure  of 
the  elastic  semilunar  valves  acting  under  the  pressure  of  the  aorta  and 
pulmonary  arteries.  This  accounts  for  the  iambic  rhythm  heard  over 
the  great  vessels. 

DISTINCTION    BETWEEN     SYSTOLE    AND    DIASTOLE    BY    MEANS 
OF    AUSCULTATION. 

One  of  the  most  important  requisites  for  the  diagnosis  of  cardiac 
lesions  is  the  ability  to  distinguish  the  systolic  from  the  diastolic  phase 
of  the  heart's  action  ;  in  other  words,  to  recognize  accurately  the  systolic 
and  diastolic  tones.  An  experienced  clinician  does  not  find  this  espe- 
cially difficult  under  normal  conditions,  because  of  the  usual  accentuation 
of  the  tones.  The  diastolic  tone  is  accentuated  over  the  great  vessels, 
and  the  systolic  tone  is  accentuated  at  the  apex  and  over  the  tricuspid 
valve. 

The  sequence  of  the  heart  tones  at  the  base  of  the  heart  and  at  the 


AUSCULTATION  OF  THE  HEART.  249 

auscultation  points  for  the  auriculoventricular  valves  is  shown  by  the 
following  scheme  (where  the  beginning  of  systole  is  indicated  by  a 
vertical  line)  : 

Great  vessels  :  VS       ~D         Vs       "d 

Auriculoventricular  valves :    l^       v_/         \^       <^ 

\S        D  IS        If 

Some  cases,  however,  furnish  exceptions  to  the  rule  of  accentuation 
in  that  the  first  and  second  sounds  are  heard  more  or  less  equally 
distinct.  Under  such  circumstances  the  peculiarity  of  the  pauses  fur- 
nishes the  most  efficient  means  of  differentiation.  Both  physiology  and 
clinical  experience  have  proved  that  systole  is  shorter  than  diastole ; 
therefore  the  systolic  tone  is  the  one  preceded  by  the  longer  interval 
of  silence.  In  other  words,  if  the  heart  tones  are  arranged  in  pairs, 
according  to  the  interval  of  silence,  and  practice  leads  us  to  do  this 
instinctively,  the  first  tone  of  each  pair  will  be  the  systolic,  and  the 
second  tone  the  diastolic.  In  the  following  scheme  of  the  heart  tones 
the  two  heart  tones  are  equally  accented,  but  can  be  readily  distin- 
guished by  the  relative  lengths  of  the  pauses  between  them : 


Vs     J)       \s     J? 


Even  this  method  may  be  unavailable,  because  both  the  pauses  are 
sometimes  equal  in  length  (pendulum  rhythm).  Then  the  clinician 
usually  depends  upon  palpating  the  apex  beat.  This  is  a  practicable 
method  provided  the  heart  action  is  not  too  rapid  and  the  apex  beat 
sufficiently  forcible.  If,  however,  the  heart  is  too  rapid,  the  time 
between  the  beginning  of  systole  and  diastole  is  too  short  to  associate 
the  sensation  of  touch  with  the  perception  of  sound. 

Comparing  the  heart  tones  with  the  carotid  pulse  is  even  less  reliable 
than  comparing  them  with  the  apex  beat,  as  the  apex  beat  is  synchronous 
with  the  first  tone,  while  the  carotid  pulse  corresponds  more  accurately 
to  the  expulsion  time. 

Systole  can  never  be  determined  from  the  radial  pulse  unless  the 
heart  action  is  very  slow.  If  rapid,  the  radial  pulse  is  delayed  (0.22 
seconds,  according  to  Landois),  and  so  coincides  more  nearly  with  dias- 
tole than  with  systole.  Students  should  therefore  avoid  this  method 
if  possible. 

Systole  and  diastole  can,  as  a  rule,  be  readily  distinguished  by  one 
of  these  methods,  but  under  certain  pathologic  conditions  where  the 
heart  action  is  very  rapid,  especially  if  it  is  irregular,  the  differentia- 
tion may  be  extremely  difficult.  Decision  must  be  deferred  in  some 
cases  until  the  heart  action  has  quieted  down,  either  spontaneously  by 
rest  or  with  the  aid  of  drugs  (digitalis). 

In  many  heart  lesions  systole  may  be  determined  by  certain  well- 
characterized  pathologic   heart  murmurs,  particularly  those  which  are 


250  AUSCULTATION. 

accentuated  toward  their  termination  and  which  occur  only  immediately 
before  systole — that  is,  are  presystolic  (see  p.  269  et  seq.). 

In  the  above  description  the  writer  has  enumerated  the  diiferent 
methods  for  recognizing  the  phases  of  the  heart's  action  in  the  order  of 
their  practicability.  The  most  desirable  and  the  most  commonly  em- 
ployed in  practice  is  the  determination  of  systole  by  the  accentuation 
of  the  tones  and  their  relation  to  the  pause.  Students  should  practise 
this  method  assiduously,  and  not  form  the  habit  of  determining  systole 
by  feeling  the  carotid  pulse,  or,  worse  still,  the  radial  pulse.  The  method 
recommended  affords  excellent  practice  in  training  the  ear,  and  is  of 
great  importance  to  physicians  who  have  never  studied  music. 

ABNORMAL    AUSCULTATION    SIGNS    OVER    THE    HEART. 

Only  those  abnormal  results  of  auscultation,  the  determination  of 
which  is  peculiar  to  auscultation,  will  be  discussed  here.  Abnormalities 
in  rhythm  can  usually  be  determined  quite  as  readily  from  the  pulse  and 
the  apex  beat,  and  will  be  discussed  in  the  sections  treating  of  the  Pulse 
and  the  Apex  Beat.  The  same  sections  describe  the  significance  of  the 
conditions  under  which  the  rhythm,  as  determined  by  auscultation  and 
palpation  of  the  apex  beat,  differs  from  that  obtained  at  the  radial 
pulse.  (See  p.  101  and  the  section  upon  Reduplication  of  the  Apex 
Beat.) 

ALTERATIONS    IN    THE    LOUDNESS    OR   INTENSITY    OF   THE    HEART 

TONES. 

The  intensity  of  the  heart  tones  depends  partly  upon  conditions 
within  and  partly  upon  conditions  without  the  heart.  The  thicker  the 
chest-walls  the  less  distinct  the  heart  tones.  Hence,  in  corpulent  or 
muscular  individuals,  and  particularly  in  women  with  well-developed 
breasts,  the  heart  tones  are  apt  to  be  faint,  while  in  emaciated  individuals 
they  are  generally  strong.  Edema  of  the  chest-wall  may  also  weaken 
the  heart  tones.  Similarly,  the  heart  tones  are  less  audible  if  the  heart 
is  pushed  away  from  the  chest-wall,  as  a  result  of  emphysema,  of  fluid 
in  the  pericardium,  or  of  precordial  emphysema.  If  the  pericordial 
exudation  is  extensive  the   heart  tones  are  frequently  quite  inaudible. 

They  are  intensified,  however,  if  the  lung  is  retracted  from  the  heart 
as  a  result  of  pulmonary  contraction  or  in  consequence  of  an  encroach- 
ment upon  the  intrathoracic  space  (kyphoscoliosis — high  position  of  the 
diaphragm,  or  displacement  of  the  heart). 

The  heart  tones  are  intensified  by  a  consolidation  of  the  pulmonary 
edges  about  the  heart.  The  factors  operating  here  are  probably  the 
same  as  those  which  produce  bronchial  breathing  over  consolidations 
(p.  226  ei  seq.).  The  heart  tones  are  more  perfectly  transmitted  to  the 
surface,  on  the  one  hand,  through  patent  bronchi  surrounded  by  con- 
solidated lung,  and,  on  the  other  hand,  by  resonance  of  the  air  in  the 
bronchi.  Resonance  is  also  responsible  for  the  heart  tones  being  inten- 
sified in  pneumopericardium  and  in  adjoining  cavities  of  the  lungs,  also, 


AUSCULTATION  OF  THE  HEART.  251 

again,  in  certain  degrees  of  distention  of  the  stomach  with  air.  In  all 
these  conditions  the  tones  may  acquire  a  metallic  ring. 

In  other  cases,  however,  the  heart  tones  are  intensified  on  account 
of  conditions  within  the  heart  itself.  The  intensity  depends  espe- 
cially upon  the  strength  of  the  heart.  As  a  rule,  therefore,  the  tones 
are  louder  in  strong  individuals  or  when  the  action  of  the  heart  is 
excited,  while  thev  are  less  audible  or  even  inaudible  in  weak  or  very 
sick  individuals,  during  collapse,  and  in  serious  aifectious  of  the  heart 
muscle  which  diminish  the  capacity  for  w^ork.  Many  exceptions  to 
these  rules  occur  in  individual  cases,  because,  as  we  have  already  seen, 
the  intensity  of  the  heart  tones  depends  upon  many  other  factors  besides 
the  mere  strength  of  the  heart.  The  elasticity  and  smoothness  of  the 
valves  is  one  in  point,  and  it  may  perhaps  explain  why  the  heart  tones 
are  occasionally  very  loud  in  weak  individuals  with  low  blood-pressure, 
and  in  anemic  persons. 

If  the  heart  tones  are  markedly  increased  they  are  audible  not  only 
over  the  precordia,  but  also  at  a  greater  or  less  distance  from  the  heart, 
in  the  intrascapular  space,  in  the  head,  in  the  epigastric  region,  and 
occasionally  even  at  some  distance  from  the  patient's  body. 

Increase  or  diminution  of  individual  tones  is  of  greater  significance 
than  uniform  increase  or  diminution  of  all  the  heart  tones.  In  order  to 
recognize  changes  in  the  intensity  of  individual  tones,  we  must  clearly 
appreciate  the  relative  intensity  of  the  different  heart  tones  under 
physiologic  conditions.  The  corresponding  tones  of  the  right  and  left 
heart  are  generally  conceded  to  be  of  equal  intensity.  This  is  true 
despite  the  greater  power  developed  by  the  left  ventricle,  because  the 
intensity  of  the  tone  depends  not  so  much  upon  the  absolute  value  of 
the  pressure  acting  upon  the  valves  as  upon  the  difference  between  the 
pressures  acting  upon  the  two  sides  of  the  valve  at  the  moment  of 
closure,  and  the  rapidity  of  the  increase  in  tension.  Again,  although 
the  mitral  and  aortic  tones  of  the  left  heart  are  naturally  louder  than 
the  corresponding  tones  of  the  right  heart,  this  difference  in  intensity  is 
neutralized  because  the  aortic  and  mitral  valves  are  situated  at  a  greater 
distance  from  the  chest-wall  than  are  the  valves  of  the  right  heart. 
Even  under  normal  conditions  the  corresponding  tones  of  the  right  and 
left  heart  are,  however,  occasionally  of  unequal  intensity ;  hence,  an 
increase  or  diminution  of  one  or  the  other  tone  cannot  be  considered 
pathologic  unless  the  difference  is  very  marked. 

The  second  aortic  tone  is  increased  in  hypertrophy  of  the  left  ven- 
tricle provided  the  valves  themselves  are  not  diseased  and  the  hyper- 
trophied  ventricle  is  sufficient  to  ]5roduce  an  increase  in  blood-pressure. 
This  occurs  particularly  in  arteriosclerosis  and  in  chronic  nephritis. 
The  second  pulmonic  tone  is  increased  similarly  in  the  iiypertrophy  of 
the  right  ventricle  which  accompanies  mitral  lesions,  or  in  any  other  con- 
dition obstructing  pulmonary  circulation  (emphysema).  Accentuation 
of  the  second  pulmonic  tone  is  therefore  an  im])ortant  sign  of  a  compen- 
sated mitral  lesion.  Diminution  or  weakening  of  a  second  pulmonic 
tone  which  has  been  previously  accentuated  occurs  when  the  compensa- 


252  AUSCULTATION. 

tion  in  tbese  lesions  becomes  disturbed  as  soon  as  tbe  right  ventricle 
fails  to  exert  sufficient  power.  Under  the  above  conditions,  where  the 
ventricle  develops  more  force  we  might  expect  that  the  first  aortic  and 
pulmonic  tones,  as  well  as  those  over  the  auriculoventricular  valves, 
would  be  intensified.  Although  not  usually  the  case,  this  is  occasion- 
ally true.  As  has  been  mentioned  above,  the  intensity  of  the  first 
aortic  and  pulmonic  sounds  depends  less  upon  the  absolute  pressure 
exerted  by  the  ventricles  at  the  beginning  of  systole  than  upon  the 
difference  in  pressure  on  the  two  sides  of  the  closed  valve  and  the  rapid- 
ity of  the  increase  in  tension.  Similarly,  the  intensity  of  the  auriculo- 
ventricular tones  depends  not  so  much  upon  the  absolute  force  developed 
by  the  heart  as  upon  the  degree  of  tension  and  the  rapidity  of  its  increase 
at  the  valve.  Greater  working  power  does  not  necessarily  increase  these 
two  factors,  provided  sufficient  blood  enters  the  ventricle  during  diastole 
and  at  the  same  time  places  the  valve  under  considerable  tension. 

Diminution  of  individual  heart  tones  is  caused  by  more  or  less  exten- 
sive destruction  of  the  respective  valves.  Thus,  marked  deformity  of 
the  mitral  valve  causes  diminution  of  the  mitral  tones,  and  marked 
destruction  of  the  aortic  valve  causes  diminution  of  the  second  aortic 
tone.  At  the  same  time  we  must  not  forget  that  many  erroneous  views 
are  held  about  this  point.  The  loss  of  a  portion  of  the  membrane  of  a 
valve  does  not  necessarily  cause  absence  or  even  marked  diminution  of 
the  corresponding  tone,  because  the  remaining  portions  of  the  valve 
can  still  produce  the  tones  ;  and,  besides,  not  only  the  valve  itself,  but 
also  the  surrounding  structures  contribute  to  the  production  of  tones. 
For  the  first  tone  the  walls  of  the  ventricle  and  the  conus  arteriosus, 
and  for  the  second  the  walls  of  the  first  portion  of  the  aorta  and  pul- 
monary artery,  play  an  important  part. 

The  following  rule  may  therefore  be  accepted  :  If  a  valve  is  affected 
we  shall  hear  not  only  the  murmur  it  causes,  but  also  its  corresponding 
tone.  An  experienced  clinician  can  frequently  detect  both  the  mur- 
murs and  the  heart  tone.  This  is  best  accomplished  by  holding  the  ear 
at  a  little  distance  from  the  stethoscope,  so  that  the  sounds  are  heard 
rather  faintly.  The  respective  tones  may  then  be  diminished  by  a  valvular 
lesion,  but  are  not  necessarily  so.  It  has  been  frequently  stated  that  the 
diagnosis  of  aortic  insufficiency  depends  upon  an  absence  of  the  second 
aortic  tone.  This  view  is  absolutely  incorrect.  A  practised  ear  can 
hear  the  second  aortic  tone  in  most  cases  of  aortic  insufficiency,  although 
frequently  it  is  diminished.  Absence  or  marked  diminution  of  the 
second  aortic  tone  may,  however,  aid  in  some  cases  in  the  diagnosis  of 
aortic  insufficiency. 

It  is  interesting  and  quite  important  diagnostically  to  remember 
that  with  a  marked  insufficiency  of  the  auriculoventricular  valve  not 
only  the  auriculoventricular  tone,  but  all  the  tones  of  that  side  of 
the  heart  become  very  much  diminished  or  disappear  entirely.  The 
absence  of  the  first  tone  is  not  due  to  the  impossibility  of  producing 
a  first  tone  in  an  extensive  destruction  of  the  valve,  for,  as  was  noted 
above,  the  systolic  tone  originates  in  all  that  part  of  the  heart  put  into 


AUSCULTATION  OF  THE  HEART.  253 

a  state  of  tension  during  systole — namely,  the  walls  of  the  ventricle  and 
the  arterial  openings.  For  example,  a  marked  mitral  insufficiency 
may  show  no  systolic  tone  at  any  point  over  the  left  heart,  and  not 
merely  the  first,  but  also  the  second,  tone  over  the  aortic  area  may  be 
entirely  absent.  The  cause  of  this  peculiarity  is  at  first  glance  rather 
difficult  to  understand,  but  it  may  be  explained  as  follows  :  On  account 
of  the  existence  of  mitral  insufficiency  the  closure  time  of  the  heart  dis- 
appears, but  its  place  is  usurped  by  a  period  during  which  the  heart 
does  contract  about  its  contents,  but  the  rapidity  of  increase  of  tension 
is  very  slow,  because  the  blood  in  the  ventricle  immediately  escapes  into 
the  auricle.  Consequently,  the  mitral  valve  is  never  brought  into  a 
state  of  rapid  and  strong  tension,  because,  as  soon  as  the  blood  escapes 
into  the  auricle,  both  sides  of  the  valve  are  subjected  to  about  the  same 
degree  of  pressure.  Hence,  the  mitral  tone  is  very  faint  or  entirely  lack- 
ing on  account  of  the  absence  of  a  closure  period.  A  further  result  of 
the  regurgitation  at  the  beginning  of  systole  is  that  the  walls  of  the  ven- 
tricles, the  conus  arteriosus,  and  the  closed  aortic  valves  are  not  suf- 
ficiently nor  rapidly  enough  stretched  to  produce  a  strong  systolic  tone. 
Consequently,  either  no  systolic  tone  or  only  a  rudimentary  one  is 
heard  over  the  ventricle  and  over  the  beginning  of  the  aorta.  In  addi- 
tion, a  marked  mitral  regurgitation  may  also  cause  diminution  or  absence 
of  the  second  aortic  tone,  because  the  blood  regurgitated  into  the  auricle 
by  the  ventricular  pressure  rushes  back  again  into  the  ventricle  at  the 
beginning  of  diastole,  thus  reducing  below  the  normal  the  difference  in 
pressure  upon  the  two  sides  of  the  valves,  and  the  tension  of  the  valves. 
Other  things  being  equal,  the  same  reasoning  applies  to  the  right  heart 
and  to  tricuspid  insufficiency.  All  the  heart  tones  may  be  diminished 
or  entirely  absent  in  a  combined  mitral  and  tricuspid  insufficiency. 
The  absence  of  the  heart  tones  in  insufficiency  of  the  auriculoventricular 
valves  is  of  double  diagnostic  significance.  In  the  first  place,  it  aids  in 
determining  the  degree  of  insufficiency.  Mitral  insufficiency  with  no 
tone  over  the  left  heart  must  necessarily  be  a  serious  lesion.  This  law 
applies  only  during  the  period  of  compensation.  During  disturbance  of 
compensation  the  heart  tones  may  be  enfeebled  on  account  of  diminished 
systolic  force.  On  ihe  other  hand  the  absence  of  heart  tones  may  occa- 
sionally prove  the  existence  of  an  auriculoventricular  insufficiency  which 
could  not  otherwise  be  diagnosed  on  account  of  the  absence  of  a  mitral 
murmur.  If,  for  example,  a  compensated  mitral  stenosis  is  diagnosed, 
and  it  is  noted  that  the  heart  tones  are  absent  on  the  left  side,  the  stenosis 
is  probably  combined  with  an  insufficiency  of  the  mitral  valve. 

Finally,  in  regard  to  the  audibility  of  heart  tones  in  valvular  lesions 
accompanied  by  murmurs,  it  is  to  be  noted  that  the  statement  so  fre- 
quently made,  that  the  tones  are  masked  by  a  miu'mur,  is  based  on  an 
erroneous  conception.  The  same  change  which  disturbs  the  functions 
of  the  valves  and  produces  the  murmur  may  coincidentally  prevent  the 
production  of  a  tone  or  diminish  its  force.  The  tones  cannot,  however, 
be  masked  by  the  murmur.  Provided  the  tone  actually  exists,  its 
sound,  like  a  sharp  blow  in  the  midst  of  the  slow,  pulsating  sound  of 


254  AUSCULTATION. 

the  murmur,  can  always  be  detected  by  an  experienced  clinician,  espe- 
cially if  he  employs  the  device  of  holding  the  ear  at  a  little  distance 
from  the  stethoscope. 

In  the  graphic  representations  of  the  results  of  auscultation  the 
writer  has  expressed  the  intensity  of  the  heart  tones  by  the  heaviness 
of  the  metrical  signs  and  accents  used  to  represent  them.  (See,  for 
example.  Fig.  114,  increased  second  pulmonic  tone.) 

ALTERATIONS    IN    THE    TIMBRE    OF    THE    HEART    TONES. 

The  timbre  or  quality  of  the  heart  tone  may  vary  even  under  normal 
conditions.  Whether  the  normal  heart  tones  are  simply  noises  or  whether 
they  resemble  musical  sounds  depends  upon  a  number  of  factors  diffi- 
cult to  analyze,  especially  upon  the  elasticity  of  the  valves  and  of  the 
walls  of  the  larger  vessels.  However,  a  drum-like  tympanitic  or  singing 
quality  is  rather  rare  in  healthy  individuals.  Occasionally  the  tones 
even  in  healthy  individuals  are  not  clear ;  they  are  n.ot  like  a  single 
short  blow,  but  produce  a  rough,  irregular  sound.  The  cause  of  such 
an  impurity  in  the  tones  of  a  normal  heart  has  not  been  determined. 

Marked  variation  in  the  timbre  of  the  heart  tones  occurs  under  path- 
ologic conditions.  Thus,  in  arteriosclerosis  the  second  aortic  sound  is 
not  only  accentuated,  but  possesses  a  peculiar  ringing  quality.  More- 
over, as  has  been  mentioned  upon  pp.  250  and  251,  as  a  result  of  reso- 
nance of  air  contained  in  cavities,  the  heart  tones  are  not  only  intensified, 
but  assume  a  peculiar  metallic  character. 

The  tone  called  "  cliquetis  metallique  "  is  a  noticeably  rattling  sys- 
tolic tone  heard  over  the  ventricles  when  the  heart  action  is  stimulated, 
not  only  in  healthy  individuals,  but  also  in  heart  disease,  in  attacks  of 
nervous  palpitation,  and  in  every  form  of  cardiac  hypertrophy.  Occa- 
sionally it  can  be  heard  at  some  little  distance,  and  is  probably  due  ta 
the  violent  vibration  transmitted  to  the  chest- wall,  or  possibly  the  stomachy 
in  consequence  of  the  accelerated  cardiac  action. 

Impurity  or  roughness  of  the  heart  sounds  is  observed  in  healthy 
persons,  but  it  is  more  commonly  due  to  some  disease  of  the  heart.  It 
is  frequently  due  to  slight  changes  in  the  valve  which  do  not  necessarily 
disturb  its  function  (roughness  or  rigidity  of  the  curtains),  but  in  some 
cases  it  is  the  result  of  a  valvular  lesion  which  is  not  sufficiently  pro- 
nounced to  produce  the  characteristic  murmur.  Under  such  circum- 
stances an  impure  tone  might  be  regarded  as  a  rudimentary  murmur ; 
because,  if  the  cardiac  action  is  accelerated — e.  g.,  by  directing  the  patient 
to  get  up  and  to  sit  down  again  several  times  in  succession — the  rough 
tone  is  frequently  replaced  by  a  true  murmur.  Autopsy  findings  occa- 
sionally suggest  that  the  roughness  of  the  systolic  tone  is  due  to  changes 
in  the  muscle  sound,  the  result  of  structural  changes  in  the  heart  muscle 
(fibrosis). 

APPARENT  OR  ACTUAL  REDUPLICATION  OF  THE  HEART  TONES. 

Normally  only  two  tones  are  heard  over  every  point  of  the  heart,  a 
systolic  and  a  diastolic  tone  ;  but  under  both  physiologic  and  jiathologic 


AUSCULTATION  OF  THE  HEART.  255 

conditions  three  or  even  four  tones  may  be  distinguished.  This  pecu- 
liarity may  depend  upon  either  one  of  two  causes  :  either  there  is  only 
an  apparent  reduplication — i.  e.,  under  normal  conditions  all  systolic 
tones  and  all  diastolic  tones  occur  at  the  same  moment,  but  in  any  given 
case  such  a  coincidence  may  be  disturbed — or  else  there  may  be  an 
actual  reduplication  of  the  sounds,  due  to  the  production  of  abnormal 
tones. 

Division,  Splitting,  and  Reduplication  of  Heart  Sounds 
(^  time). — When  two  tones  with  a  very  short  interval  between  them 
are  heard  in  place  of  one  heart  tone  the  tone  is  said  to  be  split  or  redu- 
plicated. If  the  two  tones  occur  very  close  together,  we  speak  of  a 
division  or  splitting  of  that  heart  tone,  while  we  limit  the  term  redupli- 
cation  to  those  cases  where  the  two  tones  are  separated  by  a  longer  inter- 
val. The  three  tones  do  not  follow  each  other  in  ^  time,  but  the  heart 
rhythm  preserves  the  normal  |-  time.  Reduplication  of  the  first  sound 
gives  an  anapest,  -^^  -^-  —  (lubb-lubb-dupp) ;  reduplication  of  the 
second  sound,  a  dactyl,  —  ^^  w  (lubb-dupp-dupp).^  The  double 
tones  in  splitting,  which  is  only  indistinctly  separated  from  reduplica- 
tion, are  repeated  so  rapidly  that  the  examiner  obtains  the  impression 
of  a  single  tone  accented  at  the  beginning  or  at  the  end.  This  is 
commonly  expressed  by  connecting  the  metric  signs  -^^^  and  ^-^^-'. 

This  splitting  or  reduplication  may  be  caused  (a)  by  an  imperfect 
coincidence  of  the  correlated  tones  of  the  right  and  left  heart,  or  (6)  by 
the  production  of  abnormal  tones. 

(a)  Splitting  and  Reduplication  as  a  Result  of  Imperfect  Coinci- 
dence of  the  Heart  Tones. — It  is  not  surprising  that  various  conditions 
should  disturb  the  coincidence  of  the  heart  tones,  considering  the  great 
number  of  factors  influencing  the  course  of  the  heart's  action  (nervous 
influences,  variations  in  pressure  in  the  different  parts  of  the  heart 
chambers  and  in  the  rest  of  the  circulation).  It  is,  on  the  contrary, 
more  remarkable  that  any  such  coincidence  of  all  systolic  and  all  dias- 
tolic phenomena  should  occur  at  all ;  and  suggests  a  very  perfect  balance 
of  the  cardiac  mechanism. 

Faulty  coincidence,  producing  a  reduplication  or  splitting  of  the 
first  tone,  is  occasionally  caused  by  a  failure  of  the  two  ventricles  to  con- 
tract at  the  same  moment ;  under  such  circumstances  the  splitting  of  the 
tone  is  audible  over  the  entire  heart.  Splitting  or  reduplication  of  the 
first  tone  is  explained  in  most  cases  by  an  actual  increase  in  the  number 
of  heart  tones,  and  will  accordingly  be  discussed  in  the  following  sub- 
division (6,  p.  257). 

Faulty  coincidence,  producing  a  splitting  of  the  second  tone, 
is  frequently  observed  in  healthy  individuals  at  the  height  of  inspiration 

'  The  normal  accentuation  of  systole  over  the  auriculoventricular  valves  and  diastole 
over  the  great  vessels  is  effaced  by  the  splitting  of  the  tones.  Hence,  reduplication 
and  splitting  of  the  first  tone  produces  an  anapestic  riiylhm,  not  only  over  the  great 
vessels  but  also  over  the  auriculoventricular  valves.  In  the  same  way  splitting  of  the 
second  tone  produces  a  dactyl,  not  only  over  the  auriculoventricular  valves  but  also  over 
the  great  vessels. 


256  AUSCULTATION. 

and  in  mitral  lesions — both  insufficiency  and  stenosis.  A  common 
explanation  of  the  splitting  of  the  second  tone  is  that  the  aortic  and 
pulmonary  semilunar  valves  do  not  shut  at  the  same  instant.  This 
lack  of  coincidence,  under  the  above-named  conditions,  is  supposed  to 
be  due  to  an  abnormal  diiference  in  pressure  between  the  aorta  and 
pulmonary  artery.  High  pressure  closes  the  valves  sooner  than  low 
pressure.  The  second  part  of  this  explanation  is  certainly  incorrect, 
because  even  under  physiologic  conditions  the  pressure  in  the  aorta 
differs  enormously  from  that  in  the  pulmonary  artery,  and  because, 
furthermore,  Ceradini  has  demonstrated  that  the  closure  of  the  semi- 
lunar valves  occurs  instantly  and  independently  of  the  degree  of  press- 
ure in  the  artery  as  soon  as  blood  ceases  to  flow  out  of  the  heart.  The 
second  tone  is  not  caused  by  the  closure,  but  by  the  sudden  tension  of 
the  closed  semilunar  valves,  and  takes  place  at  the  moment  when,  after 
a  period  of  rest,  the  ventricular  diastole  begins.  So  far  as  any  lack  of 
coincidence  of  the  left  and  right  tones  are  concerned,  splitting  or 
reduplication  of  the  second  tone  inight  be  referred  to  lack  of  coincidence 
in  the  beginning  of  diastole,  but  such  an  assumption  is  quite  unnecessary. 
The  following  explanation  is  more  plausible  :  The  semilunar  valves, 
which  are  closed  at  the  end  of  systole  as  a  result  of  the  marked  diastolic 
drop  in  pressure  within  the  ventricles,  are  suddenly  forced  back  and 
made  tense  against  the  ventricle  by  the  pressure  in  the  aorta  and  pul- 
monary artery  at  the  beginning  of  systole.  This  produces  the  diastolic 
tone.  Any  factor  which  tends  to  prevent  a  rapid  diastolic  drop  in 
pressure  within  the  ventricles  will  probably  delay  the  corresponding 
second  tones,  while  any  factor  which  favors  a  drop  in  pressure  will 
hasten  it.  As  a  matter  of  fact,  such  factors  are  present  under  those 
conditions  where  reduplication  or  splitting  of  the  second  sound  exists. 
Inspiration  in  a  healthy  individual,  with  moderately  rapid  respira- 
tion (see  p.  119),  detains  the  blood  in  the  dilated  pulmonary  vessels, 
and  so  delays  the  ventricular  filling.  In  consequence,  the  difference 
in  pressure  between  the  aorta  and  the  left  ventricle  is  rapidly  in- 
creased, producing  sudden  diastolic  tension  of  the  aortic  valves,  and 
thus  causing  the  second  aortic  sound  to  occur  before  the  second  pul- 
monic, as  evidenced  by  reduplication  or  splitting  of  the  second  tone. 
The  conditions  are  similar  in  mitral  stenosis,  where  the  flow  of  blood 
into  the  left  ventricle  is  obstructed  by  the  narrowed  valve  ;  consequently, 
the  aortic  valve  is  put  under  tension  sooner  than  the  pulmonic.  In 
mitral  insufficiency,  on  the  contrary,  the  left  ventricle  is  filled  very 
rapidly  during  diastole,  on  account  of  the  congestion  in  the  auricle  ; 
consequently,  the  aortic  valve  is  put  under  tension  somewhat  later  and 
the  second  aortic  tone  is  delayed.  If  this  explanation  is  correct,  the 
second  aortic  tone  is  hastened  during  inspiration  of  a  healthy  individual, 
as  well  as  in  mitral  stenosis,  but  delayed  in  cases  of  mitral  insufficiency. 
This  is  actually  the  fact,  because  in  mitral  stenosis  and  in  healthy 
individuals  the  second  part  of  the  double  tone  can  be  perceived  in  the 
left  intercostal  space  as  a  loud   second   pulmonic   tone,  while  in  mitral 


AUSCULTATION  OF  THE  HEART.  257 

insufficiency,  in  the  same  place,  the  first  part  of  the  double  tone  is  more 
distinctly  heard/ 

Reduplication  of  the  second  tone  so  frequently  accompanies  mitral 
lesions  that  it  should  be  considered  as  of  some  diagnostic  significance, 
provided  that  it  can  be  proved  to  be  independent  of  any  definite  phase 
in  breathing. 

(b)  Splitting  and  Reduplication  as  a  Result  of  the  Production  of 
New  Tones. — In  some  cases  there  is  reason  to  believe  that  the  redupli- 
cation of  tones  is  not  due  to  failure  of  coincidence  of  the  normal  tones, 
but  is  caused  by  the  production  of  new  abnormal  tones. 

It  is  conceivable  that  splitting  or  reduplication  of  the  first  tone  ovei 
the  auriculoventricalar  valves  occurs  where  mechanical  conditions  prevent 
the  individual  valve  segments  from  being  put  under  tension  at  exactly 
the  same  moment,  so  that  they  produce  separate  systolic  tones. 

In  many  other  cases  the  reduplication  or  splitting  of  the  first  tone, 
which  is  heard  only  over  the  great  vessels,  might  readily  be  assumed  to 
consist  of  the  normal  first  tone,  which  is  increased  by  the  tension  of  the 
closed  semilunar  valves,  plus  a  second  part  of  the  tone  which  is  produced 
during  the  expulsion  time  by  the  pulse  wave  in  the  aortic  or  pulmonary 
artery.  As  a  matter  of  fact,  there  is  no  reason  why  the  pulse  wave 
which  can  produce  a  tone  in  the  carotid  artery  should  not  produce  such 
a  tone  in  the  aorta.  Such  a  splitting  of  tone  does  not  occur  nor- 
mally, because  the  closure  time  is  so  short  that  the  tone  of  closure 
time  and  that  of  the  expulsion  time  are  merged  into  one.  Accord- 
ingly, the  reduplication  or  splitting  of  the  first  tone  as  heard  only 
over  the  great  vessels  would  depend  upon  a  prolongation  of  the 
closure  time,  and  thus  possess  some  clinical  significance.  This  expla- 
nation agrees  with  the  physiologic  reduplication  of  the  first  tone  heard 
over  the  great  vessels,  particularly  during  those  phases  of  respiration 
where  arterial  pressure  is  elevated  (according  to  p.  119) ;  that  is,  with 
slow  respiration,  during  inspiration,  with  rapid  respiration  during 
expiration. 

In  many  cases  the  reduplication  or  splitting  of  the  second  tone  is  also 
due  to  the  production  of  new  tones  and  not  merely  to  lack  of  coinci- 
dence. Circumstances  are  conceivable  where  marked  secondary  elevations 
(dicrotism)  due  to  elasticity  or  reflected  waves  of  the  aortic  pulse  may 
cause  a  supernumerary  second  tone.  Furthermore,  a  new  diastolic 
mitral  tone  may  produce  the  rhythm  of  reduplication  instead  of  a  three- 
time  rhythm  (see  p.  259). 

We  can  usually  recognize  when  splitting  or  reduplication  is  due  to 
an  actual  increase  in  the  number  of  tones  by  the  fact  that  the  splitting 
is  then  heard  most  distinctly  exactly  over  one  valve  and  not  at  some 
point  between.  The  writer  does  not  think  this  peculiarity  is  of  any 
special  diagnostic  value. 

^  To  prove  that  this  explanation  is  correct,  we  should  determine  whether  the  inspira- 
tory can  be  changed  to  an  expiratory  reduplication  in  healthy  individuals  breathing  very 
slowly ;  because  slow  respiration  produces  exactly  an  opposite  effect  upon  the  ventricular 
filling  from  rapid  respiration. 

17 


258  AUSCULTATION. 

Triple  Rhytlim  (|  Measure). — 1.  The  triple  rhythm  of  the  heart 
tones  in  mitral  stenosis  consists  of  three  approximately  equal  tones,  heard 
either  exclusively  or  most  plainly  at  the  apex  and  over  the  mitral  area. 
There  is  no  such  grouping  of  two  of  the  three  tones,  described  above  as 
reduplication  (splitting  or  doubling),  but  the  heart,  instead  of  beating  as 
normally,  in  f,  beats  in  |  time.  The  accent  ordinarily  falls  upon  the  sec- 
ond of  the  three  tones.^  With  this  rhythm  the  typical  murmur  of  mitral 
stenosis  may  or  may  not  be  audible.  If  inaudible,  it  may  be  brought  out  by 
simply  accelerating  the  cardiac  action,  and  we  then  find  that  the  murmur 
usurps  the  place  of  the  first  of  the  three  tones,  thus  proving  that  the  latter 
is  an  abnormal  presystolic  tone.  The  second  is  the  normal  systolic  tone 
and  corresponds  to  the  apex  beat ;  and  the  third  is  consequently  the  dias- 
tolic tone.  The  localization  of  the  extra  tone  (the  first  stroke  of  the  triple 
rhythm)  at  the  auscultation  area  of  the  mitral  valve  is  another  argu- 
ment for  its  origin  from  this  valve.  It  is  therefore  an  abnormal 
presystolic  tone.  The  thickened  mitral  valve  remains  tense  during 
ventricular  diastole,  and  so  the  auricular  contraction  plus  the  valvular 
tension  produces  the  tone.  The  adherent  mitral  valve  in  this  case  forms 
a  diaphragm  between  the  auricle  and  the  ventricle  during  diastole ;  and 
just  as  the  systolic  vibration  of  this  diaphragm  occasions  a  systolic 
tone,  so  does  a  presystolic  (diastolic)  tension  from  the  auricular  con- 
traction occasion  a  new  presystolic  tone.  This  sort  of  triple  rhythm  is 
readily  appreciated  m  typical  cases  by  the  presystolic  character  of  the 
first  tone ;  and  it  is  of  diagnostic  importance  in  recognizing  cases  of 
mitral  stenosis  not  accompanied  by  a  presystolic  murmur  (see  below). 
One  should,  however,  be  careful  not  to  confuse  triple  rhythm  with 
another  very  common  peculiarity  of  mitral  lesions — viz.,  reduplication 
of  the  second  tone,  due  to  the  imperfect  coincidence  of  the  second  aortic 
and  second  pulmonic.  The  rhythm  and  the  localization  over  the  mitral 
valve  are  quite  different  (see  p.  255)  and  especially  distinctive  of  the 
presystolic  tone. 

It  must,  however,  be  stated  that  the  diastolic  mitral  valve  tone  of  mitral  steno- 
sis is  not  always  presystolic,  for  it  may  appear  at  another  period  of  diastole,  namely, 
when  tension  of  the  mitral  valve  occurs  not  only  during  the  presystolic  contraction 
of  the  auricle,  hut  also  at  any  earlier  period  of  diastole,  from  the  recoil  of  the 
blood  at  the  adherent  mitral  valve.  In  such  cases  exactly  the  same  rhji:hm  results 
as  in  reduplication  of  the  second  tone  (p.  255  et  seq.  and  p.  257)  ;_and  the  sig- 
nificance then  can  be  determined  only  by  its  appearance  over  the  mitral  valve,  as 
contrasted  with  its  ordinary  appearance  over  the  base  or  at  the  apex. 

2.  Gallojy  rhythm  is  a  triple  rhythm  heard,  for  the  most  part,  over 
the  entire  heart ;  the  tones  follow^  at  apparently  equal  intervals,  and  the 
second  ordinarily  is  accentuated  at  the  apex  and  the  third  at  the  great 
vessels ;  thus  : 

Apex :  v_/    v_/    v_/       .  v^    v«/    <^>     tatilta  tatata 

Great  vessels :     \^    \^    \^         v^    n^^    v^     tatata  tatata 

This  rhythm  means  that  an  extra  tone  occurs  during  diastole — i.  e., 

1  At  the  mitral  area  \  /  /  /  tatata  tatiita 

at  the  apex.         j  w    v_/    v.^        ^    ^    ^  \  lubblub-dupp  lubblubdupp. 


AUSCULTATION  OF  THE  HEART.  259 

before  the  normal  first  tone.  We  can  ordinarily  distinguish  it  from  the 
presystolic  tone  of  mitral  stenosis,  because  it  is  generally  to  be  heard 
equally  plainly  all  over  the  heart. 

Its  explanation  is  not  yet  quite  certain.  We  have  no  physiologic 
grounds  for  believing  the  theory  that  it  is  due  to  the  fact  that  the 
contraction  of  the  ventricle  consists  of  two  strokes.  Potain  ^  for- 
merly held  that  the  auricular  contraction  made  the  ventricular  wall 
tense  and  so  produced  the  first  of  the  three  tones ;  and  Kriege 
and  Schmall's  ^  cardiographic  representations  supported  his  theory. 
Potain,  however,  has  since  ^  modified  his  explanation.  He  now 
considers  that  the  extra  tone  which  occurs  during  diastole,  or  before 
systole,  is  not  due  entirely  to  the  contraction  of  the  auricle  making 
the  heart- walls  tense,  but  also  to  a  sudden,  abnormal  passive  tension 
of  the  ventricular  wall  during  diastole,  which  tension  is  occasioned  in  the 
first  place  by  the  vis  a  tergo  of  the  entering  blood,  and  in  the  second 
place  by  the  auricular  contraction.  The  extra  tone  frequently  coincides 
with  presystole  ;  but  sometimes  it  approaches  more  nearly  the  preceding 
diastolic  tone  than  the  following  systolic  tone,  and  so  makes  the  rhythm 
quite  different.  In  addition  to  the  normal  systolic  shock  we  can  fre- 
quently feel  or  see  a  diastolic  or  presystolic  shock  of  the  anterior  heart- 
wall,  coinciding  with  the  extra  tone.  This  corresponds  to  the  Kriege- 
Schmall  cardiogram,  so  that  the  above  explanation  seems  quite  probable. 

Such  an  explanation  makes  gallop  rhythm  the  expression  of  an 
abnormally  stimulated  heart  activity,  which  produces  either  an  abnor- 
mally quick  diastolic  relaxation  and  a  consecutive  sudden  passive  tension 
of  the  ventricular  wall  from  the  entering  blood,  or  an  increased  con- 
traction of  the  auricle.  Conditions  which  apparently  are  directly 
opposed,  produce  a  gallop  rhythm — viz.,  cardiac  insufficiency,  which  is 
always  connected  with  an  irritability  of  the  heart ;  and  the  stimulated 
cardiac  action  of  health,  of  exophthalmic  goiter,  and  of  nephritis  with  high- 
tension  pulse.  Potain  distinguishes  between  a  gallop  of  the  right  and 
of  the  left  heart,  according  to  whether  the  rhythm  is  heard  more  plainly 
over  the  right  or  the  left  side. 

Gallop  rhythm,  then,  is  a  diastolic  phenomenon.  Potain's  "  systolic 
gallop  rhythm"  is  better  called  a  doubling  of  the  first  tqne  (p.  257).  It 
is  heard  over  the  great  arteries,  and  is  due  to  a  prolongation  of  the 
closure  time. 

PENDULUM  OR    FETAL  RHYTHM   OF  THE  HEART  TONES  (Embryocardia). 

By  this  is  understood  a  rhythm  in  which  the  pauses  between  the 
systolic  and  diastolic  equal  those  between  the  diastolic  and  the  systolic 
tones — i.  e.,  the  short  and  the  long  pauses  are  equalized.  Pendulum 
rhythm  has  been  principally  observed  with  increased  tension  in  the 
arterial  system  (nephritis).  Pawinski's*  experiments  seem  to  prove 
that  it  depends  upon  a  prolongation  of  the  systole,  and  essentially  of  its 

1  Union  med.,  1875,  Nov.  11  and  18;  187G,  Jan.  6  and  27;  Feb.  29,  Mar.  11. 

2  ZeitH.f.  klin.  Med.,  1891,  vol.  xviii.,  Parts  3  and  4.         ^  Sem.  mtd.,  1900,  p.  22. 
*  Deutsch.  Med.  Woch.,  1891,  No.  4. 


260  AUSCULTATION. 

closure  time,  due  in  turn  to  the  increased  arterial  pressure  the  ventricle 
has  to  overcome  before  it  can  open  the  semilunar  valves. 

Von  Huchard  designated  as  evibryocardia  a  characteristic  form  of  cardiac  action 
observed  in  severe  infectious  conditions  and  in  the  terminal  stages  of  heart  disease. 
On  account  of  the  great  rapidity  of  cardiac  action,  the  duration  of  both  pauses,  as 
well  as  the  resonating  character  of  both  tones,  appears  almost  entirely  equalized. 
Embryocardia  should  therefore  be  defined  as  tachycardia  plus  pendulum  rhythm. 
Stokes  described  the  same  phenomenon  some  time  ago  under  the  name  of  fetal- 
heart  tones.     Its  explanation  is  still  unknown. 

HEART  MURMURS. 

These  are  variable  sounds  heard  either  in  addition  to  the  tones  or 
sometimes  usurping  their  place.  They  are  nearly  always  due  to  some 
diseased  condition,  but  they  are  occasionally  heard  in  health. 

An  exact  distinction  between  tone  and  murmur  is  not  essential  here. 
Acoustically,  the  heart  tones  depend  as  much  as  the  murmurs  upon 
non-periodic  sound  vibrations  ;  so  that  it  is  not  correct  to  describe  tones 
as  consisting  of  regular,  and  murmurs  of  irregular,  sound  vibrations. 
An  approximate  periodicity  or  regularity  of  the  vibrations  in  these 
sounds,  and  thereby  an  approach  to  a  definite  pitch,  is  doubtless  far 
more  applicable  to  murmurs  than  to  tones — e.  (/.,  many  murmurs  are 
best  described  as  being  musical.  For  practical  diagnosis  the  distinc- 
tion between  tone  and  murmur  depends  chiefly  upon  the  method  of 
origin.  The  tones  of  the  heart  (and  of  the  vessels)  arise  from  a  single 
sudden  disturbance  of  eqnilil^rium  of  the  sound-producing  body  ;  the 
Tnurmurs,  on  the  contrary,  from  several  repeated  disturbances  of  equilib- 
rium. Any  evident  duration  in  the  tone  must  depend  upon  continued 
vibrations  of  the  part  due  to  its  inertia ;  in  the  murmur,  on  the  con- 
trary, upon  repeated  fresh  vibrations  due  to  new  applications  of  the 
moving  force.  Thus,  a  tone  may  be  compared  to  the  sound  produced 
by  striking  once  upon  a  drum;  and  a  murmur,  to  the  sound  produced 
as  long  as  one  blows  in  a  pipe.  Acoustically,  they  are  noises  in  either 
case,  though  they  may  approach  more  or  less  nearly  to  a  musical  tone 
or  resonance.  Miirmurs,  then,  can  be  differentiated  from  tones,  whether 
of  the  heart  or  of  the  vessels  (see  284  et  seq.),  essentially  by  their  pro- 
longation and  their  lengthened  resonance. 

Some  of  the  murmurs  heard  over  the  heart  originate  from  within, 
some  from  without ;  the  former  are  called  endocardial,  the  latter  j^ara- 

cardial. 

Endocardial  Murmurs. 

These  are  of  two  kinds  :  valvular  murmurs,  depending  upon  a  dis- 
turbance of  the  cardiac  valves,  and  accidental  murmurs,  having  no 
connection  with  a  disturbed  valve  function. 

Endocardicd  murmurs  are  more  or  less  prolonged  noises  (thus  con- 
trasting with  the  heart  tones,  which  are  brief  and  sound  sharply  cut). 
They  are  very  diverse  in  character,  generally  blowing  or  puffing,  some- 
times scraping,  musical,  even  singing  or  whistling.  The  heart  tones 
are    expressed    symbolically  by  the    metric  signs    1   and  — ^  and  the 


AUSCULTATION  OF  THE  HEART.  261 

endocardial  murmurs  by  the  crescendo  and  decrescendo  signs  <  and  >.  - 
Two  elementary  forms  of  murmurs  may  be  differentiated  : 

1.  >  Decrescendo  murmurs,  which  begin  sharply  and  gradually 
fade  away. 

2.  <   Crescendo   murmurs,  which  begin  gradually  and  end  sharply. 
Two  combined  forms  may  be  derived,  thus  : 

3.  <(|J>   Murmurs  Avhich  begin,  and  fade  away,  gradually. 

4.  \/   Murmurs  which  begin  and  end  sharply,  and  which  in  the 

middle  are  of  minimum  intensity. 

In  most  cases  the  endocardial  murmurs  are  audible  only  to  ausculta- 
tion ;  but  exceptionally  they  may  be  heard  at  a  distance,  or  even 
appreciated  by  the  patient  himself.  These  so-called  distance  murmurs 
have  generally  a  musical,  singing,  or  whistling  character. 

We  are  indebted  to  the  experiments  and  researches  of  Corrigan, 
Kiwisch,  Heynsius,  Thomas  Weber,  Chauveau,  Marey,  Thaun,  Nolet, 
and  others^  for  the  physical  explanation  of  the  peculiarities  of  endo- 
cardial murmurs  such  as  those  mentioned  above.  Normally,  the  blood 
flows  through  the  heart  chambers  without  noise,  so  that  a  murmur  must 
be  attributed  to  some  abnormality  of  the  blood-current  in  the  heart, 
as  the  following  experiment  illustrates  : 

If  we  have  a  glass  tube  (a-b  in  Fig.  103,  I.)  through  which  a  stream 
of  water  is  flowing,  no  murmur  can  be  heard  at  the  point  c  so  long  as 
the  current  is  moderate.  If,  now,  the  rapidity  of  the  current  is 
increased  by  supplying  more  water,  a  continuous  blowing  sound  can  be 
appreciated  at  c,  which  simulates  to  a  certain  extent  an  endocardial 
murmur.  Such  a  simple  experiment  explains  the  first  essential  for  the 
origin  of  endocardial  murmurs,  namely,  the  rapidity  of  the  current,  which, 
other  conditions  remaining  the  same,  naturally  depends  upon  the  hydraulic 
pressure  causing  the  stream. 

By  narrowing  or  widening  the  caliber  of  the  tube  at  a  certain  place 
(c  in  Fig.  103,  II.,  III.,  and  IV.)  we  possess  another  means  of  pro- 
ducing a  murmur  in  the  silent  current,  always  provided  the  rapidity  of 
the  stream  is  sufficient.  If  in  such  a  tube  the  murmur  is  not  heard, 
it  may  be  produced,  or  if  very  faint,  it  may  be  intensified  by  increasing 
the  rapidity  of  the  flow,  although  the  same  rapidity  in  the  straight  tube 
would  furnish  no  sound.  This,  then,  explains  the  second  essential  in  the 
formation  of  endocardial  murmurs — viz.,  alterations  in  the  caliber  of  the 
blood-channel. 

In  order  to  clear  up  these  fundamental  principles  let  us  assume,  as  is  pictured 
in  Fig.  103,  III.,  that  the  fluid  flows  from  a  narrower  into  a  wider  part  of  the  tube. 
Experimental  physics  teaches  us  that  under  such  circumstances  the  fluid  exerts  a 
certain  suction  jjower  upon  its  surroundings.  This,  in  our  supposed  case,  to  a 
certain  extent  narrows  the  widened  portion  of  the  more  or  less  elastic  tube.  Hence 
the  difference  in  the  lumen  is  lessened  ;  the  suction  ceases,  the  walls  of  the  tube 
bulge  again,  and  the  process  is  repeated  over  and  over  again  as  long  as  the  cur- 
rent flows.     Thus  the  current  occasions  lateral  vibrations  of  the  widened  part  of 

^  An  excellent  historical  presentation  of  our  knowledge  of  heart  murnmrs  is  found 
in  Rosenstein's  section  on  Heart  Diseases,  in  Ziemssen's  Handbuch  der  Hper.  Pathol,  n. 
Therapie,  vol.  vi. 


262 


AUSCULTATION. 


the  tube-wall ;  and,  secondarily,  of  the  narrower  part,  which  alternate  with  those 
of  the  widened  part  and  follow  the  same  rhythm.  Thomas  Weber  claims  that  the 
murmurs  arise  from  these  vibrations  of  the  tube-wall,  and  that  they  are  trans- 
mitted just  as  well  against  as  with  the  stream.  If  the  narrowing  is  sharply  local- 
ized, as  in  Fig.  103,  II.,  the  result  is  the  same.  And  even  as  in  Fig.  103,  IV., 
where  a  widened  tube  is  suddenly  and  permanently  narrowed,  the  origin  of  the 
vibrations  of  the  wall  are  exactly  the  same,  whether  the  current  is  in  the  direction 
of  the  lower  or  of  the  upper  arrow.  In  the  former,  suction  takes  place  as  in  III. 
In  the  latter,  the  fluid  streams  from  the  wide  into  the  narrow  tube,  and  the  action 
of  the  pressure  occasioned  by  the  narrowing  is  like  that  of  the  suction  in  III.  It 
is  easily  understood  that  a  sufficiently  rapid  current  will  produce  murmurs  even  in 
tubes  of  uniform  caliber,  as  in  I.  For  friction  is  always  to  be  found  in  the  exter- 
nal layers  of  streams,  and  so  the  layers  quiescent  against  the  wall  rubbed  upon  by 
the  more  active  middle-current  layers,  act  quite  like  an  infinite  number  of  micro- 
scopic stenoses.  Weber  has  proved  in  these  experiments  that  the  murmurs  over 
the  wider  part  of  the  tube  always  appear  stronger  than  over  the  narrow.  And 
this  is  easily  understood  when  we  remember  that,  according  to  Pascal's  law  (the 


a 


NOONOVJ 


vavO^O^O^OVOV3NO^--O^OV3  O 


3  ^O/^O/O^O/^  ^O/O 


It 


II. 


a 


III.  IV. 

Fig.  103.— The  origin  of  current  murmurs :  a,  b,  Current  of  water ;  c,  stethoscope. 

law  of  the  hydraulic  press),  the  vibrations  in  the  wall  causing  the  sound  increase 
in  proportion  to  the  size  of  the  surface  vibrating  between  fluid  and  wall.  This  is 
of  great  importance  in  the  explanation  of  the  relations  of  transmission  of  the  car- 
diac murmurs.  It  can  be  demonstrated  experimentally  only  upon  rubber  tubes, 
since  stiff"  tubes  (of  glass  or  metal)  transmit  the  sound  too  perfectly  and  too  far. 

The  following  experimental  facts  adduced  by  Weber  are  of  sufficient  pathologic 
interest  to  be  mentioned  : 

1.  Murmurs  arise  more  readily  if  the  walls  of  the  tube  are  thin  than  if  they 
are  thick. 

2.  If  the  inner  surface  of  the  tube  is  roughened,  friction  increases  and  mur- 
murs arise  more  readily,  requiring  a  less  rapid  current. 

3.  A  much  greater  rapidity  of  current  is  necessary  to  give  rise  to  murmurs  in 
glass  or  brass  than  in  yielding  or  distensible  tubes  (rubber  tubes,  intestines,  veins). 

4.  Quicksilver  causes  murmurs  more  readily  than  water,  water  more  readily 
than  milk,  milk  more  readily  than  blood  mixed  with  water,  heavy  fluids  more 
readily  than  light  fluids,  thin  fluids  more  readily  than  tenacious  fluids. 

5.  Sometimes  the  vibrations  of  the  tube  become  so  strong  that  they  can  be 
appreciated  not  only  by  the  ear  but  also  by  the  sense  of  touch.  They  feel  like 
sand  running  over  the  finger. 


AUSCULTATION  OF  THE  HEART.  .    263 

6.  With  a  certain  grade  of  rapidity  of  the  current  and  narrowing  of  the  tube  a 
finer,  more  singing  tone  (musical  murmur)  can  sometimes  be  heard. 

7.  Increased  or  diminished  tension  of  the  wall  (by  means  of  increased  j^ressure 
of  the  fluid)  has  little  influence  upon  the  murmur  so  long  as  the  rapidity  remains 
the  same. 

8.  If  we  gradually  narrow  a  tube  through  which  fluid  is  running,  a  murmur 
■will  appear  after  a  certain  degree  of  this  compression.  Increasing  the  compression 
will  increase  the  intensity  of  the  murmur  up  to  a  maximum,  then  diminish  it,  and 
finally  cause  it  to  disappear. 

The  diagrams  make  it  plain  that  under  the  conditions  which  occasion  current 
murmurs,  whirling  movements  of  the  fluid  arise  at  the  point  in  question.  These 
can  be  plainly  demonstrated  by  using  a  glass  tube  and  suspending  a  light,  soluble 
powder  (lycopodium)  in  the  flowing  liquid.  It  has  been  supposed  that  these 
whirling  movements  were  the  causes  of  the  current  murmur.  ^  But  such  a  supposi- 
tion is  only  partially  correct,  because  the  only  jDarts  which  produce  actual  sound 
must  be  in  permanent  vibration,  and  fluids  remain  in  permanent  vibration  only 
with  difficulty.  Moreover,  the  approximately  estimated  number  of  vibrations  of 
the  current  murmur  is  irreconcilable  with  the  possible  number  of  vibrations  of  the 
columns  of  fluid  in  question.  It  is,  however,  clear  that  the  whirling  movements 
are  an  integral  part  of  the  effect,  and  that  they  are  essential  to  the  origin  of  per- 
manent vibrations  of  the  tube-wall.  They  must  exist  together.  Thomas  Weber 
has  aptly  compared  the  part  of  the  whirling  movements  to  the  role  of  the  moving 
violin  bow,  the  part  of  the  vessel-wall  vibrations  to  the  role  of  the  sounding  string. 

Valvular  Murmurs. — Valvular  Murmurs  in  General ;  Organic 
and  Functional  Valvular  Murmurs. — To  explain  their  elementary 
relations,  it  is  better  for  the  moment  to  neglect  the  part  played  by  the 
current  rapidity. 

Valvular  murmurs  may  arise  at  any  valve  when  the  blood-current, 
either  during  systole  or  diastole,  flows  into  an  adjoining  chamber,  through 
a  narrow  orifice.  Such  a  result  may  happen  in  one  of  two  different 
ways  :  either  the  valves  do  not  open  completely,  forming  a  stenosis,  or 
they  do  not  close  completely,  and  so  allow  a  blood-stream  flowing  in  an 
abnormal  direction  to  escape  through  a  narrowed  opening,  thus  forming 
an  insuffioiency  or  regurgitation. 

Anatomically,  a  stenosis  is  caused  by  adhesion  of  the  individual 
segments  of  the  semilunar  or  of  the  auriculoveutricular  valves,  or  else 
by  a  shrinkage  of  the  orifice.  Insufficiency  of  the  valves  arises  from 
the  shrinkage  of  the  curtains  in  their  long  axes,  from  partial  destruction 
or  perforation  of  the  valves,  from  tearing  free  of  the  entire  curtain,  or 
from  the  deposition  of  irregular  new  growths,  which  mechanically  pre- 
vent a  perfect  closure  of  the  valves.  In  any  of  these  cases  we  speak 
of  an  organic  or  anatomic  valvular  lesion. 

Without  being  anatomically  diseased  a  valve  may,  however,  be 
incapable  of  closing  if  the  orifice  at  which  it  is  inserted  becomes  dilated. 
This  is  called  a  relative  insufficiency.  The  curtains  no  longer  suffice  to 
close  the  widened  orifice,  or  the  position  of  the  papillary  muscles  is  so 
distorted  by  the  ventricular  dilatation  that  the  valves  can  no  longer 
perfectly  close.  Widening  of  the  orifice  in  relative  insufficiency  of  the 
semilunar  valves — i.  e.,  dilation  of  the  walls  of  the  aorta  or  the  pul- 
monary artery — depends  upon  increased  blood-pressure,  upon  loss  of 
elasticity  of  their  walls  (arteriosclerosis),  or  upon  deposition  of  histo- 
^  Heynsius  is  the  chief  advocate  of  this  theory. 


264  AUSCULTATION. 

logic  elements  in  them  (inflammatory  swelling).  On  the  contrary, 
relative  insufficiency  of  the  auriculoventricular  valves,  for  the  most 
part,  dependent  upon  a  diastolic  distention  of  the  ventricle,  signifies  too 
great  an  influx  of  blood  from  the  veins,  or,  with  insufficient  cardiac 
power,  an  incomplete  emptying  of  the  ventricle.  An  innervation 
disturbance  of  the  papillary  muscles  (chorea)  may  occasion  relative 
insufficiency  of  the  auriculoventricular  valves.  If  such  relative  insuf- 
ficiencies are  not  permanent,  but  depend  upon  some  transitory  disturbance 
of  function  (transitory  dilation),  they  are  called  functional  insivfficiencies. 

The  blood-current  producing  the  murmur  in  a  valvular  stenosis  is 
directed  normally  ;  in  an  insufficiency,  abnormally — flowing  backward. 
So,  without  further  explanation,  it  is  apparent  that  a  murmur  of  stenosis 
is  heard  during  that  phase  of  cardiac  action  in  which  the  valves  are 
opened ;  an  insufficiency  murmur,  on  the  contrary,  during  that  phase  in 
which  the  valves  should  shut. 

Compare  here  the  following  schem'e : 

Systolic  murmurs  Diastolic  murmurs 

Insufficiencies /  of  mitral,  _  of  aorta. 


{: 

1.  of  pulmonary.  of  tricuspid. 


.  of  tricuspid.  of  pulmonary. 

Stenoses f  of  aorta,  of  miti-al. 


Valvular  lesions  are,  as  a  rule,  accompanied  by  murmurs  ;  yet  not 
rarely  decided  lesions,  which  perhaps  were  only  suspected  intra  vitam 
from  some  other  clinical  conditions,  are  found  post  mortem  in  hearts 
that  never  gave  a  murmur.  This  is  easily  understood  when  we  recall 
that  a  definite  minimum  of  current  rapidity  for  each  grade  of  flowing 
mass  is  essential  to  cause  a  murmur.  Mitral  stenosis,  e.  g.,  may  occur 
without  a  murmur,  because  the  diastolic  current  is, relatively  too  slow, 
since  diastole  lasts  much  longer  than  systole.  For  this  reason  a  val- 
vular lesion  must  be  considered  as  a  possibility  in  every  case  of  heart 
disease  whether  associated  with  a  murmur  or  not. 

Significance  of  the  Timbre  (Quality  of  the  Sound)  and  of  the 
Loudness  (Intensity)  of  the  Valvular  Murmur. — We  were  formerly 
inclined  to  attribute  a  definite  diagnostic  significance  to  the  timbre 
of  an  endocardial  murmur  and  to  draw  conclusions  from  it  as  to  the 
conditions  of  the  altered  valves.  It  has,  however,  been  proved  that 
all  conclusions  based  upon  the  rough,  blowing,  musical,  whistling  or 
singing  character  of  the  murmur  are  entirely  untrustworthy.  Such  a 
quality  varies  so  much  with  the  accidental  configuration  of  the  damaged 
valves  that  we  deem  it  of  very  little  importance.  Nevertheless,  the 
musical  or  scratching  character  of  a  heart  murmur  certainly  argues  against 
its  being  of  accidental  nature  (see  p.  274  et  seq.). 

Even  the  loudness  of  the  murmur  does  not  necessarily  correspond 
to  the  degree  of  a  valvular  lesion  as  some  physicians  are  still  inclined 
to  believe,  for,  as  the  experiments  with  the  tubes  prove  (see  p.  263, 
Law  8),  a  certain  rapidity  of  current  is  requisite  to  bring  out  a 
maximum  murmur  through  a  definite  narrowing.  If  the  narrowing 
of  the  tube  is  too  slight  the  murmur  is   weak  ;    if  the  narrowing  is 


AUSCULTATION  OF  THE  HEART.  265 

too  pronounced  the  murmur  is  still  weaker,  probably  on  account  of 
the  great  loss  in  energy.  In  every  valvular  lesion,  whether  insuf- 
ficiency or  stenosis,  as  the  defect  increases  the  murmurs  increase  in  inten- 
sity until  a  maximum  is  attained ;  then^  despite  further  increase  in  the 
valvular  defect,  the  murmur  diminishes  again.  Now,  it  is  not  possible 
in  a  given  case  to  determine  from  the  character  of  the  murmur  whether  the 
valve  lesion — i.  e.,  the  narrowed  channel — has  already  overstepped  or 
has  not  yet  reached  its  acoustic  maximum,  so  once  more  no  safe  infer- 
ence can  be  drawn  from  the  loudness  of  the  murmur.  Much  more 
trustworthy  conclusions  are  to  be  deduced  from  carefully  heeding  the 
various  cardiac  functions  and  from  other  methods  of  examination, 
particularly  the  estimation  of  the  size  of  the  heart. 

How  little  the  loudness  of  the  murmur  shows  the  severity  of  a 
valvular  lesion  is  proved  by  the  clinical  fact  that  cardiac  invalids  with 
exceptionally  loud  murraui's  may  live  for  years,  whereas  others,  with 
scarcely  audible  or  even  no  murmurs,  may  very  soon  succumb  to  their 
malady. 

Murmurs  vary  a  great  deal  in  the  same  patient,  depending  upon  the 
kind  of  cardiac  activity.  Even  a  very  brief  medical  experience  teaches 
that  the  patient's  condition  is  by  no  means  always  the  best  if  the  mur- 
mur is  scarcely  audible,  but  frequently  the  worst.  The  first  essential 
for  murmurs  mentioned  in  our  theoretic  discussion — viz.,  current 
rapidity — easily  explains  this  seeming  inconsistence.  If  the  patient's 
condition  is  good,  a  vigorous  current  is  flowing  through  the  diseased 
valve,  and  the  murmur  is  therefore  strong  and  loud.  If  by  paraly- 
sis of  the  cardiac  power  the  patient's  condition  is  impaired,  the  cur- 
rent which  causes  the  murmur  is  diminished,  the  murmur  weakens, 
and  finally  even  disappears.  This  sometimes  makes  the  diagnosis  of 
valvular  lesions  very  difficult,  especially  because  we  generally  examine 
patients  when  things  are  not  going  well  with  them.  We  must  there- 
fore often  withhold  our  opinion  until  our  treatment  has  improved  the 
patient's  condition  sufficiently  to  bring  out  the  murmurs  ;  or  we  may 
temporarily  increase  the  current  rapidity  and  so  bring  out  a  suspected 
murmur  by  causing  the  patient  to  execute  some  active  movement,  and 
so  augmenting  the  heart  action. 

The  influences  external  to  the  heart  which  modify  the  loudness  of 
the  valvular  murmiu^s  are  the  same  as  those  affecting  the  heart  tones 
(see  p.  250). 

We  should  always  auscultate  a  patient  in  different  positions,  par- 
ticularly standiug  and  lying  down.  This  is  especially  important  in  the 
determination  of  murmurs,  because  position  has  a  great  influence  upon 
their  character  and  intensity.  Frequently  a  certain  murmur  can  be 
heard  only  in  the  recumbent,  another  only  in  the  erect,  posture.  This 
cannot  always  be  satisfactorily  explained  by  the  fact  that  the  blood- 
current  and  the  blood-pressure  are  decidedly  influenced  by  posture. 
We  will  refer  under  the  individual  valvular  lesions  to  the  physical 
relations  which  apply  to  this  point. 

A  very,  loud   murmur  is  only   rarely   accidental ;  so  that  although 


266  AUSCULTATION. 

the  loudness  of  a  murmur  is  not  necessarily  a  measure  of  its  severity 
(p.  274  et  seq.),  still  it  is  an  argument  against  its  accidental  nature. 

The  Localization  of  Valvular  Murmurs  in  Simple  Valvular 
Lesions. — The  essential  requisite  for  an  exact  diagnosis  of  a  valvular 
lesion  consists  in  localizing  the  murmur — i.  e.,  in  recognizing  at  what 
valve  it  arises.  This  is  not  always  easy,  because  murmurs  are  heard 
not  only  where  they  arise,  but  by  transmission  elsewhere.  In  general 
the  same  rules  apply  to  the  localization  of  murmurs  as  to  the  localiza- 
tion of  tones  (p.  246  et  seq.) — l.  e.,  murmurs  of  the  mitral  should  be 
heard  at  the  apex  ;  of  the  tricuspid,  at  the  lower  end  of  the  sternum  ; 
of  the  pulmonary,  in  the  second  intercostal  space  to  the  left  of  the 
sternum ;  and  of  the  aortic  valve,  in  the  second  intercostal  space  to  the 
right  of  the  sternum. 

Exceptions  to  these  rules  are  so  numerous  that  some  explanation  seems 
necessary.  If  the  heart  chambers  at  either  side  of  a  narrowing  are  of 
unequal  size,  a  stronger  (louder)  murmur  arises  over  the  larger  than 
over  the  smaller  chamber  (see  Weber's  experiments,  p.  262).  If  the 
murmur  originates  at  some  distance  from  the  chest-wall,  it  may  be 
heard  more  plainly  at  a  spot  upon  the  thorax  quite  remote  from  the 
point  of  projection  of  its  place  of  origin.  This  depends  upon  its 
so-called  transmission  through  the  medium  of  the  blood-stream,  either 
with  or  against  the  current.  If  transmitted  in  the  direction  of  the 
stream,  the  murmur  is  louder  than  if  transmitted  against  the  current, 
just  as  "  the  wind  carries  the  sound." 

1.  Systolic  murmurs  arising  at  the  aortic  valve  are  ordinarily  heard 
loudest  at  the  aortic  area  (the  auscultation  spot  for  the  aortic  tones), 
because  here  the  aorta  lies  near  the  thorax-wall,  and  because  the  blood- 
current  causing  the  murmur  is  directed  to  that  side.  They  are  trans- 
mitted, however,  strongly  upward  to  the  carotids  ;  this  latter  fact  may 
be  utilized  in  doubtful  cases  in  order  to  distinguish  between  mitral 
insufficiency  and  aortic  stenosis.  Not  infrequently  systolic  aortic  mur- 
murs are  heard  plainly  over  the  left  ventricle  as  well — i.  e.,  at  the  apex. 
This  is  simple  enough  to  understand,  because  they  arise  also  in  the 
left  ventricle  (p.  262)'! 

2.  Ordinarily,  the  diastolic  murmur  of  aortic  insufficiency  (see  p.  328) 
is  not  heard  as  plainly  at  the  aortic  area  as  further  below,  nearer  the 
apex,  perhaps  most  frequently  at  the  middle  of  or  to  the  left  of  the 
lower  part  of  the  sternum.  The  reasons  are  :  first,  that  the  aortic  valves 
are  situated  deeply,  at  a  distance  from  the  aortic  area  (see  p.  248) ;  second, 
that  the  murmur  arises  principally  in  the  diastolic  dilated  left  ventricle 
(p.  262);  and  third,  that  the  current  causing  the  murmur  is  directed 
from  the  aorta  to  this  chamber.  The  murmur  of  aortic  insufficiency  is 
also  frequently  to  be  heard  over  the  neck  vessels. 

3.  The  systolic  murmur  of  mitral  insufficiency  (see  p.  321)  is  ordi- 
narily heard  best,  not  over  the  mitral  area,  but  at  tlie  auscultation  spot 
of  the  mitral  tone — if.  e.,  at  the  apex.  Despite  the  location  of  the  valve 
and  the  better  transmission  of  the  murmur  through  the  blood-current 
which  is  directed  upward,  the  upper  part  of  the  left  ventricle  is  so  com- 


AUSCULTATION  OF  THE  HEART.  267 

pletely  covered  by  the  right  ventricle  and  lung  that  the  murmur  is  heard 
plainest  at  the  apex.  Another  reason  is,  that  at  the  beginning  of  systole 
the  left  ventricle  is  much  larger  than  the  auricle,  and  so  a  louder  sound 
is  heard  over  the  ventricle  (/.  e.,  apex)  than  over  the  auricle.  There  are 
instances,  however,  where  the  systolic  mitral  murmur  is  best  heard  at 
the  base  of  the  heart,  in  the  vicinity  of  the  left  auricle,  to  the  left  of  the 
sternum.  Probably  this  occurs  chiefly  when  there  is  a  marked  dilatation 
of  the  left  auricle.  This  dilatation  is  responsible  for  the  fact  that  the  mur- 
mur arises  strongly  over  the  left  auricle  and  that  the  latter  chamber  is 
more  closely  applied  to  the  chest-wall,  the  lung  having  been  pushed 
aside,  which  naturally  facilitates  the  appreciation  of  the  murmur  over 
this  area.  Besides,  the  current  causing  the  murmur  is  directed  to  the 
region  of  the  left  auricle.  Marked  dilatation  of  the  left  ventricle  also 
pushes  the  maximum  point  of  the  systolic  murmur  from  the  heart  apex 
upward,  because  such  a  dilated  left  ventricle  crowds  the  right  ventricle 
-and  the  lung  and  applies  itself  more  completely  to  the  thorax. 

4.  In  mitral  stenosis  (see  p.  324)  the  direction  of  the  current  causing 
t;he  murmur  is  an  especial  reason  for  the  sharp  localization  of  the  dias- 
tolic murmur  of  this  valve  lesion  (even  more  than  the  mitral  tone, 
see  p.  248)  at  the  apex.  If  faint,  the  diastolic  murmur  of  mitral 
stenosis  can  very  often  be  heard  only  just  outside  the  apex.  A  real 
presystolic  mitral  murmur  is  heard  loudest  over  the  left  ventricle 
(p.  269  et  seq.)  for  the  same  reason,  and  even  more,  because  the  left 
auricle  during  presystole  is  small  and  the  left  ventricle  large.  But  a 
pure  diastolic  mitral  murmur  (p.  270)  is  frequently  heard  best  over 
the  auricle  because  it  arises  at  the  beginning  of  diastole,  when  the  left 
auricle  is  wide,  and  the  left  ventricle,  in  comparison,  is  still  narrow. 

5.  The  systolic  murmur  of  tricuspid  insufficiency  (p.  335  et  seq.),  in 
spite  of  the  direction  of  the  current  upward,  is  heard  most  distinctly  at 
the  tricuspid  area,  the  lower  end  of  the  sternum  or  somewhat  to  the 
right  of  it,  because  here  the  right  ventricle  as  well  as  the  right  auricle 
lies  near  the  thoracic  wall  (Fig.  74).  Other  systolic  murmurs,  except- 
ing perhaps  the  systolic  murmur  of  the  rare  pulmonary  stenosis,  are  not 
plainly  transmitted  to  this  spot. 

6.  The  diastolic  murmur  of  tricuspid  stenosis  (see  p.  337),  a  rare 
lesion,  has  its  maximum  intensity  at  the  tricuspid  area,  the  lower  end 
of  the  sternum,  because  the  current  from  the  affected  valve  above  is 
directed  toward  this  spot,  and  because  both  cavities,  right  auricle  and 
right  ventricle,  here  lie  close  to  the  thoracic  wall. 

7.  The  systolic  murmur  of  pulmonary  stenosis  (see  p.  340)  is  auscul- 
tated at  the  pulmonic  area,  the  second  left  intercostal  spaces  and  over  the 
right  ventricle. 

The  murmur  of  pulmonary  stenosis  is  frequently  heard  over  the  greater  part 
of  the  anterior  surface  of  the  heart,  because  the  right  ventricle  is  ordinarily  so 
dilated  in  this  lesion  that  it  occupies  most  of  this  area  ;  and  because  (p.  262)  the 
murmur  arises  not  only  at  the  stenotic  valve,  but  also  over  the  right  ventricle. 
This  is  a  point  which  should  be  carefully  heeded  to  prevent  confusion  in  diagnosis. 

The  pulmonary  stenotic  murmur  should  be  plainly  transmitted  into 


268  AUSCULTATION. 

the  interior  of  the  lung ;  it  should  also  be  heard  very  distinctly  beneath 
the  left  clavicle  (where  aortic  murmurs  are  only  faintly  transmitted),  or 
behind,  between  the  shoulder  blades,  and,  in  contrast  to  the  murmur  of 
aortic  stenosis,  it  is  either  not  transmitted  at  all  or  only  very  slightly 
into  the  neck  vessels. 

8.  The  diastolic  murmur  of  pulmonary  insufficiency  is  auscultated  at 
the  pulmonic  area.  Like  the  murmur  of  aortic  insufficiency,  it  can, 
however,  be  heard  more  plainly  over  the  lower  end  of  the  sternum, 
because  it  arises  essentially  in  the  right  ventricle  (p.  262),  and  because 
the  blood-stream  producing  the  murmur  is  directed  downward.  Unlike 
the  aortic  murmur,  it  is  not  transmitted  into  the  neck  vessels. 

Some  of  the  above  rules  do  not  apply  if  the  heart  is  pushed  from 
its  normal  position  to  any  extent.  This  must  happen  frequently,  because 
valvular  lesions  cause  marked  dilatations  and  alterations  of  individual 
heart  chambers. 

Exact  Time  Relations  of  the  Valvular  Murmurs  to  the  Heart 
Tones ;  Real  Diastolic  Murmurs,  and  Modified  Diastolic  or  Presys- 
tolic Murmurs ;  Prediastolic  Murmurs ;  Distinction  Between  the 
Systolic  Murmurs  Arising  Over  the  Arterial  Orifices  and  Those 
Over  the  Auriculoventricular  Orifices. — The  heart  tones  are  fre- 
quently heard,  as  well  as  murmurs,  both  over  the  intact  valves  and  over 
the  diseased  valves  which  give  rise  to  the  murmur.  In  the  first  place 
the  tones  may  be  transmitted  from  one  of  the  unaffected  valves ;  in  the 
second  place,  the  walls  of  the  heart  and  of  the  great  vessels  participate 
in  forming  the  tones  ;  and  in  the  third  place,  the  diseased  valve  is  hardly 
ever  destroyed,  and  so  its  tone  may  still  be  produced  (p.  252,/).  By 
listening  to  the  tone,  a  skilled  examiner  can  determine  the  phase  of  car- 
diac action  to  which  a  certain  murmur  belongs.  Everything  which 
occurs  between  the  beginning  of  the  systolic  tone  and  the  next  succeed- 
ing diastolic  tone  belongs  to  systole ;  and  everything  which  occurs 
between  the  diastolic  tone  and  the  next  systolic  tone  belongs  to  diastole. 
So  a  murmur,  though  very  close  to  the  systolic  tone  and  quite  remote 
from  the  diastolic  tone,  is  still  diastolic  so  long  as  it  occurs  before  the 
beginning  of  the  systolic  tone — e.  g.,  a  presystolic  murmur  is  really 
diastolic. 

The  murmurs  of  the  different  valvular  lesions,  together  wdth  their 
tones  in  their  proper  time  relations,  are  represented  in  the  following 
scheme  : 

MM  tasnfficienc,  I  |£->^  [/>^        ^^^ 


Aortic  stenosis  \  I     -"^.^  _/_  I    -^,,^^   /        tafta,  tafta. 


Tricuspid 

Aortic 
Pulmonary 

Mitral  stenosis  )    _^ — 1/  ^,---'^/ 

Tricuspid  "  J    ^^-J"        '"■^*^^^--^~         ^         ftata  ftdta. 


AUSCULTATION  OF  THE  HEART.  269 

The  vertical  lines  mark  the  beginning  of  systole.  This  scheme 
shows  us  that  the  acoustic  picture  of  a  valvular  lesion  is  a  very  varying 
one.  The  beginner  can  represent  the  tones  sufficiently  accurately  by  the 
syllables  "  ta-ta,"  the  murmurs  by  the  letter  "  f,"  as  in  the  scheme. 

Although  it  is  plain  that  each  pair  of  these  eight  valvular  lesions 
are  acoustically  related,  yet  there  is  less  confusion  than  one  might  sup- 
pose, because  the  murmur  of  every  lesion  has  a  definite  point  of  maxi- 
mum intensity  and  every  lesion  occasions  distinct  circulatory  disturbances. 
A  differentiation  is  thus  possible  in  almost  all  cases. 

Most  murmurs  are  represented  by  the  decrescendo  sign,  because  their 
intensity  is  greatest  at  the  beginning  of  the  phase  of  cardiac  action  to 
which  they  belong.  The  reason  is  that  the  blood-current  is  then  most 
rapid.  The  diastolic  murmurs  of  the  auriculoventricular  stenoses  are 
the  only  exceptions,  because  the  auricular  contraction  increases  the  cur- 
rent rapidity  and  they  are  represented  by  the  crescendo  sign. 

It  should  be  noted  that  an  actually  uniform  crescendo  may  occur  during  the 
progressive  contraction  of  the  auricle  and  the  concomitant  dilatation  of  the  ventricle. 
The  murmur  really  increases  during  the  course  of  the  auricular  systole  on  account 
of  the  increasing  difference  between  the  sectional  area  of  the  contracted  auriculo- 
ventricular oritice  and  that  of  the  ventricle.  (See  Weber's  Laws  of  Origin  of 
Murmurs,  p.  262.) 

Tricuspid  stenosis  is  so  rare  as  to  be  practically  neglected,  so  that 
a  presystolic  accentuation  at  the  end  of  the  murmur  is  practically  pathog- 
nomonic of  mitral  stenosis.  In  puzzling  cases  this  very  characteristic 
accentuation  at  the  end  of  tiie  murmur  sometimes  aids  in  distinguishing 
the  phases  of  cardiac  action.  Although  theoretically  it  is  not  a  uni- 
formly regulated  crescendo,  the  duration  of  the  whole  sound  is  so  short 
that  the  ear  receives  the  impression  that  it  is. 

L^         s-/<Cr'^  r~  Presystolic  accentuation  of  the  diastolic  murmur. 

1^         v>      <!n —  Pure  presystolic  murmur  (most  common). 

1/  ^v^,.^/.  Diastolic  murmur  accentuated  at  the  beginning  and  at  the  end  of 

P"         "^P^vf"  diastole. 

l£.         v_/*^      r^  Pure  diastolic  murmur  (least  common). 

The  pure  presystolic  murmur  is  still  more  common  in  mitral  stenosis. 
This  is  represented  by  a  short  crescendo  sign,  for  there  seems  to  be  an 
actual  pause  between  the  diastolic  tone  and  the  murmur.  Another 
modification  consists  of  an  accentuation  both  at  the  heginning  and  at  the 
end  of  the  murmur.  This  depends  on  the  fact  that  the  blood  flows  into 
the  empty  ventricle  with  greater  ra])idity  at  the  beginning  of  diastole 
than  during  its  middle  period,  when  the  difference  of  ]iressure  between 
the  auricle  and  ventricle  has  been  to  a  great  extent  equalized.     The  last 


270  A  USCULTA  TION. 

modification,  the  jpure  diastolic  murmur,  is  the  least  common.  The 
murmur  follows  the  diastolic  tone  directly  and  then  decreases  in  intensity 
without  any  subsequent  presystolic  accentuation.  These  four  varieties 
of  murmurs  due  to  auriculoventricular  stenosis  can  be  illustrated  by 
the  preceding  scheme. 

All  these  modifications  of  the  murmurs  obviously  depend  upon  the 
varying  relations  of  the  factors  which  influence  the  intensity  of  the 
murmur  at  each  moment — i.  e.,  upon  tiie  degree  of  the  stenosis  and  upon 
the  rapidity  of  the  blood-current.  Therefore  it  is  easily  understood  that 
in  one  and  the  same  case,  depending  upon  the  rapidity  of  the  cardiac 
action,  we  hear  one  modification  at  one  time  and  another  modification  at 
another  time.^ 

We  have  yet  to  mention  a  characteristic  sort  of  valvular  murmur, 
designated  as  a  prediastolic  murmur,  to  be  heard,  of  course,  during 
systole— not  in  the  beginning,  but  only  toward  its  end.  It  may  be 
expressed  symbolically  thus  ^    i  /    ^^ 

and  reproduced  by  the  sound  ''  ta-fta."  It  arises  at  the  auriculoventric- 
ular valves,  and  is  limited  to  the  end  of  systole,  probably  because  at 
the  beginning,  and  perhaps  even  during  the  greater  portion  of  systolic 
contraction,  the  valves  remain  closed,  and  only  relax  and  bend  toward 
the  auricle  when  the  intraventricular  pressure  has  reached  a  certaia 
height — i.  e.,  shortly  before  or  during  the  time  of  expulsion.  This  may 
be  due  to  an  incomplete  contact  of  the  curtains,  or  to  an  anomaly  in 
the  cordse  tendinse  or  papillary  muscles.  If  this  supposition  is  correct, 
a  prediastolic  murmur  would  argue  for  a  moderate  grade  of  auriculo- 
ventricular insufficiency,  which  would  be  diflFerentiated  from  the  ordinary 
insufficiency  by  the  fact  that  the  closure  time  is  in  part  or  entirely 
retained.  Ordinary  systolic  murmurs  may  be  either  accidental  or 
organic,  whereas  prediastolic  murmurs  are  always  pathognomonic  of 
real  auriculoventricular  insufficiency.  It  is,  however,  also  conceivable 
that  an  insufficiency  of  the  auriculoventricular  valve  produces  a  pre- 
diastolic murmur  because  the  origin  of  the  murmur  is  especially  favored 
by  the  decided  dilatation  of  the  auricle  at  the  end  of  ventricular  systole. 
(According  to  Thomas  Weber's  Fundamental  Laivs,  p.  262.) 

We  must  call  attention,  finally,  to  the  difference  first  noted  by  v.  Noorden 
between  systolic  murmurs  arising  at  the  greater  vessels  and  those  arising  at  the 

1  It  cannot  be  decided  absolutely  in  a  given  case  that  these  modifications  are  safe 
diagnostic  signs.  The  question  should  be  tested  at  autopsy,  in  order  to  determine  whether 
(supposing,  of  course,  a  normal  current  rapidity — ('.  e.,  a  compensated  case)  the  pure 
diastolic  murmui-s  correspond  to  the  slightest,  the  diastolic  murmui-s  with  the  presystolic 
accentuation,  to  the  moderate,  and  the  pure  presystolic  murmurs,  to  the  most  severe 
grades  of  stenosis.  Certainly  this  explanation  is  partially  correct,  since  it  is  plain  that 
with  a  moderate  stenosis  the  current  giving  rise  to  the  murmur  will  be  maximal  at  the 
beginning  of  diastole  and  at  its  end  (during  the  auricular  contraction)  ;  whereas,  with 
a  very  marked  stenosis,  it  requires  an  exceptionally  active  contraction  of  the  auricle  to 
force  a  sufficiently  rapid  current  into  the  ventricle"in  order  to  give  rise  to  a  murmur. 

Sometimes  in  one  and  the  same  case  a  pure  diastolic  murmur  is  heard  at  the  base 
of  the  heail,  whereas  at  the  apex  most  of  what  is  heard  is  the  presystolic  portion  (p.  267,, 
Law  4). 


AUSCULTATION  OF  THE  HEART.  271 

auriculoventricular  orifices.  With  a  moderate  degree  of  auriculoventricular  in- 
sufficiency the  systolic  murmur  begins  exactly  at  the  commencement  of  systole,  with 
the  first  tone,  because  the  insufficiency  deprives  the  ventricle  of  a  proper  closure 
time,  and  because  the  blood,  overcoming  the  low  auricular  pressure,  regurgitates, 
even  at  the  very  beginning  of  the  ventricular  contraction.  It  is  another  thing 
with  aortic  and  pulmonary  systolic  murmurs.  Here  the  murmur  appears  first  at 
the  beginning  of  the  expulsion  time — i.  e.,  after  the  closure  time  is  completed,  the 
intraventricular  pressure  overcomes  the  aortic  pressure.  This  causes  a  delay  of  the 
systolic  murmur  as  contrasted  with  the  first  tone  ;  and  though  slight,  a  skilled  ear 
can  frequently  appreciate  and  make  use  of  it  in  diagnosing  systolic  murmurs  of 
the  great  vessels  from  those  of  the  auriculoventricular  orifices.  The  distinction 
may  be  designated  symbolically  thus  : 

Mitral  and  tricuspid  insufficiency.  Aortic  and  pulmonary  stenosis. 

Only  very  close  attention  will  detect  this  distinction.  The  closure  time  between 
the  systolic  tone  and  the  murmur  is  so  short  (0.07  to  0.14  second,  according  to 
Martius,')  that  the  interval  cannot  be  detected  as  a  distinct  pause,  but  merely  gives 
an  impression  of  a  somewhat  less  close  connection  between  the  murmur  and  the 
tone. 

We  need  not  fear  confusion  with  a  prediastolic  murmur,  because  the  latter  is 
separated  from  the  systolic  tone  by  a  longer  pause,  which  is  very  plain  ;  and  because 
the  succeeding  diastolic  tone  follows  so  closely  that  it  seems  a  part  of  the  murmur. 

Combinations  of  Murmurs  from  Multiple  Valvular  Lesions. — The 

same  valve  is  frequently  both  narrowed  and  insufficient ;  hence  we  may 
meet  with  the  following  combinations  of  murmurs  and  tones  : 

Mitral  insufficiency  and  stenosis  f       ftafta  ftafta       '\l — J^  ^-^  I 

Tricuspid  insufficiency  and  stenosis  \  '  ' 

Aortic  insufficiency  and  stenosis  f       taftaf  taftaf  L>>  ^^     I 

Pulmonary  insufficiency  and  stenosis        (.  I    ^'^        -'^       I 

When  several  valves  are  affected  at  the  same  time,  the  murmurs,  if 
loud  enough,  may  be  transmitted  over  the  entire  heart — e.  g.,  with  a 
combination  of  mitral  and  aortic  insufficiency.  In  case  the  aortic  murmur 
is  transmitted  to  the  apex,  we  may  hear  the  following : 


Y>->   K>->   I 


taftaf  taftaf 


If  there  is  a  mitral  stenosis  in  addition,  we  shall  hear  at  the  apex  this 
modification  : 


<l^>->  <F>->  <1 


ftdftaf  ftaftaf 


Method  of  Localizing  Murmurs  in  Multiple  Valvular  Lesions ; 
Maximum  and  Minimum  Points. — If  several  valves  are  diseased,  and 
if  one  of  them  is  doubly  so — that  is,  with  a  stenosis  and  insufficiency — 
the  murmurs  will  be  transmitted  in  all  directions,  and  the  diagnostic 

'  Zeit.J.  klin.  Med.,  vol.xiii.,  1888. 


272 


AUSCULTATION. 


picture  will  become  so  complicated  that  it  may  be  very  diflScult  to 
determine  where  each  murmur  really  arises  and  where  each  one  is  to  be 
heard  merely  by  transmission.  If,  for  example,  a  systolic  murmur  is 
heard  at  two  orifices — e.  g.,  at  the  mitral  and  the  aortic — it  is  very  dif- 
ficult to  say  whether  the  murmur  at  the  aorta  depends  upon  an  aortic 
stenosis  or  is  merely  the  transmitted  mitral  murmur.  It  is  very  easy 
to  make  a  mistake  in  either  direction. 

The  best  way  to  solve  such  a  problem  is  to  first  represent  upon  a 
chest  chart,  as  in  Fig.  104,  the  two  murmurs,  the  tones  and  the  cardiac 
dulness,  and  then  to  decide,  after  very  careful  auscultation,  whether  any 
difiereuce  in  the  acoustic  quality  of  the  two  murmurs  can  be  detected. 

Should  the  two  murmurs  exhibit  a  slight  difference  in  quality — for 


example,  one  rough,  the  other  smooth  ;  one  musical  or  whistling,  the 
other  blowing — it  is  probable  that  each  murmur  has  a  separate  origin. 
But  one  must  be  somewhat  cautious  in  drawing  this  conclusion,  as 
the  quality  as  well  as  the  intensity  of  a  murmur  may,  of  course,  be 
slightly  altered  by  transmission. 

If  no  distinction  in  quality  can  be  distinguished,  a  careful  ausculta- 
tion will  usually  determine  that  the  murmur  is  heard  more  distinctly  or 
intensely  at  one  point  than  at  another.  Then  the  following  possibilities 
will  exist : 

1.  If  the  murmur  is  equally  intense  at  both  orifices,  it  is  probable 
that  a  separate  murmur  arises  at  each  spot,  because  transmission  gen- 
erally deprives  a  murmur  of  some  of  its  intensity.  Very  loud  murmurs 
might,  however,  be  heard  over  the  entire  heart  with  equal  intensity. 


AUSCULTATION  OF  THE  HEART. 


273 


2.  If  the  murmur  is  heard  at  the  two  orifices  with  unequal  intensity 
— e.  g.,  over  the  aortic  much  less  distinctly  than  over  the  mitral — the 
weaker  murmur  would  generally  be  transmitted.  This  is  not  necessarily 
so,  however,  as  a  faint  murmur  might  arise  from  the  aortic,  and  a  very 
loud  murmur  from  the  mitral.  To  clear  up  the  difficulty,  we  should  aus- 
cultate from  the  one  orifice  to  the  other  along  the  line  A  31,  Fig.  105,  I. 
If  the  murmur  A  is  merely  transmitted  from  Jf,  its  intensity  will 
steadily  increase  from  A  to  31  (represented  diagrammatically  by  a 
wedge-shaped  figure,  whose  breadth  at  each  spot  is  a  measure  of  the 
intensity  of  the  murmur).  But  if,  on  the  contrary,  in  auscultating  from 
A  to  31,  we  find  that  the  intensity  of  the  murmur  at  first  diminishes, 
reaches  a  minimum  somewhere  between  A  and  31,  then  increases  again 


III. 

Fig  105. — Diagram  of  the  relations  of  transmission  of  cardiac  murmurs :   Maximum  and 

minimum  points. 

up  to  a  second  maximum  at  3/ (Fig.  105,  II.),  so  that  there  are  two 
maximal  points,  then,  even  though  the  murmur  is  weaker  at  A  than  at 
31,  we  can  be  sure  that  there  are  two  different  murmurs. 

Supposing,  as  is  so  often  the  case,  that  the  systolic  murmur  can  be 
heard  not  only  at  A  and  31,  but  also  (Fig.  105,  ]li.  and  TV.)  at  Tand  P 
(tricuspid  and  pulmonary  areas),  the  question  arises  whether  at  these  four 
points  we  have  to  do  with  transmitted  or  original  murmurs.  Here  we  must 
again  carefully  heed  the  resonating  quality  and  then  auscultate  along  the 
lines  A  P  and  A  T,  3f  Tand  31  P.  The  relations  of  intensity  expressed 
in  Fig.  105,  III.  show  that  the  murmurs  P  and  T  are  merely  trans- 
mitted from  A  and  3f,  whereas  those  in  Fig.  105,  IV.  show  that  sepa- 
rate murmurs  arise  at  A,  31  and  T,  but  that  the  murmur  at  P  is  only 
transmitted. 

18 


274  AUSCULTATION. 

In  this  way  the  beginner  learns  to  orient  himself  upon  the  points 
of  origin  of  murmurs  in  complicated  valvular  lesions.  The  important 
point  is  merely  to  proceed  systematically.  If  systolic  and  diastolic 
murmurs  are  both  present,  first  analyze  the  diastolic,  not  heeding  the 
systolic,  and  later  proceed  in  the  same  way  with  the  systolic.  With 
diastolic  murmurs  the  problem  is  often  simplified  by  remembering  that 
modified  diastolic  murmurs — /.  e.,  presystolic  or  presystolic  accented 
murmurs — can  arise  only  at  the  auriculoventricular  valves.  Another 
almost  constant  law  is  that  aortic  murmurs,  especially  the  systolic 
variety,  are  strongly  transmitted  to  the  neck  vessels. 

We  hardly  need  mention  that  no  importance  should  be  attached  to  slight  dif- 
ferences of  intensity,  because  they  may  arise  from  causes  we  do  not  yet  comprehend. 
The  diagnosis  of  a  combination  of  an  aortic  and  a  mitral  murmur  which  occupy 
the  same  phase  of  heart  action  requires  especial  attention.  We  not  infrequently 
find  two  plainly  marked  maximal  points  with  an  intermediate  minimum,  as  in  Fig. 
105,  II.,  due  to  one  single  murmur  ;  because  murmurs  arising  from  the  left  heart 
are  best  transmitted  to  the  surface  wherever  the  left  heart  is  most  closely  approxi- 
mated to  the  thoracic  wall — viz.,  in  the  region  of  the  aorta  and  at  the  apex — whereas 
at  other  places  the  superimposed  right  ventricle  makes  the  appreciation  more  dif- 
ficult. If  a  murmur  is  musical  and  of  the  same  quality  and  pitch  both  at  A  and  M, 
this  explanation  is  pretty  safe.  The  resonating  quality  in  any  case  should  therefore 
be  closely  studied.  The  above-mentioned  ditficulties  render  it  practically  impos- 
sible for  auscultation  alone  to  differentiate  between  the  single  and  double  origin  of 
a  murmur  ;  hence,  all  the  other  relations  should  be  carefully  heeded. 

Other  Methods  of  Bxamination. — Variations  in  the  size  of 
the  heart  and  changes  in  the  circulation  are  quite  as  important  in  deter- 
mining a  valvular  lesion  as  is  the  existence  of  murmurs. 

So-called  Accidental  Heart  Murmurs. — Many  cardiac  mur- 
murs depend  upon  relative  or  functional  insufficiencies  of  the  valves, 
and  are  called  relative  or  functional  murmurs.  They  generally  depend 
upon  a  dilatatiou  of  the  valvular  ring  (p.  263  et  seq.).  To  all  intents 
and  purposes  we  can  consider  them  under  the  same  heading  as  organic 
murmurs,  and  whatever  we  have  said  thus  far  under  the  latter  head  will 
apply  to  these  functional  murmurs. 

Accidental  murmurs^  on  the  contrary,  are  entirely  independent  of 
the  valvular  mechanism,  and,  although  acoustically  they  cannot  be 
distinguished  from  the  murmurs  of  true  valvular  lesions,  at  autopsy  the 
valve  is  found  to  be  perfectly  normal. 

They  are  frequently  called  inorganic  or  functional  murmurs.  ' '  Functional ' ' 
seems  to  the  writer  as  incorrect  a  term  as  ' '  inorganic, ' '  because  real  valvular  mur- 
murs may  depend  upon  purely  functional  disturbance,  and  some  accidental  mur- 
murs have  an  anatomic  origin.  For  example,  anemia  is  certainly  an  anatomic 
disease.  Accidental  murmurs  have  also  been  described  as  "anemic."  This  is 
inaccurate,  because  all  accidental  murmurs  do  not  depend  upon  anemia,  nor  are  all 
anemic  murmurs  accidental  (relative  insufiiciency  occasioned  by  anemia,  p.  277). 
The  only  way  to  escape  this  confusion  is  to  distinguish  valvular  murmurs  sharply 
from  accidental  murmurs,  and  to  separate  relative  insufficiency  murmurs  from  acci- 
dental murmurs  and  to  classify  them  with  the  true  organic  murmurs. 

Although  the  real  origin  of  accidental  murmurs  still  remains 
unproved,  the  writer  will  attempt  to  state  his  own  views  upon  the  sub- 
ject in  what  follows  : 


AUSCULTATION  OF  THE  HEART.  275 

Accidental  murmurs  are,  with  few  exceptions,  systolic  in  time. 
They  are  not  at  all  uncommon  in  health,  and  are  then  heard  for  the 
most  part  either  at  the  apex  or  over  the  pulmonary  artery.  Autopsies 
furnish  negative  results,  so  that  we  have  no  pathologic  help  in  regard 
to  their  origin.  Acoustically,  they  are  not  essentially  different  from 
valvular  murmurs ;  therefore  we  assume  that  they,  too,  are  current 
murmurs  arising  in  conformity  with  the  laws  applied  to  valvular  defects. 
In  the  normal  heart  the  experimental  conditions  (p.  261  et  seq.)  essen- 
tial to  valvular  murmurs  are  surely  present,  and  it  is  certainly  more 
astonishing  that  ordinarily  the  blood  flows  through  the  heart  without 
murmur  than  that  murmurs  may  arise  in  perfectly  sound  individuals. 
Consider  the  irregularly  formed  inner  surface  of  the  ventricle,  the  chances 
for  friction  associated  with  this,  and  the  alteration  in  cross-section  in  the 
connecting  portion  between  the  ventricle  and  aorta  or  pulmonary  artery. 
Indeed,  it  is  almost  more  logical  to  attempt  to  explain  how  it  is  possible 
for  tones,  and  not  murmurs,  to  arise  over  the  normal  heart.  Perhaps 
it  is  because  the  normal  blood-current  is  not  rapid  enough  to  give  rise 
to  murmurs.  Accidental  murmurs  would  then  depend  upon  an  increased 
rapidity  of  the  blood.  The  latter,  in  so  far  as  it  concerns  systole, 
depends  apparently  upon  the  rapidity  with  which  the  ventricle  contracts 
and  upon  the  mass  of  blood  to  be  emptied — i.  e.,  upon  the  amount  of 
diastolic  filling  of  the  heart.  Stolnikow  ^  has  demonstrated  experi- 
mentally that  the  rapidity  of  the  blood-current  may  vary  a  great  deal. 
In  one  experiment  he  found  that  the  maximum  was  sixteen  and  one- 
half  times  greater  than  the  minimum  current. 

How  completely  the  ventricle  is  filled  during  diastole  appears  to 
be  of  especial  importance.  For  v.  Frey  and  Krehl  ^  found  in  their 
experiments  that  slowing  the  heart  action,  and  thereby  increasing  the 
diastolic  filling  of  the  heart  (vagus  irritation  or  suffocation),  only 
slightly  prolongs  the  duration  of  the  ventricular  contraction.  As  a 
direct  consequence,  the  pulse  is  slowed  and  the  current  rapidity  is 
increased.  But,  so  far  as  the  writer  knows,  no  direct  experiments 
show  that  the  current  rapidity  with  low  arterial  pressure — i.  e.,  with 
slight  resistance  to  systole — or  with  altered  innervation  of  the  heart  can 
be  considerably  accelerated  without  altering  the  frequency  of  the  beat 
or  the  diastolic  filling.     Nevertheless,  this  does  seem  probable. 

Accidental  murmurs  may  therefore  arise  if  the  diastolic  filling 
increases  while  the  expulsion  time  remains  constant,  or  if  the  ventricle 
contracts  more  rapidly  while  the  diastolic  filling  remains  constant.  The 
latter  possibility  seems  possible,  because  accidental  murmurs,  like  many 
valvular  murmurs,  sometimes  arise  Avhen  the  heart  action  has  been 
excited  or  mad^  rapid.  But  even  so,  this  does  not  explain  why  they 
are  ordinarily  to  be  heard  over  the  pulmonic  or  over  the  left  ventri- 
cle, and  very  rarely  over  tlie  aortic  or  over  tlie  right  ventricle,  unless 
it  is  on  account  of  the  varying  anatomic  configuration  of  the  right  and 
left  ventricles  and  of  the  conus  arteriosus. 

They  rarely  appear  during  diastole,  because  the  diastolic  current,  on 

1  Arch.  f.  Anal.  u.  Physiol.,  Physiologic  Part,  188G.  ^  Xbid,,  1890,  No.  47. 


276  AUSCULTATION. 

account  of  the  longer  duration  of  diastole  and  its  weaker  power,  is 
much  slower  than  the  systolic.  Besides,  the  diastolic  current  does  not 
encounter  any  such  alteration  in  the  cross-section  of  the  heart  as  does 
the  systolic  current  in  its  entrance  into  the  aorta  or  pulmonary  artery.^ 
Experience  with  mitral  stenosis  shows  that  the  conditions  in  the  interior 
of  the  heart  are  not  especially  favorable  for  the  formation  of  diastolic 
murmurs,  for  frequently  the  diastolic  murmur  can  be  heard  only  during 
the  presystolic  accentuation  of  the  auriculo ventricular  current  (p.  269). 
Again,  no  other  valvular  lesion  is  so  apt  to  run  its  course  without  a 
murmur  as  mitral  stenosis  (p.  264). 

Accidental  murmurs  appear  most  often  when  the  ventricle  contracts 
quickly ;  therefore  we  should  expect  them  most  frequently  in  strong 
people  with  good  blood-pressure,  and  yet  the  reverse  of  this  is  true. 
To  this  objection  the  writer  can  only  reply  that  rapid  contractions  of 
the  ventricle  are  in  no  way  to  be  identified  with  high  blood-pressure. 
Since  the  blood-pressure  furnishes  a  resistance  to  the  cardiac  contrac- 
tion, it  is,  ou  the  contrary,  probable  that  the  ventricle  would  contract 
more  rapidly  with  low  pressure  than  with  high.  Xo  special  researches, 
so  far  as  the  writer  knows,  have  been  made  upon  this  point.  To  claim 
that  because  high  blood-pressure  increases  the  friction  it  favors  murmur 
formation  is  the  same  as  saying  that  the  pressure,  in  so  far  as  it  does 
not  influence  the  rapidity  of  current,  has  little  or  no  effect  upon  mur- 
mur formation.  (See  the  experiments  of  Weber,  Heynsius,  Xolet,  and 
Thamm,  pp.  261-263.) 

The  question  now  comes  up  :  Are  we  justified  in  believing  that  gen- 
eral weakness,  fever,  and  anemia  favor  this  explanation  of  the  origin  of 
murmurs  ?  For  under  these  conditions  accidental  murmurs  are  certainly 
very  common.  In  so  far  as  general  weakness  is  combined  with  low'  blood- 
pressure,  its  effect  has  been  already  discussed.  In  fever  the  acceleration 
of  the  pulse  and  the  decreased  tension  of  the  arteries,  expressed  by  the 
sphygmogram,  would  make  the  supposition  of  a  rapid  expulsion  of  the 
blood  from  the  heart  probable.  Riiedi's  experiments,  the  so-called 
"  tachogram  "  of  the  fever  pulse,  also  add  some  weight.  In  regard  to 
anemia,  we  must  distinguish  between  the  acute  anemia  of  hemorrhage  and 
the  chronic  anemias  or  oligochromemias  ;  in  the  former  the  low  blood- 
pressure,  in  the  latter  the  diminished  cohesion  of  the  blood,  probably 
occasions  an  increased  flow  from  the  heart  by  lessening  the  resistance. 
Cohnheira  proved  that  artificial  hydremia  accelerates  the  blood-current, 
thus  explaining  the  "venous  hum"  of  cblorotics  (see  p.  285  et  seq.). 
In  chlorosis  and  other  oligochromemias  the  diminished  cohesion  of  the 
blood  may  also  favor  murmur  formation  (according  to  p.  262,  Law  4). 

The  hypothesis  advanced  by  many  authors,  that  accidental  murmurs 
depend  upon  an  abnormal  facility  of  vibration  of  the  valves  and  of  the 
arterial  walls,  seems  to  the  author  absolutely  inexplicable.  Whoever 
appreciates  the  fundamental  difference  between  the  much  prolonged 
acoustic  character  of  a  murmur  and  the  stroke-like  character  of  a  heart 

^The  difference  of  cross-section  between  the  veins  leading  to  the  heart  and  the 
auricle  is  much  less  than  that  between  the  distended  ventricle  and  its  etierent  arteries. 


AUSCULTATION  OF  THE  HEART.  277 

tone  will  probably  not  be  satisfied  with  the  supposition  that  the  tension 
of  even  a  relaxed  and  irregular  vibrating  membrane  can  produce  such 
a  blowing  murmur. 

Special  roughness  of  the  walls  through  which  the  blood-current 
passes  (p.  262,  Law  2),  independent  of  valvular  disturbances,  does  prob- 
ably play  a  certain  part  in  the  origin  of  accidental  murmurs,  as  in  athe- 
roma of  the  aorta  and  of  the  endocardium.  This  explanation  evidently 
cannot  apply  to  accidental  murmurs  in  general,  however,  because  acciden- 
tal murmurs  are  only  rarely  heard  loudest  over  the  aortic  orifice  ;  because 
the  pulmonary  artery  is  almost  never  atheromatous ;  and  because  cases 
presenting  accidental  murmurs  during  life  show  no  atheroma  post 
mortem.  In  certain  exceptional  cases,  so-called  accidental  murmurs 
are  nothing  more  than  vesicular  breathing  (p.  221). 

So  much  for  systolic  accidental  murmurs.  The  conditions  in  the 
heart  itself  are  very  unfavorable  for  producing  diastolic  accidental 
murmurs ;  but  in  rare  cases  a  diastolic  murmur  with  its  maximum 
over  the  aorta,  and  so  easily  confused  with  an  aortic  insufficiency 
murmur,  does  appear  without  being  dependent  upon  any  valvular 
lesion.  In  anemic  individuals  such  a  murmur  is  to  be  regarded  as 
the  diastolic  accented  portion  of  the  venous  hum  transmitted  from  the 
jugular  veins  to  the  adjoining  portions  of  the  innominate  veins  and  the 
vena  cava  superior  to  the  heart  (p.  285).  By  auscultating  from  the 
aorta  upward  to  the  jugular  vein,  one  can  generally  convince  one's  self 
that  the  diastolic  murmur,  heard  perhaps  loudest  over  the  aorta,  gradu- 
ally merges  above  into  the  rhythmic  diastolic  accentuation  of  a  con- 
tinuous venous  hum.  The  severest  cases  of  oligochromemias  (with 
15  to  25  per  cent,  hemoglobin)  sometimes  furnish  an  accidental  dias- 
tolic murmur  audible  all  over  the  precordia  and  not  connected  with 
a  venous  hum.  There  is  very  little  more  known  about  diastolic  acci- 
dental murmurs,  and  in  general,  when  diastolic,  a  murmur  is  nearly 
always  valvular. 

The  most  practical  points  for  distinguishing  accidental  from  valvular 
murmurs  may  now  be  profitably  reviewed.  If  nothing  points  to  a 
valvular  lesion,  a  systolic  murmur  may  be  rightly  considered  acci- 
dental. By  nothing  the  writer  means  no  preceding  etiologic  factor, 
such  as  inflammatory  rheumatism,  no  abnormality  of  the  pulse  or  of  the 
circulation,  no  abnormality  of  the  tone  intensity,  and  no  demonstrable 
dilatation  of  any  cardiac  chamber.  Anemia,  fever,  atheroma,  or  a 
venous  hum  favors  the  diagnosis  of  an  accidental  murmur.  Still,  not 
every  murmur  heard  over  an  anemic  individual's  heart  is  necessarily 
accidental ;  for  relative  insufficiencies  are  very  often  caused  by  anemic 
dilatation  of  the  heart,  and  can  be  distinguished  from  anatomic  valvular 
lesions  only  by  the  fact  that  they  diminish  or  disappear  with  the 
improvement  of  the  anemia.  They  are  limited  to  the  mitral  and 
tricuspid,  and  are  governed  by  the  same  diagnostic  rules  as  the  ana- 
tomic varieties.  (See  the  Special  Diagnosis  of  Mitral  and  Tricuspid 
Insufficiencies.)  Location  of  the  maximum  point  of  a  doubtful  sys- 
tolic murmur  over  the  pulmonic  valve  argues  in  favor  of  its  being 


278  AUSCULTATION. 

accidental.  The  accidental  murmurs  of  atheroma,  in  accordance  with 
the  anatomic  seat  of  the  atheroma,  are  preferably  localized  at  the  aortic 
orifice,  as  well  as  frequently  at  the  apex.  Though  signifying  no  valvular 
lesion,  they  are  really  of  serious  import,  because  they  depend  upon  ana- 
tomic changes  which  may  later  occasion  fatal  disturbances. 

Diastolic  accidental  murmurs  are  exceedingly  rare,  are  almost  always 
associated  with  a  venous  hum,  very  often  with  a  systolic  murmur,  and 
are  confined  to  serious  anemia  (oligochromemia). 

It  is  questionable  whether  accidental  murmurs  can  really  be  distin- 
guished by  any  acoustic  peculiarity  from  valvular  murmurs.  In  general 
they  are  not  as  loud  as  the  valvular  (see  p.  266)  ;  nevertheless,  we  do  hear 
very  loud  accidental  murmurs,  and,  conversely,  faint  valvular  murmurs, 
even  in  serious  lesions.  Similarly,  the  particular  quality  of  a  murmur, 
its  blowing,  scraping,  or  musical  nature,  is  not  distinctive,  although 
the  latter  two  characteristics  generally  depend  upon  some  abnormal 
configurations  of  the  cardiac  cavities  or  orifices  and  rarely  appear  with 
purely  accidental  murmurs.  The  prediastolic  character  of  a  systolic 
murmur  argues  with  certainty  against  its  being  accidental,  and  in  favor 
of  a  mild  insufficiency  of  the  auriculo ventricular  valve.  It  expresses 
merely  a  yielding  of  that  valve  during  the  maximum  of  systolic  ven- 
tricular pressure.  A  prediastolic  murmur  would  never  be  accidental 
(see  p.  270), 

Influence  of  Breathing  Upon  Endocardial  Murmurs. — Whether  valvular 
or  accidental,  endocardial  murmurs  are  influenced  by  the  phases  of  respiration  in 
numerous  ways.  On  the  one  hand,  the  extent  to  which  the  lung  overlaps  the  heart 
is  variable,  depending  upon  the  diflferent  phases  of  breathing  ;  on  the  other  hand, 
the  breathing  favors  or  hinders  the  current  of  blood  through  the  heart. 

So  far  as  the  overlapping  of  the  lung  is  concerned,  inspiration  always 
weakens  a  murmur,  because  the  heart  is  then  more  perfectly  covered  by  the 
lung  ;  expiration,  on  the  contrary,  intensifies  it.  The  eflFect  of  breathing  upon 
the  blood-current  is  more  complicated  (see  p.  116  et  seq.).  The  entrance  of 
blood  to,  and  the  exit  from,  the  right  heart  is  always  favored  by  inspiration.  In 
the  left  heart  it  depends  upon  the  rapidity  of  breathing.  During  rapid  breath- 
ing the  entrance  to,  and  the  exit  from,  the  left  heart,  in  consequence  of  the 
increased  capacity  of  the  pulmonary  vessels  and  of  the  retention  of  more  blood  in 
the  lungs,  is  hindered  by  inspiration.  With  slow,  deep  respiration,  however,  this 
influence  can  be  noted  only  during  the  first  half  of  inspiration,  because  the  dilata- 
tion of  the  pulmonary  vessels  diminishes  the  resistance  in  the  pulmonary  channels, 
and  so  must  favor  the  passage  of  blood  through  to  the  left  heart.  Expiration  works 
exactly  in  the  opposite  way.  It  retards  the  blood- current  through  the  right  heart 
somewhat,  because  it  diminishes  the  negativity  of  the  intrathoracic  pressure.  Yet 
this  influence  is  insignificant  so  long  as  expiration  is  merely  passive.  For  the  left 
heart  the  effect  of  expiration  depends  upon  whether  it  is  quick  or  slow.  With 
slow  breathing  the  first  part  of  expiration  aids  the  flow  by  compressing  the  pul- 
monary vessels,  while  the  second  part  hinders  the  filling  of  the  left  heart  by 
increasing  the  resistance  in  the  pulmonary  circulation.  With  quick  breathing, 
on  the  contrary,  only  the  first  eflPect  of  expiration  is  felt,  and  the  filling  of  the 
left  heart  is  improved.  This  influence  is  sometimes  very  plainly  observed  in  val- 
vular lesions,  since  any  increased  current  through  a  cardiac  orifice  necessarily  in- 
tensifies a  murmur  arising  there.  Very  important  points  for  differentiating  right- 
and  left-sided  valvular  lesions  will  sometimes  be  ftirnished  by  carefully  heeding 
these  facts  about  the  influence  of  quick  breathing.  It  may  be  further  mentioned 
that  the  Valsalva  experiment  (see  p.  280)  directly  dimiiushes  the  endocardial  mur- 


AUSCULTATION  OF  THE  HEART.  279 

murs  of  the  right  heart  by  inhibiting  the  venous  current.  It  also  diminishes  the 
murmurs  of  the  left  only  after  an  initial  but  transitory  increase.  This  brief  inten- 
sification is  due  to  the  pressure  suddenly  exerted  upon  the  pulmonary  vessels. 

Paracardial  Murmurs. 

Under  this  title  are  included  all  murmurs  synchronous  with  the  heart 
action  which  depend  upon  changes  outside  of  the  heart  chamber — i.  e., 
in  the  pericardium  or  its  immediate  neighborhood.  They  include  (1) 
the  pericardial  friction  rub  ;  (2)  the  pleuropericardial  rub  ;  (3)  the  pre- 
cordial emphysematous  murmur  ;  (4)  the  pericardial  splashing. 

Pericardial  Rub. — Analogous  to  the  pleural,  the  pericardial  rub 
arises  from  the  rubbing  of  the  two  pericardial  surfaces  when  roughened 
by  the  deposition  of  inflammatory  fibrinous  or  connective  tissue,  by  tuber- 
cles, by  tumors,  or  by  abnormal  dryness  (in  cholera).  Pericardial  rubs 
present  exactly  the  same  acoustic  varieties  as  pleural  rubs — e.  g.,  they  are 
sometimes  finely  creaking,  sometimes  crackling,  sometimes  scratching. 
Fine  pericardial  friction  rubs,  caused  by  an  exceptionally  slight  roughness 
of  the  pericardium,  are  sometimes  confused  with  endocardial  murmurs. 
To  make  a  diagnosis  in  such  cases  (as  well  as  conversely  in  exceptionally 
rough  endocardial  murmurs),  it  is  very  essential  to  pay  close  attention  to 
the  phases  of  cardiac  action.  Endocardial  murmurs  conform  most  accu- 
rately to  the  phases  of  cardiac  actiou,  coinciding  with  either  the  systolic 
or  diastolic  tone ;  pericardial  murmurs,  on  the  contrary,  occur  halfway 
between  the  tones,  overstep  the  boundary  between  systole  and  diastole, 
or  even  quickly  change  phases,  which  endocardial  murmurs  never  do. 
Sometimes  pericardial  murmurs  are  to  be  heard  as  a  continuous  scratch- 
ing, which  is  merely  intensified  during  the  phases  of  cardiac  activity. 
All  this  is  perfectly  comprehensible  when  we  consider  that  the  point 
of  time  during  which  a  pericardial  murmur  is  to  be  heard  depends  much 
less  upon  the  phase  of  the  heart  action  than  upon  the  chance  position 
of  a  roughness,  which  very  frequently  alters  its  form  and  extent.  In 
explaining  why  the  systolic  part  of  the  pericardial  murmur  does  not 
exactly  tally  with  the  beginning  of  systole,  Geigel  noted  that  the  great- 
est systolic  excursion  of  the  surface  of  the  heart  and,  of  course,  of  its 
pericardium  does  not  occur  during  the  closure,  but  during  the  expulsion 
time  of  systole,  and,  the  writer  believes,  even  at  the  termination  of  the 
latter  period. 

We  make  use  of  the  sign  aWW  to  describe  and  picture  symbolically 
the  pericardial  murmurs.  The  height  of  the  teeth  expresses  the  intensity 
of  the  murmur  at  a  given  moment.  The  following  diagrams  exhibit 
different  types  of  pericardial  murmurs  (see  also  p.  268)  : 

Ki/     Pericardial  rub  in  the  middle  of  systole  and  in  the 
aAa      AaA  middle  of  diastole. 

l/_  1/      Pericardial  rub  systolic  in  time  but  also  prolonged  into 

*    A/WvAAfA     '  diastole. 

1^       w         I—   Continuous  scraping  pericardial  rub,  intensified  in  the 
wwvvaAVvwMi<a/VWaa«/        middle  of  systole  and  in  the  middle  of  diastole. 


280  AUSCULTATION. 

Though  pericardial  murmurs  may  arise  from  the  entire  pericardium, 
the  rubbing  of  the  anterior  surface  of  the  heart  is  all  that  is  usually- 
heard,  and  more  particularly  of  that  portion  uncovered  by  the  lung  or 
overlapped  merely  by  a  thin  pulmonary  covering.  These  murmurs  are 
therefore  heard  most  distinctly  over  the  area  of  superficial  cardiac  dul- 
ness  and  over  the  sternum,  and  they  may  frequently  be  felt  there. 

Pericardial  rubs  depend  in  most  cases  upon  inflammatory  deposits. 
They  may  come  quickly,  change  their  character  quickly,  and  disappear 
quickly.  Their  disappearance  may  depend  (a)  upon  the  retrogression 
of  the  inflammation,  (6)  upon  the  formation  of  adhesions,  or  (c)  upon 
the  collection  of  a  fluid  exudate,  which  separates  the  pericardial  layers 
from  each  other.  A  pericardial  rub  may,  however,  persist  despite  the 
presence  of  an  effusion,  for  the  fluid  may  be  mostly  collected  in  the 
lateral  parts  of  the  pericardium  and  against  the  great  vessels,  and  leave 
enough  of  the  rough  visceral  layer  exposed  anteriorly  to  still  grate  upon 
the  parietal  pericardium.  Again,  even  with  large  exudations,  friction 
rubs  may  arise  from  the  inferior  pericardium  if  the  weight  of  the 
heart  has  displaced  the  fluid  and  brought  the  two  roughened  layers  in 
contact  inferiorly. 

The  most  trustworthy  signs  to  distinguish  pericardial  rubs  from  endocardial 
murmurs  are  :  the  acoustic  peculiarity  of  the  former,  its  decided  variability,  and 
its  lack  of  correspondence  to  the  cardiac  phases.  Pressure  of  the  stethoscope 
intensifies  a  rub  but  does  not  affect  a  murmur.  Bending  forward  from  a  sitting 
posture  in  bed  will  accentuate  a  pericardial  friction  rub,  whereas  a  more  decided 
change  of  position  is  required  to  affect  an  endocardial  murmur.  Pericardial  mur- 
murs can  be  influenced  by  the  breathing  in  as  many  ways  as  endocardial.  Valsalva's 
experiment  weakens  or  abolishes  a  valvular  murmur,  while  it  often  intensifies  a 
pericardial  rub.  This  experiment  is  practised  in  the  following  way  :  After  a  deep 
inspiration  the  patient  attempts  an  expiration  with  a  closed  glottis,  and  at  the  same 
time  exerts  strong  abdominal  pressure.  This  maneuver  raises  the  intrathoracic 
pressure  and  prevents  the  entrance  of  the  blood  into  the  heart  from  the  great  veins. 
The  test  is  not  suitable  for  very  sick  people.  Faint  pericardial  murmurs  are  not 
transmitted  as  well  as  are  endocardial  of  the  same  intensity,  because  the  latter 
are  not  only  favored  by  the  blood-current,  but  arise  from  each  of  the  heart 
chambers  bounding  the  lesion.  Loud  pericardial  murmurs  can,  however,  be  heard 
over  the  entire  precordia.  Finally,  all  the  other  signs  of  pericarditis,  on  the  one 
hand,  and  of  endocarditis  on  the  other,  should  in  doubtful  cases  be  utilized  to 
clear  up  the  diagnosis. 

Pleuropericardial  Rub  (Extrapericardial ;  Pseudopericardial). — Peri- 
cardial may  be  confused  with  pleural  rubs  when  the  latter  arise  near  the  heart, 
because  friction  of  pleura  costalis  or  pulmonalis,  on  the  one  hand,  and  pleura  peri- 
cardiaca  on  the  other,  may  be  brought  out  by  movements  of  the  heart  as  Avell  as  of 
the  lung.  They  are  called  pleuropericardial,  extrapericardial,  or  pseudopericardial 
rubs.  One  of  the  most  essential  points  in  differentiation  is  that  the  maximum 
intensity  of  true  pericardial  rubs  is  in  the  region  of  superficial  cardiac  dulness  and 
over  the  sternum,  whereas  the  extrapericardial  are  best  heard  outside  this  area  ; 
again,  the  latter  possess  distinct  cardiac  and  respiratory  phases,  while  the  former 
are  less  influenced  by  the  respiration  than  by  the  heart  action.  If  the  deposit  is 
quite  circumscribed,  holding  the  breath  in  extreme  inspiration  or  expiration  will 
decrease  or  abolish  pleuropericardial  rubs,  but  not  true  pericardial  rubs,  with  any 
degree  of  ease.  If  this  diminution  or  disappearance  occurs  at  the  end  of  inspira- 
tion, the  roughness  will  be  situated  upon  the  pleura  pericardiaca,  and  so  sei^arated 
by  the  inflated  lung  edge  from  the  corresponding  roughness  upon  the  pleura  costalis 
(Fig.  106,  a);  whereas,  if  at  the  end  of  expiration,  the  roughness  will  be  upon  the 


AUSCULTATION  OF  THE  HEART.  281 

pleura  pericardiaca  and  pleura  pulmonalis,  which  are  then  no  longer  in  contact 
(Fig.  106,  b).  True  pericardial  rubs  are,  on  the  contrary,  usually  intensified  by 
holding  the  breath  in  extreme  inspiration,  especially  if  abdominal  pressure  is  exerted 
(Valsalva's  experiment,  p.  280);  but  this  is,  of  course,  better  ap^jreciated  over  the 
superficial  cardiac  dulness,  where  the  distended  lung  edge  does  not  overlap  the 
heart. 

Precordial  Emphysematous  Murmur. — If  from  the  rupture  of  alveoli,  air 
escapes  along  the  interstitial  pulmonary  tissue  to  the  hilus,  and  from  there  to  the 
connective  tissue  of  the  anterior  mediastinum,  the  superficial  cardiac  dulness  will 
be  diminished,  the  heart  tones  weakened,  and  resonating,  crepitating,  or  metallic 
noises  simulating  rales  may  appear  over  the  heart.  They  will  be  synchronous  with 
the  cardiac  action,  not  with  the  respiration,  and  thus  can  be  distinguished  from 
the  rales  of  interstitial  emphysema  (p.  240).  From  the  cardiac  rales  which  may 
be  heard  over  consolidations  and  cavities  in  the  neighborhood  of  the  heart,  they 
can  be  differentiated  by  paying  attention  to  the  relations  of  the  cardiac  dulness,  of 
the  heart  tones,  and  of  the  respiratory  murmur,  by  the  demonstration  of  signs  of  a 


Lung. 


Heart  covered  with  vis-  ^  -        \     n    ^  ^    ^ 

ceral  pericardium.      v».  \     Costal  pleura. 

Pericardial  pleura. 


I  Pleural  deposits. 


Lung. 
[  Pleural  deposits. 


Costal  pleura. 

Pericardial  pleural. 

Fig.  106.— Two  possibilities  in  pleuropericardial  rubs.    Diagrammatic  horizontal  section  of 

the  chest. 

pulmonary  emphysema  or  of  an  emphysema  of  the  skin,  and  by  the  considera- 
tion of  the  accompanying  appearances  and  the  history. 

Pericardial  Splashing^. — If  the  pericardium  contains  both  air  and  fluid,  a 
characteristic  splashing  noise  arises  synchronously  with  and  in  consequence  of  the 
heart  action.  It  will  resemble  what  we  hear  by  shaking  a  patient  with  pneumo- 
thorax, and  sometimes  will  be  metallic.  The  heart  tones  will  then  be  diminished 
or,  by  the  resonance,  sometimes  increased  (pp.  250  and  257),  and  in  the  latter  event 
will  present  a  metallic  character.  The  cardiac  dulness  disappears  in  the  recumbent 
posture,  whereas  in  the  sitting  position  the  fluid  pushes  the  deeper  portion  of  the 
heart  forward  and  occasions  dulness.  The  heart  action  may  produce  similar 
splashing  when  there  is  a  distended  stomach,  large  cavities,  or  a  pyopneumo- 
thorax, so  that  we  must  note  the  spots  where  the  murmur  is  most  intensely  heard, 
the  severe  signs  of  pericarditis  or  pericardial  perforation,  the  relations  of  the  car- 
diac dulness,  the  exact  conditions  of  the  lungs,  and  the  modifications,  if  any, 
produced  by  emptying  and  filling  the  stomach. 


282  A  USCUL  TA  TION. 

AUSCULTATION    OF  THE  VESSELS. 

Both  tones  and  murmurs  can  be  heard  over  the  vessels  as  vi^ell  as 
over  the  heart.  (See  pp.  260  and  261  et  seq.  and  p.  245  et  seq.  in  regard 
to  the  definition  of  tones  and  murmurs  and  the  discussion  of  their  origin.) 
Some  of  them  are  transmitted  from  the  heart.  The  stethoscope  is  always 
used  to  auscultate  the  vessels,  and  care  should  be  taken  to  avoid  any 
pressure. 

AUSCULTATION  OF   THE  ARTERIES. 

The  carotid  is  auscultated  at  the  angle  of  the  jaw  or  at  the  inner  edge 
of  the  sternocleidomastoid ;  the  subclavian,  above  the  clavicle,  between 
it  and  the  sternocleidomastoid,  or  below  the  clavicle,  in  the  so-called 
"  Mohreuheim's  groove,"  between  the  pectoralis  major  and  the  deltoid ; 
the  brachial,  at  the  inner  edge  of  the  biceps,  or  at  the  bend  of  the 
elbow  with  a  slightly  bowed  arm ;  the  radial,  at  the  place  where  one 
ordinarily  feels  the  pulse ;  the  crural,  just  below  Poupart's  ligament. 

NORMAL  CONDITIONS. 

Two  tones  are  heard  normally  over  the  carotid  and  subclavian — a  systolic,  from, 
the  systolic  tension  of  the  vessel-walls,  and  a  diastolic,  transmitted  from  the  aortic 
valves.  Over  the  crural  and  over  the  abdominal  aorta  we  normally  hear  either 
nothing  at  all  or  a  systolic  tone.     The  small  arteries  are  normally  toneless. 

A  so-called  "pressure  murmur"  can  be  produced  by  applying  a  stethoscope 
with  some  force  upon,  the  larger  and  even  upon  the  smaller  arteries,  such  as  the 
brachial.  This  is  frequently  a  very  loud,  vibrating,  systolic  murmur,  and  is  due  to 
the  artificial  stenosis  of  the  artery.  (See  Auscultation  of  the  Heart,  p.  261. )  If  strong 
enough  pressure  is  applied  to  occlude  the  lumen  of  the  artery,  a  systolic  "pressure 
tone  "  is  produced.  Pressure  tones  and  pressure  murmurs  are  perfectly  physiologic, 
so  that,  to  bring  out  pathologic  tones  or  murmurs,  with  the  exception  of  Duroziez's 
double  murmur,  we  should  never  employ  pressure  of  the  stethoscope  in  auscul- 
tating the  vessels.  A  systolic  murmur  is  sometimes  heard  over  the  skull  of  children 
from  the  third  month  to  the  sixth  year,  perhaps  best  over  the  vertex ;  it  proba,bly 
arises  in  the  internal  carotid — exactly  how  we  do  not  know — is  normal  and  with- 
out diagnostic  importance.      [Fisher  called  attention  to  it  in  rickets. — Ed.] 

PATHOLOGIC    CONDITIONS. 

The  diastolic  and  especially  the  systolic  murmurs  of  aortic  lesions  are  readily 
transmitted  to  the  vessels  of  the  neck.  When  the  second  aortic  tone  disappears 
in  aortic  insufficiency,  ordinarily  but  one  systolic  tone  can  be  heard  over  the  neck 
vessels. 

A  systolic  tone  may  be  appreciated  even  over  toneless  arteries  with  a  pulsus 
celer  of  fever  or  of  aortic  insufficiency  ;  and  with  the  latter  a  tone  may  be  appre- 
ciated over  very  small  arteries — e.  g.,  the  radial,  dorsalis  pedis. 

A  crural  double  tone  is  occasionally  audible  in  aortic  insufficiency  with  an  ex- 
quisite pulsus  celer  ;  then  both  the  systolic  tension  and  the  diastolic  relaxation  of 
the  arteries  give  rise  to  a  plain  tone.  This  same  phenomenon  hap  been  noted, 
though  very  rarely,  in  chlorosis,  pregnancy,  and  chronic  lead-poisoning. 

The  so-called  Duroziez's  double  murmur  is  more  common  in  aortic  insufficiency 
than  the  crural  double  tone.  If  the  pressure  of  the  stethoscope  over  the  crural  or 
brachial  artery  is  gradually  increased,  the  following  series  of  sounds  can  be  heard  : 
without  pressure  the  single  or  double  arterial  tone ;  with  somewhat  stronger  press- 
ure the  normal  systolic  pressure  murmur  ;  with  a  farther  very  carefully  adjusted 
amount  of  pressure  the  systolic  murmur,  followed  by  a  second,  generally  much 


AUSCULTATION  OF  THE  VESSELS.  283 

fainter,  diastolic  murmur  ;  finally,  ^dth  still  more  pressure,  a  single  or  double 
tone  again.  This  second  diastolic  murmur  is  caused  by  the  diastolic  reflux  of 
blood  through  the  artificial  stenosis  of  the  crural.  Aortic  aneurism  will  sometimes 
furnish  this  double  murmur  if  there  should  be  a  diastolic  reflux  of  blood  into  the 
sac.  It  may  also  be  found  -with  any  pulsus  celer — e.  g.,  in  chlorosis  and  exoph- 
thalmic goiter.  The  writer  has  heard  it  over  the  left  lobe  of  the  liver  in  a  case  of 
inflammatory  liver  pulse  (see  p.  300)  by  applying  strong  pressure  with  the 
stethoscope.  A  good  deal  of  patience  is  required  for  the  demonstration  of  the 
Duroziez  phenomenon,  because  it  is  a  question  of  ajiplying  just  the  proper  amount 
of  pressure. 

A  systolic  murmur  heard  only  over  one  subclavian  artery,  when  the  arm  is 
hanging  down  and  when  no  pressure  is  exerted  by  the  stethoscope,  suggests  chronic 
disease  of  the  apex  of  the  corresponding  lung.  Pleural  adhesions  to  the  subclavian 
vessel  sheath  probably  twist  the  artery,  and  so  cause  the  murmur.  Inspiration 
applies  the  thorax  more  closely  against  the  stethoscope,  so  that  we  must  be  careful 
to  avoid,  any  pressure.  Sometimes,  however,  a  subclavian  murmur  can  be  heard 
on  both  sides,  more  rarely  on  one  side,  in  perfectly  healthy  people,  and  in  many 
persons  such  a  murmur  may  also  be  caused  artificially  by  certain  jjositions  of  the 
arms  which  compress  the  artery  against  the  clavicle  or  against  the  subclavian  and 
pectoralis  minor  muscles. 

Systolic  murmurs  heard  over  the  arteries,  especially  the  carotids,  without  stetho- 
scopic  pressure,  possess  some  diagnostic  interest.  They  may  arise  in  anemia  in  the 
same  way  as  accidental  heart  murmurs  (p.  277),  and  if  not  transmitted  from  the 
heart  they  are  often  of  the  greatest  importance  in  verifying  the  accidental  charac- 
ter of  a  heart  murmur  in  the  same  way  as  the  venous  hum  (p.  285).  The  in- 
crease of  the  systolic  blood-stream  in  the  pulsus  celer  of  aortic  insufiiciency, 
exophthalmic  goiter,  and  chlorosis  can  cause  murmurs  over  the  arteries,  indepen- 
dent of  any  transmission. 

Localized  arteriosclerosis  will  furnish  a  systolic  murmur  over  an  artery.  A  case 
of  this  kind  was  of  considerable  interest  to  the  author.  An  old  man  presented  a 
loud  systolic  murmur  over  the  left  carotid  for  months,  and  the  diagnosis  of  an 
arteriosclerosis  of  that  carotid  was  confirmed  later  by  the  origin  of  a  left-sided 
cerebral  thrombosis.  Slight  pressure  of  the  stethoscope — not  enough  to  cause  a 
murmur  in  a  normal  artery — \\i\\  sometimes  bring  out  such  an  arteriosclerotic 
murmur.  Litten  recently  emphasized  their  diagnostic  importance,  and  described 
them,  as  phenomena  of  palpation,  under  the  name  "spritzen."  They  may  be 
heard  over  the  abdominal  aorta  as  well  as  over  the  carotids. 

Systolic  and  diastolic  murmurs  are  frequently  heard  over  the  enlarged  thijroid 
of  exophthalmic  goiter.  The  systolic  are  doubtless  arterial,  dependent  upon  a 
pulsus  celer.  It  has  not  been  determined  whether  the  diastolic  are  arterial,  and, 
like  the  second  part  of  the  Duroziez  double  murmur,  a  consequence  of  pulsus 
celer;  or  whether  they  are  the  diastolic  portion  of  venous  murmurs  (p.  286), 
isolated  and  strengthened  because  the  veins  are  compressed  or  closed  by  the  arteries 
during  systole. 

Anyone  Avho  takes  the  trouble  to  auscultate  the  vessels  frequently  will  hear 
sounds  which  have  never  been  described  and  many  which  have  not  been  thoroughly 
explained.  The  writer  mentions  as  an  examj^le  the  occurrence  of  three  sounds  in 
the  carotid  in  cases  of  aortic  insufficiency,  which  together  give  a  rhythm  completely 
analogous  to  the  gallop  rhythm  of  the  heai-t,  although  such  a  rhythm  is  not  present 
in  that  organ.  It  is  probably  produced  by  a  combination  of  the  transmitted  first 
sound  of  the  heart  with  two  local  sounds  occurring  somewhat  later  in  the  artery. 
In  aortic  insufficiency  the  writer  has  also  repeatedly  heard  a  presystolic  murmur — 
i.  e.,  presystolic  in  reference  to  the  local  arterial  sounds — which  is  probably  pro- 
duced by  the  marked  increase  in  the  velocity  of  the  current  (pulsus  celer)  which 
precedes  the  distention  of  the  artery. 


284  AUSCULTATION. 

AUSCULTATION   OF  THE   VEINS, 

TONES    OVER  THE  VEINS. 

The  blood  flows  through  the  veins  normally  without  tones  and  with- 
out murmurs.  The  so-called  venous  hum  is  only  very  rarely  heard  in 
healthy  individuals.  The  reflux  blood-wave  of  the  regurgitating  venous 
pulse  in  the  greater  veins  (especially  in  the  jugular  vein,  and  in  the 
bulb)  may  cause  a  systolic  tone,  due  to  the  relaxation  of  the  valves  and 
of  the  walls  of  the  vein.  This  systolic  bulb-valve  tone  can  be  differ- 
entiated from  the  synchronous  systolic  carotid  tone  only  by  observing 
that  it  slightly  precedes  the  latter,  forming  a  sort  of  preface  (see  p.  151). 

MURMURS    OVER  THE  VEINS ;   VENOUS  HUM. 

Most  venous  murmurs  are  continuous,  because  the  current  in  the 
veins  varies  so  little  in  rapidity.  The  most  important  is  the  so-called 
"venous  hum,"  " nun's- murmur,"  or  "bruit  du  diable."  It  is  heard 
over  the  jugular  vein  very  frequently  in  anemic  and  chlorotic  individ- 
uals, but  rarely  in  health.  It  exhibits  a  characteristic  continuous  sound, 
sometimes  blowing,  sometimes  humming,  and  sometimes  musically 
whistling,  with  a  rhythmic  accentuation  corresponding  to  systole,  to 
diastole,  and  to  the  phase  of  respiration.  It  is  heard  most  plainly  on  the 
right  side,  over  the  carotid,  in  the  angle  between  the  sternum  and  the  cla- 
vicular portions  of  the  sternocleidomastoid.  The  patient  should  stand 
erect  and  hold  his  head  straight,  because  the  recumbent  posture  dimin- 
ishes the  intensity  of  the  murmur  and  sometimes  causes  it  to  disappear. 
Turning  the  head  to  the  opposite  side  ordinarily  increases  the  murmur. 
Pressure  of  the  stethoscope  should  be  avoided,  for  if  marked  pressure 
is  exerted  the  murmur  practically  always  disappears,  and  then  the  carotid 
tone  or  an  artificial  murmur  of  the  stenosed  carotid  is  all  that  is  heard. 
If  faint,  we  can  sometimes  distinguish  only  the  accentuated  systolic,  dias- 
tolic, and  inspiratory  portions  of  the  venous  hum.  Such  an  interrupted 
murmur  may  be  confused  with  an  arterial  or  with  a  res])iratory  murmur. 
Pressing  very  lightly  with  the  stethoscope  or  turning  the  patient's  head 
toward  the  opposite  side  will,  however,  intensify  the  hum  and  trans- 
form the  interrupted  murmur  into  a  continuous  roar,  and  so  clear  up 
the  diagnosis.  The  diastolic  accentuation  of  a  venous  hum  may  be 
transmitted  to  the  cardiac  region  and  simulate  a  diastolic  accidental 
murmur,  but  auscultating  from  the  heart  to  the  jugular  will  generally 
distinguish  the  one  from  the  other  (p.  277). 

To  explain  the  venous  hum  Ave  must  start  with  the  fact  that  it 
occurs,  although  not  exclusively  yet  much  the  most  commonly,  in 
anemic  individuals ;  and  then  we  must  turn  to  the  general  physical  laws 
applying  to  the  origin  of  murmurs  in  flowing  currents  (p.  261  et  seq.). 
The  two  factors  which  are  all  important  in  producing  current  murmurs 
are  :  (1)  the  presence  of  abnormal  narrowiugs  or  widening*  in  the  tube, 
and,  (2)  the  current  rapidity.  To  explain  the  venous  hum  in  anemic 
individuals,  the  hypothesis  has  been  advanced  that  the  jugular  veins 
collapse  in  consequence  of  a  diminished  mass  of  blood,  whereas  the 


AUSCULTATION  OF  THE   VESSELS.  285 

bulbils  remains  distended  in  virtue  of  its  attachment  to  the  cervical  fascia. 
An  abnormally  pronounced  change  of  lumen  thus  results  between  the 
vein  and  the  bulb,  and  so  produces  the  murmur.  Tliis  explanation  is 
certainly  incorrect,  because,  in  the  first  place,  in  those  anemic  individ- 
uals in  whom  the  venous  hum  is  most  common  (chlorotics),  the  suppo- 
sition of  a  diminished  blood-mass  is  quite  erroneous,  and  because,  in  the 
second  place,  it  is  easy  to  see  that  in  chlorosis  the  jugular  veins  are 
generally  well  filled,  and  indeed  often  abnormally  so.  Since  we  must 
give  up  the  hypothesis  of  a  change  of  lumen  at  the  auscultation  spot  of 
the  jugular  vein  as  an  explanation  of  the  murmur,  we  must  turn  our 
attention  to  the  second  of  the  above-named  factors — viz.,  the  current 
rapidity.  Have  we  any  proof  that  anemic  blood  flows  with  increased 
rapidity?  Cohnheim's  experiment  in  submitting  the  mesentery  of  an 
artificially  hydremic  animal  to  direct  observation  proved  that  hydremic 
blood  actually  flows  more  quickly  than  normal  blood,  and  probably  on 
account  of  its  diminished  cohesion  or  viscosity.^  Though  anemics 
usually  exhibit  a  diminution  of  the  blood-coloring  matter,  their  blood  is 
not  necessarily  hydremic,  Nevertheless,  specific-gravity  estimations  of 
their  blood  do  show  that  it  is  very  frequently  hydremic  ;  and,  besides, 
it  is  perfectly  conceivable  that  the  cohesion  of  anemic  blood  is  dimin- 
ished even  without  actual  hydremia,  and  so  the  friction  between  the 
layer  of  blood  against  the  vessel-wall  and  the  circulating  current  would 
be  diminished,  and  hence  result  in  an  increase  of  the  current  rapidity. 
An  increased  current  rapidity  would  naturally  offset  to  some  extent  the 
disadvantage  of  a  deficient  hemogloblin.  The  explanation  that  the 
venous  hum  in  anemic  individuals  depends  upon  an  increased  rapidity 
of  the  current  is  certainly  the  most  probable.  Of  course,  this  theory 
assumes  a  normal  change  in  lumen  between  the  jugular  vein  and 
the  bulbus.  The  venous  hum  which  is  quite  rarely  observed  in  per- 
fectly healthy  individuals  may  reasonably  be  supposed  to  depend  upon 
individual  anatomic  relations  or  conditions  of  distention  of  the  vein 
sufficient  to  narrow  its  lumen  and  produce  a  murmur  with  normal 
current  rapidity.  The  current  rapidity  of  the  blood  may  perhaps  also 
vary  considerably  within  normal  limits. 

.  We  explain  the  accentuation  of  the  hum  in  the  standing  position  by 
the  influence  of  gravity  upon  the  column  of  venous  blood ;  it  exercises 
suction,  thereby  narrows  the  vein,  and  so  hastens  the  jugular  blood- 
stream. The  murmur  is  more  plainly  heard  upon  the  right  side,  because 
the  right  jugular  vein  is  almost  a  direct  linear  continuation  of  the  vena 
innominata  dextra ;  whereas  the  left  jugular  empties  into  the  innomi- 
nata  sinistra  at  an  oblique  angle,  and  so  there  is  less  obstacle  to  the 
current  on  the  right  side.  By  turning  the  head  to  the  opposite  side, 
the  upper  part  of  the  vein  is  compressed  by  the  sternocleidomastoid 
and  omohyoid  ;  hence  this  movement  accentuates  the  venous  hum. 
The  accentuation  due  to  the  stethoscopic  pressure  needs  no  further 
explanation. 

The  rhythmic  accentuation  of  the  hum  requires  explanation.     The 
1  AUg.  Path.,  1882,  vol.  i.,  p.  441. 


286  AUSCULTATION. 

inspiratory  intensification  is  easily  explained  by  the  increased  rapidity 
of  the  venous  blood  during  inspiration.  The  systolic  and  diastolic 
accentuation  are  more  complicated.  The  curve  of  the  physiologic  venous 
pulse  (Fig.  68)  seems  to  show  that  the  venous  current  is  hastened 
during  ventricular  systole ;  slowed,  on  the  contrary,  during  diastole, 
judging  from  the  small  secondary  oscillations  in  the  ascending  limb  of 
the  curve.  Hence,  the  systolic  accentuation  of  the  venous  hum  may  be 
explained  by  the  systolic  increase  of  rapidity  of  the  blood-current, 
whereas  the  diastolic  accentuation  must  depend  upon  another  cause. 
The  conditions  of  change  of  lumen  which  the  vein  suffers  coincident 
with  the  ascending  limb  of  the  venous  pulse — i.  e.,  diastole — at  the  place 
where  the  wave  crest  passes  over  into  the  wave  trough  may  favor  the 
origin  of  a  murmur  by  helping  the  vibrations  of  the  vessel-wall  with 
the  accompanying  whirling. 

Murmurs  similar  in  character  and  origin  to  the  venous  hum  may  also 
be  heard  over  the  crural  vein  and  over  a  vascular  goiter.  In  the  latter 
they  may  be  favored  by  irregularity  of  the  blood-vessels  and  tortuosity 
of  the  veins. 

The  writer  attributes  considerable  diagnostic  significance  to  the 
presence  of  a  venous  hum.  If  not  absolutely  pathognomonic,  it  at  least 
suggests  the  presence  of  anemia.  The  demonstration  of  a  venous  hum 
confirms  the  diagnosis  of  an  accidental  heart  murmur.  A  venous  hum 
is  also  found  in  exophthalmic  goiter,  and  is  located  most  frequently  over 
the  goiter.  Here,  too,  it  probably  depends  upon  an  increased  rapidity 
of  blood-current. 

AUSCULTATION   OF   THE   ABDOMEN, 

Excepting  for  the  sounds  heard  over  the  pregnant  uterus  (fetal  heart  tones, 
uterine  and  placental  bruits,  and  cord  murmurs),  described  in  obstetric  text-books, 
auscultation  of  the  abdomen  is  generally  barren  of  results.  (Compare  the  section 
upon  Auscultation  of  the  Vessels  (p.  282  et  seq.)  in  regard  to  the  examination  of 
the  abdominal  aorta.)  Friction  murmurs  synchronous  with  respiration,  caused  by 
peritoneal  exudations  over  the  liver  or  spleen  (ordinary  palpable  as  well),  have  a 
certain  importance  (perihepatitic  and  perisplenic  friction  murmurs).  Gerhardt 
claims  that  most  cases  of  cholelithiasis  furnish  such  friction  sounds  in  the  gall- 
bladder region.  Similar  friction  murmurs  arise  over  other  parts  of  the  abdomen 
between  roughened  surfaces  of  the  peritoneum,  but  they  are  generally  better  appre- 
ciated by  lialpation  than  by  auscultation,  because  they  are  mostly  brought  out  by 
manipulation.  In  normal  cases  intestinal  movements  proceed  so  quietly  that 
only  very  faint  intestinal  murmurs  are  to  be  heard ;  but  in  pathologic  increase 
of  peristalsis  the  intestinal  movements  can  sometimes  be  heard  at  a  distance,  the 
so-called  "borborygmi."  Further,  the  coincident  presence  of  gas  and  fluid  in  the 
abdominal  cavity  may,  in  moving  a  patient  with  perforative  peritonitis,  cause  suc- 
cussion  murmurs  in  the  abdomen,  frequently  metallic  in  character  and  similar  to 
the  succiissio  Hippocratis  (p.  240).  They  may  be  sometimes  heard  by  means  of  the 
stethoscope,  sometimes  at  a  distance.  They  possess  a  certain  interest  but  no  great 
diagnostic  significance,  since  in  the  very  diseases  whose  differentiation  from  perfora- 
tive peritonitis  is  desired — for  example,  in  ileus  and  in  non-perforative  peritonitis — • 
there  is  ordinarily  an  accumulation  of  air  and  fluid  in  the  stomach  and  distended 
intestines  capable  of  giving  rise  to  the  same  sort  of  a  succussion  murmur.  The 
so-called  "splashing  noise"  will  be  mentioned  under  Palpation  of  the  Abdomen. 
In  the  diagnosis  of  intestinal  stenosis  (from  tumors)  the  writer  has  several  times 


ABNORMAL  PULSATIONS.  287 

been  aided  by  the  presence  of  a  sizzling  or  whistling  stenotic  murmur,  appreciable 
sometimes  at  a  distance  even  by  the  patient  himself,  sometimes  by  means  of  a 
stethoscope,  and  sometimes  by  palpation.  This  is  due  to  peristalsis,  gas  and  fluid 
being  forced  through  a  stenosis  in  the  intestines.  A  peristaltic  wave  or  a  colicky 
pain  will  point  to  the  best  time  for  examination.  (See  Auscultatory  Percussion  of 
the  Abdomen,  p.  185  et  seq.) 

Auscultation  of  the  esophagus.     (See  the  section,  Examination  of  the 
Esophagus.) 


PALPATION    OF   THE    LUNGS  AND    PLEURA. 

(In  regard  to  the  inspection  of  these  parts,  see  the  section,  Relations 
of  Respiration,  p.  77  et  seq.) 

As  has  been  ah^eady  mentioned  in  several  places  (Rales,  Rubs,  Suc- 
cussion  Murmurs),  palpation  of  the  lungs  and  of  the  pleura  serves  partly 
to  confirm  symptoms  recognized  by  auscultation,  partly  to  furnish  inde- 
pendent results.  Examining  for  fluctuation,  changes  of  resistance  of 
the  thorax,  abnormal  pulsations  and  pectoral  (tactile)  fremitus  belong 
to  the  special  province  of  palpation. 

DETERMINATION    OF    FLUCTUATION    AND    CHANGES 
OF  RESISTANCE  IN  THE  THORAX. 

'  Superficial  purulent  affections  of  the  thorax  or  a  purulent  pleurisy  which  has 
broken  through  the  chest-wall  directly  under  the  skin  (a  so-called  empyema  neces- 
sitatis) fluctuate.  No  real  fluctuation  can  ever  be  appreciated  over  a  serous  or 
non-perforating  purulent  pleurisy,  because  of  the  tension  of  the  intercostal  soft 
parts. 

But  a  kind  of  fluctuation  or  thrill  (vibratory  fluctuation)  can  be  obtained  over 
an  effusion  by  vigorously  percussing  the  posterior  thorax,  and  at  the  same  time 
with  the  other  hand  palpating  the  anterior  corresponding  half  of  the  thorax 
(bimanual  palpation  percussion).  The  appreciation  of  this  phenomenon  requires 
a  very  nice  sense  of  touch.  The  writer  has  noticed  it  in  exceptional  cases  in 
sero-  and  pyopneumothorax,  where  the  free  mobility  of  the  fluid  permits  a  strong 
vibration  wave.  Here  the  phenomenon  has  some  diagnostic  importance,  because 
the  fluid  concealed  beneath  the  lung  in  a  j^neumothorax  is  often  demonstrable 
only  with  considerable  strength  of  percussion  (see  p.  207).  The  succussion  mur- 
mur felt  in, sero-  and  pyopneumothorax  is  an  accentuation  of  the  same  phenomenon. 

Palpation  over  pleuritic  exudations  and  the  different  kinds  of  lung  infiltra- 
tions ordinarily  appreciates  an  increase  of  resistance,  which  frequently  the  finger 
as  plexor  also  appreciates  during  percussion. 

ABNORMAL  PULSATIONS  IN  THE  REGION  OF  THE 
LUNGS  AND  PLEURA. 

Pulsation  over  the  precordia  will  be  described  later  (p.  299  et  seq.).  Where 
pulsating  tumors  have  pushed  the  lungs  aside  and  lie  against  the  thorax,  inspec- 
tion or  palpation,  one  or  both,  may  appreciate  such  pulsation  over  the  lungs. 
In  marked  mitral  lesions,  especially  insufficiency,  one  can  palpate  here  and  tliere 
through  the  thoracic  wall  diffuse  pulsations  of  the  lungs.  This  can  be  appreciated 
better  with  the  ear  or  the  single-barrel  stethoscope  against  the  chest  than  with  the 
hand.     The  phenomenon  must  be  distinguished  from  a  mere  mechanical  shaking 


288  PALPATION  OF  THE  LUNGS  AND  PLEURA. 

of  the  thorax  diffusely  transmitted  from  the  heart.  A  puhnonary  pulse  may  also 
be  detected  in  insufficiency  of  the  pulmonary  valves  (pulsus  celer  of  the  pul- 
monary artery).  Pleuritic  exudations  may  pulsate  in  the  intercostal  spaces  (pul- 
sating pleurisy)  by  transmitting  the  heart  movements  through  the  fluid  to  the 
thoracic  spaces.  This  phenomenon  is  very  rare,  because  the  tension  of  the  inter- 
costal soft  parts  is  too  great  unless  they  and  the  pleura  itself  become  softened  and 
decomposed  from  the  inflammation,  and  unless  the  intrapleuritic  tension  dimin- 
ishes to  equal  that  of  the  atmosphere.  In  short,  empyemas,  but  only  very  few 
serous  exudations,  pulsate. 

TESTING  THE  VOCAL  (TACTILE)  FREMITUS. 

By  vocal  (tactile)  fremitus  is  meant  the  purring  vibration  appreciated 
by  the  hand  placed  upon  the  thorax  of  a  person  speaking  or  singing. 
It  arises  from  the  transmission  of  the  glottis  vibrations  through  the  air 
column  of  the  trachea  and  bronchi  to  the  thoracic  wall.  Physiologically, 
the  louder  and  deeper  the  voice,  the  stronger  the  fremitus.  The  fremitus 
frequently  cannot  be  appreciated  in  women  and  children  with  high 
voices,  in  very  fat  people,  and  in  patients  too  sick  to  speak  aloud.  The 
fremitus  is  strongest  at  the  upper  posterior  JDarts  of  the  thorax,  over  the 
great  bronchi.  From  there  downward  and  outward  it  gradually  dimin- 
ishes. 

Differences  in  the  fremitus  over  different  places  of  the  thorax  are 
appreciated  by  comparative  palpation  while  the  patient  speaks  the  same 
words  aloud  ;  for  example,  "  one,  two,  three,"  or  "  ninety-nine."  The 
ulnar  edge  of  the  hand,  which  is  generally  endowed  with  a  very  keen 
sense  of  touch,  appreciates  the  fremitus  most  accurately.  The  naked 
ear  applied  to  the  thorax  will  serve  the  double  purpose  of  auscultation 
and  palpation.  Naturally,  we  should  only  compare  symmetric  parts, 
and  we  should  remember  that  the  fremitus  is  normally  somewhat  stronger 
upon  the  right  than  upon  the  left  side,  on  account  of  the  greater  breadth 
and  the  more  direct  branching  of  the  right  bronchus. 

Similar  rules  apply  to  the  increase  and  decrease  of  the  fremitus 
as  to  the  voice  itself  and  to  the  physiologic  laryngotracheal  breathing 
murmur.  The  fremitus  is  increased  wherever  bronchophony  appears 
(p.  241  et  seq.) — i.  e.,  over  infiltrations  and  other  consolidations  of  the 
pulmonary  parenchyma  so  long  as  the  bronchi  remain  patent — over 
cavities  and  over  dilated  bronchi.  It  is  diminished  if  the  bronchi  are 
plugged,  or  if  gases,  fluid,  or  solid  tissues  intervene  between  the  pulmonary 
surface  and  the  chest-wall  (pneumothorax,  pleural  exudates,  tumors). 
Increased  fremitus  corresponds,  as  a  rule,  to  bronchial  breathing  and  to 
bronchophony ;  diminished  fremitus,  to  diminished  breathing  and  lack 
of  bronchophony.  Yet  frequently  in  one  and  the  same  case  there  are 
factors  working  at  variance  with  each  other  for  the  production  of  bron- 
chial breathing,  bronchophony,  and  increased  fremitus.  Such  factors  do 
not  always  affect  them  equally.  So,  although  these  three  signs  are  of 
the  same  diagnostic  import,  we  must  determine  each  one  separately. 
For  example,  in  pleuritic  effusions  the  exudation  decreases,  Avhile  the 
pulmonary  compression  increases  bronchophony,  bronchial  breathing, 
and  fremitus ;  but  the  effect  upon  each  of  these  signs  is  not  the  same, 


HEART  BEAT  AND  APEX  BEAT.  289 

for  frequently  over  a  moderate-sized  pleural  exudation  we  get  bronchial 
breathing,  bronchophony,  but  diminished  fremitus. 

Fremitus  is  always  increased  over  pulmonary  infiltrations  except 
when  the  bronchus  leading  to  the  infiltrated  part  is  occluded  by  secre- 
tion, by  a  foreign  body,  or  by  a  compressing  tumor.  It  is  then  absent 
or  decidedly  diminished,  although  usually  not  permanently,  as  the  secre- 
tion, which  is  the  usual  source  of  tlie  plugging,  may  be  coughed  up. 

The  rule  that  the  fremitus  is  diminished  over  fluid  exudations  and 
over  pneumothorax  also  has  exceptions,  because  if  the  exudation  is 
small  the  compressed  lung  increases  the  fremitus  more  than  the  exu- 
dation diminishes  it.  This  is  rare  ;  but  increased  fremitus  as  well  as 
bronchial  breathing  is  common  at  the  upper  border  of  the  pleuritic 
exudate,  where  the  fluid  layer  is  thin  and  wedge-shaped  (see  Fig.  94, 
I.),  whereas  toward  the  base  it  is  plainly  weakened  (see  Fig.  97,  I,), 
Finally  adhesions,  if  membranous  or  string-like,  can  transmit  the  frem- 
itus to  the  surface  through  an  exudation  or  through  a  pneumothoracic 
cavity. 

One  of  the  helpful  methods  of  determining  the  level  of  the  fluid  in 
a  pleuritic  exudation  is  to  map  out  accurately  the  line  of  demarcation 
between  this  increased  and  decreased  fremitus.  In  tapping  a  chest  we 
may  sometimes  avoid  circumscribed  adhesions  within  the  area  of  a 
pleuritic  effusion  or  of  a  pneumothorax  by  testing  the  fremitus. 

Changes  in  the  thoracic  wall  also  influence  the  fremitus.  Thicken- 
ing of  the  wall,  edema,  and  the  like,  diminish  it.  Over  differently 
curved  portions  it  varies  under  otherwise  equal  conditions,  so  that  the 
relations  of  fremitus  are  not  trustworthy  in  the  scoliotic  or  deformed 
chest.  Changes  of  elasticity  of  the  thorax  decidedly  influence  the  frem- 
itus, so  that  it  may  be  diminished  over  contracted  portions  lined  inter- 
nally with  thickened  pleura,  even  without  any  exudation. 


INSPECTION   AND   PALPATION    OF  THE   HEART 
REGION    (PRECORDIA). 

We  shall  discuss  these  two  methods  of  examination  together,  because 
they  are  so  mtmiately  related.  Marked  bulgings  of  the  heart  and  of 
the  pericardium  have  already  been  described  in  the  section  upon  the 
Shape  of  the  Thorax  (p.  34). 

HEART  BEAT  AND  APEX  BEAT. 

The  heart  beat  is  the  visible  and  palpable  vil^ration  of  the  heart 
against  the  thorax  ;  the  heart  apex  beat,  more  simply  apex  beat,  the 
portion  confined  to  the  neighborhood  of  the  apex.  Most  diagnostic 
points  are  especially  concerned  with  the  apex  beat.  To  locate  the  heart 
beat  correctly,  place  the  flat  hand  upon  the  precordia  horizontally  and 
close  to  the  left  parasternal  line,  with  the  fingers  reaching  to  the  left 
axillary  line.     The  finger-tips  may,  at  the  same  time,  be  utilized  for 

19 


290     INSPECTION  AND  PALPATION  OF  THE  HEART  REGION. 

more  accurate  localization  of  the  apex  beat.  If  the  examiner  stands 
in  front  of  the  patient  he  uses  his  right  hand  ;  if  he  stands  behind 
the  patient,  the  left  hand.  In  women  with  large  breasts  the  entire 
left  mamma  must  be  drawn  up  to  the  right.  Sp.  designates  the  apex 
beat  in  our  diagrams. 

HEART  BEAT  UNDER  NORMAL  CONDITIONS. 

A  vibration  synchronous  with  the  heart  action,  and  for  the  most  part 
systolic  in  time,  can  be  felt  over  the  precordia  of  healthy  individuals. 
This  vibration  is  called  the  heart  beat,  and  with  it  a  slight  systolic 
depression  to  the  right  and  above  the  apex  can  sometimes  be  felt. 
The  actual  apex  beat  is  limited  to  a  circumscribed  area  of  this  vibra- 
tion (one  or  two  neighboring  intercostal  spaces).  It  may  be  visible  or 
palpable,  one  or  both,  and  corresponds  accurately  enough  to  the  apex 
of  the  heart — i.  e.,  to  that  point  of  the  deep  cardiac  dulness  which  lies 
farthest  to  the  left.  If  the  apex  of  the  heart  is  considerably  over- 
lapped by  lung,  the  apex  beat  lies  a  little  within  this  point.  In  adults 
it  lies  normally  in  the  lifth  intercostal  space,  somewhat  inside  of  the 
mammillary  or  midclavicular  line.  In  children  it  may  be  situated  a 
space  higher ;  in  the  aged,  a  space  lower.  Even  in  adult  life  its  posi- 
tion depends  a  good  deal  upon  the  form  of  the  thorax  ;  variations  of 
about  one  intercostal  space  may  be  within  physiologic  limits.  In  small 
children  the  apex  beat  may  lie  physiologically  somewhat  beyond  the 
midclavicular  line.  The  extent  of  the  apex  beat  varies  ;  ordinarily  it 
covers  an  area  about  2  cm.  square.  In  conformity  with  the  results  of 
topographic  percussion,  the  heart  apex,  during  median  respiration,  is 
generally  covered  only  by  a  thin  layer  of  lung,  which  cannot  interfere 
with  the  appreciation  of  the  apex  beat.  Still,  the  heart  apex  may  nor- 
mally lie  directly  against  the  thoracic  wall  and  so  render  the  apex  beat 
more  distinct.  Under  pathologic  conditions,  the  enlarged  right  ventri- 
cle, more  or  less  spread  out,  may  share  in  the  production  of  the  apex 
beat,  although  normally,  as  is  well  known,  the  heart  apex  is  produced 
by  the  left  ventricle  alone. 

The  intensity  of  the  apex  beat  varies  a  great  deal  even  under  physio- 
logic conditions,  depending  upon  the  amount  of  overlapping  lung  and 
upon  the  thickness  and  resistance  of  the  thoracic  wall.  These  varia- 
tions and  the  fact  that  the  apex  may  lie  behind  a  rib  instead  of  at  an 
intercostal  space  make  it  clear  why  quite  healthy  persons  sometimes 
show  no  apex  beat.  Normal  breathing  does  not  alter  the  position  or 
the  intensity  of  the  apex  beat,  but  deep  respiration  generally  hides 
it.  Inspiration  may  depress  it,  due  to  the  dropping  of  the  diaphragm 
and  of  the  heart  with  inspiration  ;  expiration  elevates  it  again. 

In  accordance  with  the  passive  alteration  of  the  position  of  the 
heart  described  under  Topographic  Percussion  (p.  179  d  seq.),  the  apex 
beat  can  change  its  position,  moving  to  the  left  in  left-sided  positions,  to 
the  right  in  right-sided  positions,  or  in  the  latter  being  completely  oblit- 
erated by  the  overlying  left  lung.     Bending  the  trunk  forward  in  the 


HEART  BEAT  AND  APEX  BEAT.  291 

erect  posture,  and  so  pushing  the  left  lung  edge  somewhat  aside,  fre- 
quently brings  out  the  apex  beat  more  plainly.  This  device  is  to  be 
recommended  in  attempting  to  localize  the  left  heart  boundary  when  the 
apex  beat  is  rather  indefinite.  Of  course,  any  lateral  movement  of  the 
trunk  should  be  avoided.  Similarly,  deep  expiration  will  sometimes 
bring  out  the  apex  beat,  because  the  lung  is  thus  more  completely 
retracted.  The  Valsalva  experiment,  combining  expiration  with  abdom- 
inal pressure,  is  not  applicable,  because  it  hinders  the  flow  of  venous 
blood  to  the  heart,  and  so  diminishes  its  size. 

Stimulation  to  cardiac  activity,  either  psychic  stimulation  or  bodily 
exertion,  intensifies  and  diffuses  the  apex  beat. 

According  to  physiologists,  the  essential  cause  of  the  heart  beat  is  a 
projection  of  the  heart  apex  and  the  neighboring  portions  of  the  anterior 
ventricular  wall  against  the  thoracic  wall.  Such  projection  is  caused 
by  the  systolic  change  in  the  heart's  shape.  Martins'  experiments 
demonstrated  that  the  entire  phenomenon  oi'  the  heart  beat  occurs 
within  the  systolic  "  closure  time  "  when  no  blood  has  yet  left  the  ven- 
tricle, but  still  remains  there  under  higher  tension.  These  experiments 
refuted  all  the  other  theories  (recoil  theory,  theory  of  the  stretching  of 
the  vessels).  Under  pathologic  conditions  certain  other  factors  besides 
the  change  of  form  of  the  anterior  ventricular  wall  must  have  some 
influence  in  the  causation  of  circumscribed  or  diffuse  vibrations  over 
the  precordia  (see  p.  299  et  seq.). 

PATHOLOGIC  DISLOCATION  OF  THE  HEART  BEAT, 
The  heart  beat  may  be  displaced  by  the  enlargement  of  the  heart  or 
by  its  dislocation. 

Displacements  of  the  Heart  Beat  in  Gross  Cardiac 
Changes. — The  left  ventricle  normally  gives  rise  to  the  heart  beat ; 
dilatation'  of  its  cavity  in  particular  will  therefore  displace  the  apex 
beat  to  the  left,  sometimes  even  out  to  the  left  axillary  line.  Dila- 
tation of  the  right  ventricle  may  also  cause  a  marked  displacement 
of  the  apex  beat  to  the  left,  because,  on  the  one  hand,  the  right  ven- 
tricle has  some  share  in  the  formation  of  the  apex  beat,  and,  on  the 
other  hand,  a  dilated  right  ventricle  will  push  the  entire  heart  to 
the  left  (see  p.  183).  Therefore  we  have  no  right  to  diagnose  a  dila- 
tation as  limited  to  the  left  ventricle,  because  the  apex  beat  is  dis- 
placed to  the  left,  Avithout  paying  special  attention  to  all  the  other 
pathologic  signs.  If  such  a  displacement  is  very  marked,  and  if  at  the 
same  time  there  is  no  increase  of  cardiac  dulness  to  the  right,  we  are 
justified  in  assuming  a  preponderating  dilatation  of  the  left  ventricle. 
The  heart  apex  rests  closely  against  the  surface  of  the  diaphragm,  run- 
ning obliquely  downward  and  to  the  left,  so  that  in  dilatation  of  the 
left  ventricle  an  apex  beat  pushed  to  the  left  will  also  be  situated  lower 
than  normally.  Dilatation  of  the  right  ventricle,  on  the  contrary, 
merely  dislocates  the  apex  horizontally  to  the  left,  because  an  enlarge- 
ment of  the  right  ventricle  supported  upon  the  diaphragm  tends  to  raise 
the  heart  apex  (see  Fig.  74).     This  elevation  must  naturally  follow  the 


292     INSPECTION  AND  PALPATION  OF  THE  HEART  REGION. 

dome  of  the  diaphragm,  under  the  influence  of  the  air  pressure  from  the 
abdomen.  It  is  nevertheless  doubtful  if  this  distinction  always  applies, 
because  with  marked  dilatation  of  its  chamber  the  right  ventricle  forms 
the  apex  itself,  which  must  then  drop  downward  in  the  direction  of  the 
heart's  axis. 

Simjile  hypertrophy  of  the  cardiac  muscle  without  dilatation  is  never 
sufficiently  marked  to  occasion  any  noticeable  dislocation  of  the  apex 
beati      (See  p.  182  for  exceptions  to  this  statement.) 

Only  the  most  marked  degrees  of  cardiac  atrophy  would  be  accom- 
panied by  or  associated  with  a  dislocation  of  the  apex  inward. 

Displacements  of  the  Heart  Beat  from  Dislocation  of 
the  Heart. — (See  the  section  upon  Topographic  Percussion,  p.  188 
et  seq.) 

In  situs  inversus  the  apex  beat  lies  symmetrically  placed  upon  the 
opposite  side.  In  deformities  of  the  thorax  the  apex  beat  may  be  dis- 
placed in  any  direction.  In  emphysema  it  lies  lower  than  normally, 
although  often  the  heart  is  so  thoroughly  covered  by  the  lung  that  it 
cannot  be  felt  at  all.  In  unilateral  retraction  of  the  lung  the  apex  beat 
may  be  drawn  toward  the  affected  side  and  generally  upward,  the  latter 
on  account  of  the  high  position  of  the  diaphragm.  Pleuritic  exudations 
and  pneumothorax  cause  a  purely  lateral  dislocation  of  the  apex  beat 
(see  p.  189).  If  the  dislocation  is  excessive,  there  may  be  added  a  pen- 
dulum movement.  If  a  left-sided  effusion  or  pneumothorax  extend 
around  in  front  of  the  heart,  the  apex  beat  may  disappear.  Right-sided 
effusions  will  sometimes  crowd  the  apex  beat  even  to  the  left  axillary 
line,  and  frequently  to  an  abnormal  height,  in  consequence  of  a  rotation 
or  pendulum  movement,  the  left  side  of  the  diaphragm,  of  course,  accom- 
panying the  apex.  Retraction  of  the  left  lung  and  consequent  disloca- 
tion of  the  mediastinum  would  accomplish  a  similar  result.  Increase 
of  the  intra-abdominal  pressure  from  meteorism,  ascites,  tumors,  etc.,  will 
force  the  apex  upward,  and  frequently,  in  consequence  of  a  pendulum 
movement,  somewhat  to  the  left  (see  p.  189  et  seq.). 


DMTENSMCATION    AND    DIFFUSION    OF    THE    HEART    BEAT. 

We  appreciate  the  intensity  of  the  apex  beat  both  by  inspection  and 
palpation.  If  the  palpating  finger  is  raised  quite  vigorously  the  apex 
beat  is  characterized  as  forcible  or  powerful.  Under  such  circumstances 
it  is  often  diffused,  shaking  the  entire  precordia,  although  the  actual  apex 
beat  can  almost  always  be  determined  by  localizing  a  circumscribed 
area  of  more  decided  elevation.  Such  a  strong  movement  signifies 
nothing  but  an  intensification  of  the  apex  beat  of  no  very  exact  import, 
because  the  strength  of  the  beat  varies  so  decidedly,  even  under  physio- 
logic conditions. 

The  apex  beat  is  increased  pathologically  (and  then  ordinarily  also  dif- 
fused) by  any  stimidated  condition  of  heart  action  {bodily  exertion,  nervous 
palpitation ,  exophthalmic  goiter,  chronic  tobacco-poison ing,  fever).  Cardiac 
dilatation,  even  without  any  pronounced  hypertrophy  or  increased  car- 


HEART  BEAT  AND  APEX  BEAT.  293 

diac  activity,  not  only  displaces  and  diffuses  the  apex  beat,  but  also  inten- 
sifies it.  This  seems  anomalous  ;  and  so  does  the  violent  heart  beat  with 
weakened  ])alse  which  is  so  often  observed  in  uncompensated  heart  lesions 
and  in  the  so-called  overexertion  of  the  heart.  But  Martins'  cardio- 
graphic  experiments  proved  that  the  heart  beat  occurs  during  the  closure 
time  of  systole,  and  that  it  is  entirely  independent  of  the  power  with  which 
the  ventricle  empties  its  contents.  The  larger  the  heart,  the  greater 
the  change  of  its  form  at  the  closure  time,  and  consequently  the  more 
marked  the  apex  beat,  quite  independent  of  the  heart's  power.  In  con- 
ditions of  cardiac  weakness  the  closure  time  is  prolonged  at  the  expense 
of  the  expulsion  time,  the  heart  only  moderately  diminishes  during  dias- 
tole, the  heart- wall  during  the  expulsion  time  moves  from  the  thoracic 
wall  only  a  little  and  quite  slowly,  and  so  the  change  of  form  during 
closure  time  is  emphasized,  and  the  heart  beat  seems  especially  strong. 
Conversely,  it  is  plain  that  when  the  heart's  power  improves  in  such  a 
case  the  heart  beat  will  become  weaker,  because  the  expulsion  of  the  blood 
begins  earlier,  is  more  complete,  the  heart  becomes  smaller  more  quickly 
during  systole,  and  therefore  recedes  farther  from  the  thoracic  wall. 

An  accentuation  and  diffusion  of  the  heart  beat  frequently  signifies 
merely  a  more  extensive  uncovering  of  the  heart  (pulmonary  retraction, 
high  position  of  the  diaphragm,  upward  dislocation  of  the  heart,  (see 
p.  181)). 

As  lias  been  said,  an  abnormally  powerftil  apex  beat  alone  does  not  always  sig- 
nify cardiac  hypertrophy.  But  one  form  of  increased  apex  beat,  F.  Miiller's^  so- 
called  ' '  heaving  beat, ' '  admits  of  no  doubt ;  it  always  implies  cardiac  hypertrophy. 
In  this,  although  the  heart  action  need  not  be  violent,  and  is  frequently  not  espe- 
cially diffused,  yet  the  heart  apex  lifts  the  palpating  finger  with  pressure  and  with 
unconquerable  force.  "Slow  heaving  beat"  is  a  better  term,  as  the  i^rolongation 
of  the  beat  is  so  noticeable.  Veiy  frequently  the  heart  action  is  also  slowed.  These 
cases  are  characterized,  according  to  Miiller,  by  an  exceptionally  slow  elevation  of 
the  cardiographic  curve  and  by  an  increased  systolic  intracardial  pressure,  as  well 
as  by  an  increased  resistance  to  systole.  The  slowness  of  the  heaving  depends  upon 
the  prolongation  of  the  closure  time,  whereas  the  intensification  of  the  hea^-ing  is 
the  direct  palpatoiy  expression  of  increased  intracardial  pressure.  The  high  intra- 
cardial pressure — /.  e.,  the  resistance  to  the  ventricular  contraction — may  depend 
upon  a  high  arterial  pressure  or  upon  some  opposition  to  ventricular  emptying 
between  the  heart  and  the  arteries — e.  g. ,  an  aortic  stenosis.  In  any  case  it  neces- 
sitates a  cardiac  hypertrophy  to  overcome  the  resistance,  so  that  any  permanently 
slow  heaving  may  be  regarded  as  a  safe  sign  of  cardiac  hypertropliy  (primary 
hypertrophy).  More  importance  should  be  attributed .  to  the  slowness  of  the 
heaving  than  to  its  force  and  extent,  in  order  to  prevent  confusion  with  the 
increased  beat  in  cardiac  insufficiency,  just  mentioned  above.  In  the  recognition 
of  cardiac  hypertrophy  a  slow  heaving  heart  beat  has  about  the  same  diagnostic 
significance  as  a  continual  high-tension  pulse. 

It  is  not  as  yet  certain  whether  other  forms  of  left  ventricular  hypertrophy 
which  depend  upon  increased  diastolic  ventricular  filling  (the  so-called  secondary 
hypertrophy  (see  p.  316,  2) )  may  eventually  lead  to  the  slow  heaving  apex  beat 
described  above,  or  to  a  mere  accentuation  of  the  apex  beat.  Increased  resist- 
ance, which  prolongs  the  closure  time,  does  not  seem  to  exist  in  the  secondary 
hypertrophy  depending  upon  dilatation.  The  effect  must,  however,  be  similar, 
because  (according  to  Pascal's  law  of  the  hydraulic  press)  so  long  as  the  arterial 
pressure  remains  equal,  the  total  ventricular  loading  increases  in  proportion  to  the 

'  Berlin,  klin.  Woch.,  1895,  No.  35,  p.  757. 


294     INSPECTION  AND  PALPATION  OF  THE  HEART  REGION. 

increase  of  the  inner  surface  of  the  ventricle.  Future  exact  palpatory  and  cardio- 
graphic  examinations  must  settle  the  question  whether  this  kind  of  "  overloading  " 
can  produce  the  slowly  heaving  apex  beat,  for  evidently  "overloading"  is  not 
identical  with  increased  arterial  resistance.^ 

F.  Midler'' s  '■'■vibrating  apex  beat"  differs  both  from  the  simple  increased  beat 
and  from  the  slow  heaving  beat.  Its  impulse  is  more  rapid  and  sudden,  depend- 
ing, according  to  Miiller's  experiments,  upon  a  change  in  the  form  of  cardiac 
stimulation.  It  is  practically  confined  to  subjective  cardiac  palpitation,  especially 
the  nervous  form. 

As  soon  as  the  major  part  of  the  heart  is  uncovered,  the  apex  beat  is  no  longer 
localized  ;  but  the  entire  precordia  seems  to  vibrate  with  a  wave-like  movement, 
an  undulation  in  which  the  difierent  parts  taken  by  the  movement  of  the  ventricles, 
auricles,  and  great  vessels  can  often  be  distinguished  (see  p.  299  et  seq.^. 

Compare  p.  258  et  seq.  for  the  relation  of  the  so-called  gallop  rhythm  to  the 
diastolic  recoil  of  the  ventricular  walls. 

WEAKENING  OF    THE  HEART  BEAT. 

The  heart  beat  may  be  weakened  or  may  entirely  disappear.  Either 
effect  may  be  produced  by  an  emphysematous  lung  overlapping  the  heart ; 
by  pericardial  or  left  pleural  effusions  ;  by  pneumothorax  ;  by  tumors  or 
collections  of  air  in  the  anterior  mediastinum ;  by  marked  pannicidus 
adiposus  ;  by  edema  or  emphysema  of  the  chest-wall  (see  Fig.  14). 

Its  disappearance  on  account  of  a  pericardial  effusion  is  diagnostically 
the  most  important  of  these  causes.  Before  any  conclusions  can  be 
drawn  as  to  the  presence  of  such  an  exudation,  the  character  of  the 
apex  beat  in  health  should  have  been  observed,  because  it  may  not  have 
been  typical  before  the  patient's  illness.  Pericardial  effusions  do  not 
always  hide  the  apex  beat.  The  writer  once  saw  a  case  in  which,  despite 
a  very  large  pericardial  exudation,  the  apex  beat  persisted,  because  the 
apex  of  the  heart  was  adherent  to  the  parietal  layer  of  the  pericardium. 

[One  of  us  observed  in  Dr.  Evans'  ward  at  the  New  York  City 
Hospital  a  pneumonia  patient  in  whom  the  apex  beat  was  very  plainly 
visible,  and  slightly  heaving  to  palpation  in  the  anterior  axillary  line. 
The  autopsy  revealed  a  "  pericarditis  with  localized  double  empyema  of 
the  pericardium.  The  middle  and  lower  portions  of  the  pericardium 
were  adherent  to  the  heart,  the  upper  and  right  portion  over  the  right 
auricle  was  dilated  and  filled  with  several  ounces  of  thick  greenish  pus  ; 
on  the  left  side  of  the  heart  and  directly  over  the  left  ventricle  another 
sac,  somewhat  smaller,  contained  several  ounces  of  similar  pus." — Ed.] 

Further,  as  the  persistence  of  the  pericardial  friction  proves,  a  consid- 
erable pericardial  effusion  may  collect  and  distend  the  lateral  portions  of 
the  cavity  before  it  conceals  the  apex  beat  (see  p.  280). 

A  weakening  or  disappearance  of  the  heart  beat  is  in  exceptional 
cases  observed  as  a  consequence  of  diminished  cardiac  activity ;  but 
these  are  mostly  conditions  of  excessive  cardiac  weakness  (agony,  col- 
lapse).    The  heart  beat  diminishes  when  the  cardiac  power  becomes  so 

^  O.  Frank  {Zeils.f.  Biol,  vol.  xxxii.)  and  Moritz  {D.  Arch.  f.  klin.  Med.,  vol.  Ixvi.) 
call  the  loading  of  the  ventricle  caused  by  increased  filling  "  loading"  ("  Belastung") ; 
and  that  caused  by  arterial  resistance  or  tension,  "  overloading."  They  show  that  the 
two  factors  have  an  entirely  different  importance  in  the  heart  activity.  The  original 
work  must  be  consulted  for  this  distinction. 


HEART  BEAT  AND  APEX  BEAT.  295 

weak  that  the  alteration  in  shape  of  the  heart  during  closure  time  essential 
to  the  production  of  the  heart  beat  fails.  But  before  this  point  is  reached 
the  heart  beat  will  be  vigorous  or  even  increased  in  spite  of  the  dimin- 
ishing cardiac  power. 

The  diminished  tension  of  the  radial  pulse  is  generally  a  far  safer 
guide  to  the  condition  of  the  cardiac  power  than  a  weak  heart  beat, 
especially  if  we  are  not  familiar  with  the  patient's  normal  heart  beat. 

ABNORMAL  POSITION  OF   THE  APEX  BEAT  IN  RELATION  TO 
THE  SUPERFICIAL  CARDIAC  DULNESS. 

The  apex  beat  may  lie  inside  of  the  cardiac  dulness,  or,  perhaps, 
more  clearly  expressed,  the  superficial  cardiac  dulness  may  extend  to 
the  left  beyond  the  apex  beat.  This  peculiarity  may  occur  in  a  case  of 
pericarditis,  where  the  exudation  is  collected  in  the  lateral  portions  of 
the  sac  and  the  apex  beat  still  persists.  It  is  not,,  however,  a  pathogno- 
monic sign  of  such  a  condition,  for  it  may  sometimes  be  observed  in 
<3ardiac  enlargements — e.  g.,  in  mitral  insufficiency.  In  this  lesion  there 
is  no  true  closure  time,  for  the  left  ventricle  begins  to  empty  itself  at 
the  very  onset  of  systole,  and  the  heart- wall  is  not  pushed  as  soon  as 
normally  against  the  chest  by  the  systolic  intraventricular  pressure — in 
fact,  not  until  the  left  heart  has  already  contracted  to  some  extent, 
and  has  therefore  drawn  the  apex  upward  toward  the  base.  The 
diastolic  size  of  the  heart,  of  course,  determines  the  limits  of  the  cardiac 
dulness,  and  so  the  elevated  apex  beat  lies  inside  the  dulness.  Again, 
the  same  sign  might  occur  if  an  enlarged  left  ventricle  had  compressed 
the  lung  edge  enough  to  make  it  atelectatic ;  the  apex  beat  would,  of 
course,  be  further  to  the  left  than  normal,  but  part  of  the  increased 
dulness  to  the  left  of  the  apex  would  be  formed  by  the  compressed  lung. 

SYSTOLIC  RETRACTION  AT  THE  APEX. 

This  is  sometimes  observed  instead  of  an  apex  beat.  It  can  be  shown  to  be 
systolic  by  auscultating  the  heart. 

If  noted  in  a  healthy  individual,  as  it  sometimes  is,  the  sign  cannot  be  perfectly 
explained.  The  writer's  theory,  however,  is  as  follows  :  The  change  of  form  of 
the  heart  normally  causes  a  blow  of  the  apex  against  the  chest-wall ;  at  the  same 
time  the  sections  of  the  heart  lying  above  and  within  the  apex  retreat  toward  the 
interior  of  the  thorax.  Under  physiologic  conditions  this  would  produce  a  palpable 
and  visible  systolic  retraction  of  the  thoracic  section  lying  inside  of  the  apex  beat 
(see  p.  290).  If,  then,  for  some  reason  or  other  the  apex  beat  is  absent,  we  should 
speak  of  a  systolic  retraction  of  the  heart  apex  ;  but  in  reality  the  apex  would  not 
be  systolically  retracted,  but,  rather,  a  part  of  the  anterior  cardiac  wall  lying  above 
and  inside  the  apex. 

A  systolic  retraction  at  the  aj^ex  has  been  observed  in  many  cases  which  have 
revealed  later  at  autopsy  an  adhesion  of  the  parietal  and  visceral  pericardium  or, 
in  a  few  cases,  an  adhesion  of  the  pericardium  to  the  left  parietal  pleura.  An  expla- 
nation of  the  sign  is  difficult.  Perhaps  the  cicatricial  adhesions  tie  the  heart  down, 
so  that  it  does  not  assume  its  normal  shape  and  position  during  systole,  but  some 
other  which  pulls  the  apex  backward ;  or  perhaps  some  of  the  bands  attached  at 
the  base  of  the  heart  tend  to  drag  the  apex  away  from  the  chest  at  each  contrac- 
tion of  the  base.  The  action  of  external  atmospheric  pressure  is  then  sufficient  to 
explain  the  sign  of  retraction  at  the  apex,  without  assuming  that  the  apex  of  the 


296     INSPECTION  AND  PALPATION  OF  THE  HEART  REGION. 

heart  itself  is  directly  attached  to  the  thoracic  wall  by  means  of  the  pericardium, 
A  systolic  retraction  near  the  apex  is  sometimes  observed  in  normal  cases ;  further, 
many  cases  of  adherent  pericardium  show  no  trace  of  a  systolic  retraction  during 
life,  so  we  must  acknowledge  that  this  sign,  although  often  suggestive,  is  by  no 
means  absolute  nor  pathognomonic  of  adherent  pericardium. 

DOUBLE    HEART    BEAT;    CARDIA    BIGEMINUS;    HEMISYSTOLE; 
SYSTOLIA    ALTERNANS;    PSEUDOHEMISYSTOLE. 

Two  heart  beats  may  under  certain  conditions  follow  one  another  very  quickly, 
and  jjairs  or  groups  of  two  heart  beats  be  separated  from  other  pairs  by  a  longer 
pause  (double  stroke  of  the  heart).  There  results  one  of  three  distinct  forms  of 
cardiac  activity,  distinguished  by  the  titles :  carclia  bigeminus,  hemisystole,  and  sys- 
tolia  alternans.^  These  three  merge  into  each  other  without  any  sharp  boundary 
(Unverricht  ■^ ) ,  and  are,  so  to  speak,  genetically  related.  Thus  far  they  have  been 
observed  only  in  heart  disease,  especially  in  mitral  lesions  combined  with  tricuspid 
insufficiency. 

With  cardia  bigeminus  a  peripheral  arterial  pulse  corresponds  both  to  the  first 
and  to  the  second  of  the  double  heart  beat.  The  former  is  commonly  stronger 
than  the  latter,  thus  producing  a  sort  of  pulsus  bigeminus  alternans  (Fig.  44). 
If  there  should  be  a  venous  pulse,  each  beat  of  the  heart  will  also  produce 
a  distinct  venous  pulse.  There  is  a  regular  alternation  of  stronger  and  weaker 
heart  action ;  the  first  heart  beat  has  more  strength,  probably  because  the 
preceding  longer  pause  has  enabled  a  more  complete  diastolic  filling  of  the  heart. 

If  the  second  contraction  of  the  left  heart  becomes  progressively  weaker  until 
it  finally  disappears,  perhaps  fi-om  some  obstacle  or  from  a  nervous  influence,  and 
if  at  the  same  time  both  contractions  of  the  right  heart  remain  distinct,  hemisystole 
results.  In  this  condition,  then,  the  right  heart  beats  twice  for  each  single  beat 
of  the  left  heart.  It  might  be  possible  to  diagnose  such  a  condition  in  a  tricuspid 
insufficiency,  where  a  double  heart  beat  was  localized  most  plainly  over  the  right 
ventricle,  where  the  radial  pulse  corresponded  only  to  the  first  beat,  but  where  a 
positive  venous  pulse  in  the  neck  corresponded  to  both  beats. 

Systolia  alternans  arises  from  hemisystole  when  the  first  of  the  two  beats  of  the 
right  heart  becomes  weaker  and  finally  disappears.  In  a  tricuspid  insufficiency 
with  a  regurgitating  venous  pulse  this  peculiar  condition  might  be  determined. 
The  radial  jiulse  unaccompanied  by  a  venous  pulse  would  correspond  to  the  first  beat 
of  the  heart  (left),  and  the  venous  pulse  unaccompanied  by  a  radial  pulse  to  the 
second  beat  of  the  heart  (right).  Here  contraction  alternates  between  the  right 
and  left  sides  of  the  heart. 

The  follow^ing  scheme  explains  clearly  the  transition  from  one  to  the  other : 

First  heart  beat.  Second  heart  heat. 
^     ,.    ,.        .                         r  Right  heart.             Effective.  Effective. 

Cardia  bigemmus   ....  |  LJt  heart.  Effective.  Effective. 

„      .      ^  ,  f  Riajht  heart.  Effective.  Effective. 

Hemisystole |  j^gft  }^^^^^  Eflective.  Ineffectual. 

„        -.      ,  f  Right  heart.  Ineffectual.  Effective. 

Systolia  alternans    ....   |  Left  heart.  Effective.  Ineffectual. 

It  is  self-evident  that  valvular  murmurs  which  could  be  localized  would  be  of 
great  assistance  in  distinguishing  these  three  forms  of  heart  beat,  which  Unver- 
richt has  so  cleverly  pictured  as  modifications,  one  from  the  other. 

Most  authors,  however,  agree  with  Rieger*  and  not  Avith  Unverricht.  The 
former  considers  that  the  bigeminus  is  the  only  type  of  double  heart  beat  which  has 

^  For  these  terms  the  expressions,  twin  beat,  half-beat,  and  altered  beat  of  the 
heart  may  be  employed.  -  Berlin,  klin.  Woch.,  1890,  No.  26. 

•' Riegel  and  Lachmann,  D.  Arch.  f.  klin.  Med.,  vol  xxvii.,  p.  393 ;  Riegel,  Volk- 
mann's  Vortrdge,  No.  227.  Again,  Riegel,  Zur  Lehre  vnn  der  Herzirref/ularitdt  und  Incon- 
gruenz  in  der  Tfidtigkeit  beider  Herzhdlften,  Wiesbaden,  Bergmann,  1891. 


HEART  BEAT  AND  APEX  BEAT.  297 

been  conclusively  demonstrated  in  man ;  and  that  the  hemisystole,  first  described 
by  V.  Leyden,'  and  the  systolia  alternans  assumed  by  Unverricht,  in  i-eality,  only 
belong  to  the  bigeminus. 

That  this  is  true,  so  far  as  hemisystole  is  concerned,  is  proved,  according  to  these 
authors,  by  the  fact  that  where  an  arterial  pulse  is  not  palpable  for  the  second  heart 
beat,  it  can  still  be  appreciated  in  the  sphygmogram  ;  and,  according  to  Riegel,  the 
venous  pulse  suffers  less  than  the  arterial.  Here  the  so-called  hemisystole  should  be 
regarded  as  a  bigeminus  in  which  the  second  heart  stroke  is  so  weak  that  it  is  noted 
only  in  the  venous  pulse  and  in  the  sphygmogram,  but  cannot  be  felt  at  the  wrist 
— in  other  words,  a  ^^ pseudohemisystole."  Although  physiologists  have  for  a 
long  time  demonstrated  hemisystole  upon  the  exposed  mammal  heart,  thus  far 
there  has  been  too  little  clinical  observation  to  determine  whether  it  does  actually 
appear  in  man.  Unverricht  drew  his  conclusions  '■'  about  systolia  alternans,  not 
from  the  alternation  of  the  positive  venous  pulse  with  the  radial  pulse,  but  from 
less  secure  criteria — viz.,  the  diiferent  location  of  heart  tones,  murmurs,  and  the 
beats  in  the  two  heart  actions.  The  existence  of  systolia  alternans  must  therefore 
be  left  undecided. 

A  double  heart  beat  may  quickly  change  into  normal  heart  activity.  We  do 
not  know  yet  how  to  explain  the  cause  of  such  a  peculiarity,  nor  its  prognostic 
significance. 

INEFFECTUAL    (FUTILE)    HEART    CONTRACTIONS. 

Quincke  and  Hochhaus^  designated  by  this  expression  jaeculiar  cardiac  con- 
tractions which  occur  in  heart  disease,  and  which  are  characterized  by  the  insertion 
of  a  beat  between  normal  contractions,  sometimes  periodically,  sometimes  quite 
irregularly,  and  especially  by  the  disproportion  between  the  increased  intensity  of 
the  heart  beat  and  of  the  first  tone,  on  the  one  hand,  and  the  weakness  of  the  corre- 
sponding arterial  pulse  on  the  other. 

They  are  probably  incomplete  abortive  cardiac  contractions,  with  which  the  heart 
beat  may  be  abnormally  vigorous,  while  the  arterial  jjulse  is  weak.  (See  Martins' 
explanation,  p.  293.)  In  other  words,  we  might  consider  that  an  identical  cause  pro- 
duces both  these  transitory  futile  contractions  and  the  more  permanent  conditions 
which  were  observed  and  described  by  Martins  in  the  compensatory  disturbances 
accompanied  by  an  increased  cardiac  impulse.  But  Quincke  and  Hochhaus  con- 
tend that  this  view  is  untenable,  because  the  first  sound  in  the  ineffectual  heart  con- 
tractions is  intensified  and  peculiarly  changed  in  quality  (drum-like).  They  con- 
sider it  is  a  question  not  so  much  of  a  quantitative — ?'.  e.,  a  diminution  of  the 
heart' s  action — as  of  a  qualitative  change,  which  they  liken  to  a  cardiac  ' '  spastic 
gait."  The  contractions  are  strong  enough,  but  so  spasmodic  and  so  poorly  co- 
ordinated that  they  do  not  accomplish  the  normal  amount  of  jDumping  (perhaps 
because  all  parts  of  the  ventricle  do  not  contract  simultaneously). 

Further  peculiarities  of  these  futile  contractions  are:  the  diastolic  tone  is  weak- 
ened and  premature  ;  the  abortive  contraction  itself  seems  premature — /.  e.,  it 
follows  an  apparently  shorter  and  precedes  a  longer  diastole ;  the  systolic  and 
diastolic  murmurs  accompanying  such  ineffectual  contractions  are  weakened  or  disap- 
pear ;  and  the  cardiogram  may  reveal  changes  which  it  is  impossible  to  detail  here. 
Not  infrequently  patients  coinplain  of  these  contractions  as  being  painful  or  indef- 
initely unpleasant,  or  they  may  describe  the  sensation  as  that  of  a  jolt  or  a  blow. 

HEART    BLOCKING    AND    AURICULOVENTRICULAR    ALLOR- 

RHYTHMIA. 

Under  this  term  Gaskell,  for  physiology,  and  later  W.  His,  Jr.,  clinically, 
described  a  peculiarity  which  consists  in  the  failure  upon  the  part  of  the  ventricle  * 

'  V.  Leyden,  Virchow's  Arehiv,  vol.  xliv.,  1868.  ^  Loc.  cit. 

3  D.  Arch.f.  klin.  Med.,  1894,  vol.  liii.,  p.  414. 
*  Ibid.,  1899,  vol.  Ixiv.,  p.  316. 


298     INSPECTION  AND  PALPATION  OF  THE  HEART  BEOION. 

to  follow  every  contraction  of  the  auricle.  In  other  words,  the  auricle  contracted 
oftener  than  the  ventricle.  Stannius'  experiments  proved  that  ventricular  con- 
traction is  normally  excited  from  the  auricular  wall  by  some  nervous  or  muscular 
connection,  so  the  name  "  heart  blocking  "  was  selected  to  signify  some  obstruc- 
tion in  this  connection.  W,  His,  Jr.,  demonstrated  a  more  frequent  auricular 
contraction,  in  a  case  of  Stokes- Adam' s  disease  (arteriosclerosis  with  brachycardia 
and  epilepsy),  by  comparing  the  rapid  venous  pulse  with  the  slow  radial  pulse  and 
heart  beat.  The  radial  pulse  corresponded  accurately  to  the  heart  beat  and  heart 
tones,  while  the  venous  pulse,  very  much  more  rapid,  corresponded  to  the  rhythm 
of  tones  over  the  auricle,  but  without  any  palpable  vibration  of  the  heart  region. 

This  phenomenon  might  be  confused  with  hemisystole  or  pseudohemisystole 
(p.  296  et  seq.).  In  the  latter  a  double  heart  beat  occurs,  and  one  or  two  heart 
tones  correspond  with  each  venous  pulse  and  heart  beat.  But  in  the  ' '  heart 
blocking  "  the  venous  pulse  has  no  corresponding  beat  and  tones.  The  ineflFectual 
heart  contraction  only  hurries  the  radial  pulse,  and  possesses  both  a  vigorous  heart 
beat  and  strong  tones.  From  experimental  observations  ' '  heart  blocking  "  is  sup- 
posed to  depend  upon  affection  (1)  of  the  ventricular  muscle,  (2)  of  the  vagus, 
and  ( 3)  of  the  connection  between  the  auricle  and  ventricle. 

Auriculoventricular  Allorrhythmia. — Though  this  has  been  recognized  in 
physiology,  it  has  not  been  studied  as  yet  clinically.  The  auricle  and  ventricle 
here  beat  entirely  independently  of  each  other,  not  as  in  heart  blocking. 

THE  CARDIOGRAM. 

The  cardiograph  is  an  apparatus  which  conducts  the  movements  of 
the  heart  apex  beat,  through  hollow  tubes,  so  as  to  represent  them 
graphically  upon  a  revolving  drum.  The  resulting  curves,  so-called 
cardiograms,  have  already  solved  a  series  of  very  important  questions 

Expulsion  time. 


Closure  time. 


Fig.  107.— Martius'  normal  cardiogram :  /.,  Beginning  of  systole ;  II.,  closure  of  semilunar 
valves;  III.  and  IV.,  recoil  waves  of  stasis  which  arise  in  the  aorta. 

in  heart  physiology,  and    give  promise  of   important  conclusions   for 
heart  pathology. 

Fig.  107  represents  one  of  Martins'  typical  cardiograms.  This 
author,  to  whose  experiments  ^  the  writer  refers  the  reader,  explains  the 
bearing  of  the  apparently  manifold  and  confused  curves  seen  upon  the 
drum  under  physiologic  conditions. 

'  "Graphische  Untei"suchungen  iiber  die  Herzbewegungen,"  Zeits.f.  klin.  Med.,  vol. 
xiii.,  parts  3  and  4,  1888,  p.  327 ;  Deutsch.  med.  Woch.,  1888,  JS^os.  15  and  18 ;  Zeits.  f. 
klin.  Med.,  vol.  xv.,  parts  5  and  6,  1889,  and  vol.  xix.,  parts  1  and  2, 1891. 


OTHER  PULSATIONS  IN  PBECORDIA  AND  ITS  NEIGHBORHOOD.    299 

OTHER  PULSATIONS  IN  THE  PRECORDIA  AND  ITS 
NEIGHBORHOOD. 

The  great  vessels — aorta  and  pulmonary  artery — are  normally  so 
thoroughly  covered  by  the  sternum  and  the  lung  that  their  pulsa- 
tions escape  appreciation.  Marked  dilatation  of  these  vessels  or  a 
retraction  of  the  normally  overlapping  lung  makes  their  pulsations  vis- 
ible and  palpable.  That  of  the  pulmonary  artery  appears  in  the  second 
left  space  ;  that  of  the  aorta,  in  the  second  right  (Fig.  74).  Aneurisms 
or  the  diffused  aortic  dilatation  caused  by  aortic  insufficiency  (Fig.  92) 
are  the  more  usual  causes  of  the  aortic  pulsation,  while  mitral  lesions 
are  generally  responsible  for  the  pulmonic  pulsation.  In  the  latter  the 
dilated  left  auricle  and  left  ventricle  push  the  lung  aside  and  expose  the 
vigorous  hypertrophied  right  ventricle  (see  Fig.  90).  If  the  lung  is 
retracted  by  adhesions  these  pulsations  may  become  evident  even  with  a 
normal-sized  heart  and  great  vessels.  If  the  heart  is  much  enlarged, 
slight  pulsations  of  the  anterior  ventricular  wall  are  readily  mistaken 
for  pulsations  of  the  great  vessel  trunks.  In  the  former  case  the  area 
over  which  the  heart  stroke  is  palpable  would  be  larger  and  the  pulsa- 
tion felt  earlier — i.  e.,  corresponding  to  the  closure  time  of  systole — 
while  in  the  latter  instance  the  pulsation  would  coincide  with  the  expul- 
sion time.  This  point  is  frequently  serviceable  for  distinguishing  a 
markedly  dilated  right  ventricle  from  an  aneurism.  In  case  of  an 
increased  area  of  cardiac  dulness  upward,  the  powerful  heaving  charac- 
ter of  a  pulsation  alone  should  be  sufficient  to  show  that  the  increased 
dulness  is  due  to  a  widening  or  uncovering  of  the  arterial  trunks,  and 
not  to  a  dilatation  of  the  auricle. 

The  systolic  pulsation  of  an  aortic  aneurism  may  be  diffused  over  a 
considerable  area.  This  area  will  usually  be  situated  near  the  second 
right  intercostal  space.  It  is  frequently  visible  as  an  expansile  pulsat- 
ing tumor ;  but  is,  perhaps,  better  appreciated  by  the  palpating  hand. 
If,  as  is  ordinarily  the  case,  an  aneurism  proceeds  from  the  ascending  or 
first  portion  of  the  arch,  the  pulsation  will  generally  be  visible  in  the 
jugulum,  and  can  be  very  plainly  felt  there  as  a  pulsating  tumor  by 
crooking  the  finger  behind  the  top  of  the  sternum. 

The  left  bronchus,  which  is  straddled  by  the  aorta,  will  be  depressed  by  each 
pulsation  of  a  large  aneurism,  and  will  in  turn  transmit  this  depression  to  the 
trachea,  and  so  to  the  larynx.  By  grasping  the  cricoid  cartilage  between  the  thumb 
and  forefinger  of  the  right  hand  while  facing  the  patient,  the  examiner  can  feel 
at  the  larynx  this  transmitted  pulsation  as  a  rhythmic  systolic  downward  tug,  the 
so-called  tracheal  tug  (Oliver-Car darelli  phenomenon).  A  faint  tug  is  some- 
times accentuated  if  the  patient  bends  his  head  back  and  so  increases  the  tension 
of  the  trachea.  This  procedure  may  even  make  the  tugging  visible.  The  sign 
should  not  be  confused  with  the  ordinary  carotid  pulsation,  nor  with  the  pulsation 
of  the  arteries  of  the  thyroid  gland,  neither  of  which  is  strictly  limited  to  a  down- 
ward movement.  The  same  sign  has  been  plainly  demonstrated  in  a  pulsatinfi 
■mediastinal  sarcoma  and  in  dilatation  of  the  arch  of  the  aorta,  so  that  it  can  no 
longer  be  considered  absolutely  pathognomonic  of  aneurism. 


300     INSPECTION  AND  PALPATION  OF  THE  HEART  REGION. 

A  short,  sharp  blow,  corresponding  to  the  closure  of  the  semilunar 
valves,  may  be  felt  at  the  base  of  the  heart  whenever  the  aorta  and  pul- 
monary artery,  uncovered  by  the  lung,  are  exposed  and  situated  directly 
behind  the  chest-wall.  It  is  sometimes  heard  even  without  such  un- 
covering. It  is  practically  never  visible.  Its  brevity,  which  can  be  well 
appreciated  by  palpation,  corresponds  accurately  to  that  of  the  ausculta- 
tion sound  of  the  second  tone.  It  is  to  be  felt  most  distinctly  over 
the  pulmonary  artery  in  mitral  lesions  which  are  associated  with  an 
accentuated  pulmonic  second  sound. 

A  diffuse,  feeble,  systolic  auricular  vibration  distinct  from  other  pul- 
sations of  the  heart  may  sometimes  be  felt  at  the  base  of  the  heart.  It 
comes  out  especially  plainly  when  a  marked  auricular  dilatation  from 
mitral  or  tricuspid  insufficiency  has  pushed  the  lung  away  from  the  base 
of  the  heart.  We  feel,  then,  not  auricular  contraction,  but  auricular  dias- 
tolic filling,  which  in  the  valvular  lesions  mentioned  above  is  intensified 
by  the  stasis  or  regurgitation  at  the  mitral  valve. 

A  systolic  valve  shock,  the  palpatory  equivalent  of  the  systolic  valvu- 
lar tone,  and  correspondingly  brief,  should  not  be  confused  with  this 
auricular  vibration.  The  former  is  felt  in  the  region  of  the  auriculo- 
ventricular  valves  to  the  right  and  left  of  the  sternum,  especially  when 
marked  cardiac  dilatation  pushes  the  lung  aside.  The  ear  against  the 
stethoscope  readily  appreciates  the  difference  between  it  and  the  actual 
heart  beat ;  it  is  not  really  heaving,  and  is  much  shorter  and  sharper 
than  the  latter. 

An  epigastric  pulsation,  a  visible,  palpable,  systolic  shaking  or  lift- 
ing of  the  epigastrium,  appears  in  emphysema.  The  diaphragm  is  low, 
the  heart  lies  in  more  intimate  contact  with  the  epigastrium,  the  right 
ventricle  is  hypertrophied  and  may  be  dilated ;  hence  the  heart  beat  is 
transmitted  directly  through  the  diaphragm  to  the  epigastrium.  A 
normal  heart  if  excited  sometimes  causes  an  epigastric  pulsation. 

Pulsations  of  the  abdominal  aorta  in  a  thin  patient  with  retracted 
abdominal  walls  and  partially  filled  intestines  often  resemble  an  epigas- 
tric pulsation,  but  a  careful  palpation  of  the  abdominal  aorta  from  below 
upward  will  generally  distinguish  them. 

Although  we  discussed  pulsation  of  the  liver  in  the  section  upon  the 
Venous  Pulse  (see  p.  150  et  seq.),  it  should  also  be  noted  that  an  arterial 
pulse  is  sometimes  felt  over  the  liver  (see  p.  152).  This  occurs  most 
frequently  in  aortic  regurgitation  as  a  result  of  the  pulsus  celer,  and  also 
in  inflammatory  conditions  of  the  liver.  The  writer  has  observed  such 
an  arterial  liver  pulse  in  a  case  of  infectious  cholangitis. 

In  aortic  regurgitation,  as  a  result  of  the  pulsus  celer,  the  spleen 
may  also  pulsate.  The  splenic  pulse  is  always  arterial,  since  the  splenic 
vein  empties  into  the  portal  vein,  which  never  pulsates,  as  it  is  cut  off 
from  the  heart  by  the  intervening  liver. 

The  reader  is  also  referred  to  what  has  been  said  about  pulmonary 
pulsation  and  pulsating  pleurisy  (p.  288  et  seq.). 


INSPECTION  OF  THE  ABDOMEN.  301 

PALPATION    OF  CARDIAC  MURMURS. 

(Thrill ;   Fremissement. ) 

Some  heart  murmurs  are  as  plainly  palpable  as  the  heart  tones. 
They  are  most  readily  appreciated  by  a  light  touch  of  the  finger,  or  of 
the  flat  hand  or  its  ulnar  edge. 

Pericardial  friction  rubs  are  naturally  very  distinctly  palpable  (see 
p.  280  et  seq.). 

Neither  accidental  nor  valvular  endocardial  murmurs  can  usually  be 
appreciated  by  palpation  unless  they  are  very  loud  and  vigorous.  In 
mitral  stenosis,  however,  a  distinct  presystolic  thrill  is  frequently  felt 
at  the  apex  even  when  no  murmur  can  be  heard.  This  peculiarity  is 
explained  by  the  difference  in  the  number  of  vibrations  appreciated  by 
the  sense  of  hearing  and  that  of  touch.  (See  Auscultation  with  Eefer- 
ence  to  the  Localization  of  Murmurs,  etc.,  p.  260.) 


INSPECTION  AND  PALPATION  OF  THE  ABDOMEN. 

(See  the  section  upon  the  Examination  of  the  Stomach  and  the 
Intestines,  pp.  353  and  415.) 

Inspection  and  palpation,  discussed  here  together,  are  more  reliable 
in  the  examination  of  the  abdomen  than  percussion. 

INSPECTION  OF  THE  ABDOMEN. 

This  should  be  attempted  first  with  the  patient  in  the  dorsal  decu- 
bitus ;  afterward,  if  necessary,  in  the  erect,  and  then  in  other  positions. 
We  should  first  notice  any  increase  or  decrease  of  the  general  abdominal 
volume,  the  significance  of  which  must  be  controlled  by  percussion  and 
palpation. 

Obesity  is  one  of  the  most  frequent  causes  of  abdominal  enlarge- 
ment, for  the  skin  of  the  abdomen  is  a  favorite  place  for  the  deposition 
of  fat.  The  abdomen  is  then  uniformly  arched,  when  lying  or  stand- 
ing ;  or  the  bulging  may  be  somewhat  lobulated,  owing  to  the  arrange- 
ment of  fat ;  the  navel  is  depressed,  because  the  connective  tissue  there- 
about is  so  rigid  that  fat  cannot  be  deposited.  An  attempt  to  grasj) 
the  panuiculus  adiposus  between  the  fingers  will  solve  any  doubt.  Per- 
cussion elicits  a  dulness,  the  intensity  of  which  depends  upon  the  thick- 
ness of  the  fat-layer. 

Hdema  of  the  abdominal  wall  presents  the  same  retracted  navel 
and  may  possibly  be  confused  with  a  fat  belly  ;  but  the  almost  constant 
existence  of  the  edema  elsewhere,  its  ])reponderance  in  the  lateral  and 
inferior  portions  as  contrasted  with  the  median  deposition  of  fat,  tlie 
pitting  of  the  skin,  and  other  clinical  relations  (p.  49)  will  solve  any 
doubt. 


302  INSPECTION  AND  PALPATION  OF  THE  ABDOMEN, 

Meteorism  (tympanites)  causes  abdominal  distention.  It  lessens 
or  obliterates  the  umbilical  depression  unless  the  wall  is  thickened  by 
edema  or  fat.  The  contour  of  the  stomach  or  of  the  intestinal  coils 
can  frequently  be  seen  through  thin  abdominal  walls,  especially  when 
peristalsis  is  active  or  when  the  organs  are  dilated,  particularly  if  the 
dilatation  is  dependent  upon  a  stenotic  obstruction  in  the  digestive 
tract  (pyloric  stenosis,  ileus,  intestinal  tumors).  The  intestinal  tumor  in 
ileus  is  at  first  plainly  visible  ;  but  later  the  distended  coils,  particularly 
those  in  the  neighborhood  of  the  obstruction,  become  paralyzed  and 
immobile  and  occupy  most  of  the  abdominal  surface.  By  noting 
through  the  abdominal  wall  the  contour  of  an  especially  distended  and 
completely  immobile  coil  of  intestine,  the  position  of  the  obstruction 
can  sometimes  be  determined.  In  very  marked  meteorism  the  caliber 
difference  between  the  large  and  the  small  intestine  cannot  be  appre- 
ciated. The  paralytic  immobility  of  the  visible  intestinal  contour  and 
the  absence  of  intestinal  murmurs  to  auscultation  are  important  signs 
for  the  diagnosis  of  acute  diffuse  peritonitis. 

Free  accumulation  of  air  in  the  peritoneal  cavity  from 
perforation  of  the  stomach  or  intestine  is  characterized  by  a  uniform 
distention  of  the  abdomen  without  visible  stomach  or  intestinal  contour. 

A  collection  of  free  fluid  also  produces  an  apparently  uniform 
distention  of  the  abdomen.  In  the  dorsal  decubitus  the  fluid,  when 
under  no  great  tension,  is  mostly  accumulated  in  the  lateral  portions,  so 
that  the  abdomen  seems  proportionately  broad.  In  case  the  fluid  reaches 
so  high,  the  navel  (as  contrasted  with  its  position  in  meteorism)  protrudes 
slightly.  Percussion  of  an  abdomen  containing  free  fluid  elicits  a  dul- 
ness  of  the  dependent  portions  (see  p.  216).  this  dulness  shifts  with 
change  of  position.  Still  more  essential  to  the  diagnosis  of  free  fluid  is 
the  so-called  fluctuation  irave,  which  can  sometimes,  w^hen  the  patient  is 
moved,  be  appreciated,  even  by  inspection,  as  a  characteristic  flopping. 
If  the  tension  of  the  abdominal  contents  is  increased,  this  flopping  is 
not  visible,  but  frequently  the  peculiar  way  in  which  a  patient's  move- 
ment makes  the  abdomen  fall  to  one  side  like  a  heavy  body  shows  the 
presence  of  fluid,  in  contrast  to  mere  meteorism. 

The  presence  of  dilated  veins  in  the  abdominal  wall  (p.  55 
et  seq.)  aids  in  diagnosing  the  cause  of  the  free  fluid  in  the  abdominal 
cavity.  If  they  are  limited  to  the  sides  of  the  abdominal  wall  (Fig. 
17),  and  if  an  examination  shows  that  they  conduct  the  blood  from 
below  upward,  they  present  the  type  of  collateral  circulation  ob- 
served most  plainly  in  thrombosis  of  the  vena  cava  inferior.  In  this 
case  a  part  of  the  blood  which  should  proceed  through  the  vena  cava 
inferior  is  deflected,  and  flows  directly  from  the  lower  extremities, 
through  the  veins  of  the  anterior  abdominal  wall,  into  the  vena  cava 
superior.  Any  fluid  eff'usion  in  the  abdominal  cavity  might  compress 
the  vena  cava  inferior  enough  to  cause  some  obstruction  ;  hence,  this 
sign  of  a  collateral  circulation  is  of  slight  value  unless  the  venous  dila- 
tation is  very  marked.  Then  it  would  point  to  an  actual  thrombosis  of 
the  inferior  vena  cava.     On  the  contrary  (p.  56  et  seq.),  dilated  veins 


INSPECTION  OF  THE  ABDOMEN.  303 

which  occupy  more  the  middle  of  the  abdominal  wall,  radiating  from 
the  umbilicus  in  the  form  of  a  so-called  "  caput  Medusae,"  and  whose 
blood-current  plainly  flows  in  every  direction  from  the  umbilicus, 
would  point  to  an  anatomic  obstruction  of  the  portal  cir'culation  (cir- 
rhosis of  the  liver,  thrombosis  of  the  portal  vein).  It  must  be  acknow- 
ledged that  this  radiating  arrangement  is  not  a  striking  factor  in  every 
case  of  portal  obstruction,  but  its  median  position  and  the  direction 
of  the  blood-current  away  from  the  navel  is  constant  enough  to  be 
Sufficiently  diagnostic  (see  Fig.  18).  One  might  think  that  the  high 
pressure  of  any  effusion  in  the  peritoneal  cavity  would  cause  a  certain 
degree  of  portal  stasis  from  its  compressing  action,  and  therefore  pro- 
duce a  similar  collateral  circulation.  Yet  experience  shows  that  this 
type  of  collateral  circulation  is  practically  characteristic  of  cirrhosis  of 
the  liver  or  of  portal  thrombosis,  because  the  small  anastomotic  branches 
lying  between  the  portal  and  the  peritoneal  cavity  veins,  and  essential 
to  the  formation  of  this  collateral  circulation,  are  just  as  much  com- 
pressed by  ascites  as  the  portal  vein  is  itself  (see  p.  56  et  seq.).  It  is 
a  different  thing  with  the  portal  stasis  in  a  limited  sense,  which  arises 
from  a  portal  obstruction  due  to  hepatic  cirrhosis,  or  due  to  thrombosis 
of  the  portal  trunk  near  its  entrance  to  the  liver.  The  collateral  circu- 
lation is  then  undertaken  by  the  veins  of  the  ligamentum  teres  and  of 
the  serous  covering  of  the  liver. 

I/arge  ovarian  tumors  or  other  abdominal  cysts  are  differentiated 
from  effusions  of  free  fluid  by  inspection,  palpation,  and  percussion 
(p.  215  et  seq.).  With  them  the  greatest  degree  of  prominence  and 
resistance  is  in  the  median  line  of  the  abdomen,  not  in  the  more  depend- 
ent portions.  But  all  other  methods  of  examination  must  frequently 
be  employed  for  a  certain  differentiation. 

Knteroptosis  presents  to  inspection  a  peculiarly  characteristic  and 
practical  clinical  picture.  This  condition  depends  upon  a  relaxation  of 
the  abdominal  walls,  of  the  mesentery,  and  of  the  parietal  peritoneum ; 
it  is  more  frequently  observed  in  the  female  sex,  and  is  due  either  to  a 
marked  loss  of  the  subperitoneal,  submesenteric,  and  subcutaneous  fat, 
and  to  an  atrophy  of  the  abdominal  muscles,  or,  following  pregnancy,  to 
an  impaired  tension  of  the  stretched  abdominal  walls  and  peritoneum. 
In  the  latter  case  there  is  almost  always  associated  a  loss  of  fat  of  the 
abdominal  walls  and  of  the  abdominal  contents,  a  certain  atrophy,  and 
frequently  even  a  spreading  of  the  recti  muscles.  As  a  consequence 
the  abdominal  organs  are  abnormally  mobile  ;  the  liver  and  the  kidneys 
in  the  erect  posture  are  situated  lower  than  normal ;  the  right  kidney 
especially  gradually  draws  down  a  mesentery  for  itself  and  becomes  a 
movable,  or  even  a  genuine  floating,  kidney.  Without  sufficient  sup- 
port the  stomach  and  transverse  colon  may  drop  and  sink  deep  into  the 
abdomen.  The  weight  of  its  contents  causing  passive  distention,  fre- 
quently dilates  the  stomach.  When  the  physiologic  support  of  the 
abdominal  wall  fails,  the  intestines  become  distended  with  gas.  The 
skin  of  the  abdomen  becomes  lean,  withered,  and  frequently  wrinkled  ; 
in  patients  who  have  born  children  it  is  covered  with  striae.     The  walls 


304  INSPECTION  AND  PALPATION  OF  THE  ABDOMEN. 

are  so  thin  that  the  contour  of  the  stomach  and  intestines,  especially 
in  the  dorsal  decubitus,  can  be  made  out  very  plainly.  In  the  erect 
posture  a  veritable  paunch  is  noticed,  and  through  the  gaping  breach 
between  the  recti  abdominales  a  considerable  portion  of  the  abdominal 
contents  projects  like  a  hernia. 

Empty  intestines  in  inanition — e.  g.,  from  starvation  or  esophageal 
stenosis — produce  a  very  decided  retraction  of  the  abdomen.  A  similar 
appearance  in  tubercular  meningitis,  the  so-called  "  scaphoid  belly ,'^  is 
due  to  a  contraction  of  the  intestinal  muscles,  and  perhaps  of  the  abdom- 
inal muscles  as  well.  Inspection  sometimes  reveals  local  prominences 
(cysts,  tumors,  enlargement  of  the  abdominal  organs)  and  their  mobility 
with  respiration. 

PALPATION  OF  THE  ABDOMEN. 

METHOD  OF  PALPATION. 

The  first  requisite  is  a  thorough  relaxation  of  the  patient's  abdom- 
inal walls.  Therefore,  if  his  condition  permits,  place  the  patient  in  the 
dorsal  decubitus,  take  away  everything  from  under  his  head  except  a 
very  thin  pillow,  and  get  him  to  breathe  quietly,  regularly,  and  without 
exerting  abdominal  pressure.  Sometimes  flexing  the  knees  slightly  will 
help  to  relax  the  abdominal  walls.  Considerable  tension  of  the  belly, 
if  due  to  meteorisni,  can  frequently  be  relieved  and  the  examination  be 
facilitated  by  first  emptying  the  colon  of  feces  and  gas  with  the  aid  of 
a  copious  water  enema.  Great  tension  and  extreme  sensitiveness  of  the 
abdomen  may  necessitate  the  employment  of  anesthesia.  It  should, 
therefore,  never  be  neglected  in  any  serious  and  doubtful  case  if  there 
is  a  question  of  an  operation,  as  the  absolutely  relaxed  walls  under 
anesthesia  enable  the  examiner  to  make  a  more  thorough  examination.^ 

The  physician  himself  can  prevent  a  reflex  spasm  of  the  abdominal 
muscles  by  his  method  of  palpation.  If  his  hands  are  cold,  they 
shoukl  be  warmed  before  he  touches  the  patient's  belly.  He  should  not 
palpate  with  the  finger-tips,  but  always  with  the  flat  hand,  with  gradu- 
ally increasing  pressure.  All  hurried  movements  annoy  the  patient, 
render  the  examination  difficult,  and  are  therefore  to  be  avoided.  The 
more  superficial  should  precede  deeper  palpation,  because  the  former  is 
less  disagreeable  to  the  patient.  The  expiratory  retraction  of  the 
abdominal  walls  enables  one  to  press  the  hand  gradually  into  the  depths. 
At  first  the  hand  shoukl  be  placed  upon  the  spot  to  be  examined,  and 
left  there  quietly  during  both  inspiration  and  expiration.  The  way 
the  parts  under  the  hand  move  during  the  respiratory  excursion  should 
be  noted  ;  and  only  after  this  procedure  should  tactile  movements  be 
made  use  of  to  feel  the  entire  abdominal  surface.  In  palpating  painful 
affections  it  is  a  good  rule  to  begin  with  the  painless  parts,  thus  gaining 

'  According  to  the  writer's  view,  an  ether  examination  should  be  limited  to  the  deter- 
mination of  some  condition  which  might  require  a  decided  chanjje  in  therapy.  He 
emphasizes  this  because  such  examinations  and  exploratory  lai)arotomies,  the  former 
sometimes  not  less  dangerous  than  the  latter  to  the  patient's  well-being,  are  often  abused. 


PALPATION  OF  THE  ABDOMEN,  305 

the  patient's  confidence  and  distracting  his  attention.  This  is  especially 
to  be  recommended  in  examining  children.  The  examiner's  hand  should 
rest  as  comfortably  as  possible,  otherwise  its  sensitiveness  is  impaired. 
Bimanual  palpation  frequently  furnishes  very  useful  results ;  one  hand 
placed  upon  the  lateral  or  anterior  surface  of  the  abdomen  presses  the 
parts  against  the  other  hand  in  the  flanks,  in  the  vagina,  or  in  the 
rectum. 

In  all  difficult  cases  it  is  of  decided  advantage  to  palpate  in  differ- 
ent positions  of  the  body — e.  g.,  in  the  dorsal  decubitus,  the  right  and 
left  lateral,  the  erect,  and  the  knee-chest  posture. 

Rubbing  the  skin  of  the  abdomen  with  oil  or,  even  better,  with 
powdered  chalk  frequently  facilitates  an  examination.  The  palpating 
fingers  slip  over  the  skin  more  readily,  and  so  their  sensitiveness  is 
increased.  This  device  makes  palpation  less  disagreeable  and  less  pain- 
ful to  the  patient,  and  is  therefore  to  be  recommended. 

Jerky  or  interrupted  palpation  ("  dipping ")  is  often  advantageous 
for  certain  purposes.  The  palpating  hand  is  placed  flat  upon  the  part 
of  the  abdomen  to  be  examined  ;  then  quite  powerful  but  short  strokes 
are  employed  with  the  flat  hand  or  sometimes  with  the  fingers.  This 
method  may  demonstrate  the  collection  of  fluid  in  the  abdomen,  or  the 
presence  of  deeply  placed  solid  masses  covered  by  fluid  which  ordinary 
palpation  does  not  reach.  In  favorable  cases  the  deeply  placed  solid 
parts  seem  to  strike  the  palpating  hand,  because  the  blow  excites  such 
a  great  wave  movement  in  the  fluid.  The  same  method  of  palpation  is 
employed  in  obstetric  examinations,  the  so-called  "  ballotteraent "  of 
the  child's  head.  "  Dipping "  can  be  recommended  to  demonstrate 
enlargement  of  the  liver  or  of  the  spleen,  deep-lying  tumors  or  a  distended 
gall-bladder,  and  for  palpating  an  abdomen  tensely  distended  with  fluid 
where  ordinary  palpation  as  well  as  percussion  leaves  one  in  doubt. 

An  important  rule  in  palpating  the  abdomen  is  to  proceed  very 
cautiously,  since  roughness  can  very  easily  do  harm,  especially  in  acute 
inflammatory  afiections. 

GENERAL  RESULTS  OF  ABDOMINAL  PALPATION. 

Abdominal  palpation  should  appreciate  the  general  relations  of 
resistance  in  the  belly  (both  of  the  walls  and  of  the  abdominal  contents), 
the  palpable  boundaries  of  the  organs,  their  sensitiveness  to  pressure, 
and  any  local  resistances  and  tumors.  Palpation  then  quickly  confirms, 
completes,  and  corrects  the  results  of  inspection  in  regard  to  tlie  presence 
of  fat-accumulation,  of  edema  in  the  abdominal  wall,  of  fluid  within 
the  abdominal  cavity,  or  of  raeteorism.  The  "  fluctuation  wave  "  is  the 
best  method  o^  demonstrating  fluid.  One  hand  strikes  a  short,  sharp 
blow  upon  one  side,  over  a  dependent  portion  where  the  fluid  is  sus- 
pected, and  if  fluid  is  really  present  the  other  liand,  upon  a  diametrically 
opposite  spot  of  the  abdomen,  will  then  feel  a  ])lain  wave  transmission. 
Fluctuation,  in  the  ordinary  sense  of  the  word — /.  e.,  the  transmission 
of  slow  pressure  movements  through  the  abdomen — cannot  be  relied 

20 


306  INSPECTION  AND  PALPATION  OF  THE  ABDOMEN. 

upon  to  demonstrate  fluid  in  the  belly,  because  the  normal  intestines 
filled  with  air  fluctuate  in  that  sense.  The  distinct  transmission  of 
short  blows  is,  on  the  contrary,  quite  characteristic  of  the  presence  of 
fluid  rather  than  of  gas,  because  the  phenomenon  requires  a  considerable 
mass  and  there  is  the  delay  of  inertia  in  the  moved  substance. 

Enteroptosis  presents  to  palpation  an  abnormal  thinness  and  flabbi- 
ness  of  the  abdominal  walls,  and  hyperesthesia.  The  organs  may  all 
be  palpated  and  bounded  just  as  if  there  was  no  covering.  Tense 
intestinal  coils  and  a  stomach  distended  with  gas  are  often  much  more 
readily  outlined  by  palpation  than  by  percussion,  on  account  of  their 
firm  resistance,  like  an  air  cushion.  Contracted  intestinal  loops  feel 
like  tubes,  varying  in  size  from  the  little  finger  to  the  thumb.  They 
are  generally  movable  enough  to  be  rolled  under  the  finger.  The 
"  haustra "  of  the  large  intestines  can  sometimes  be  plainly  felt.  In 
palpating  abdominal  organs  this  respiratory  mobility  is  always  im- 
portant. (See  Special  Palpatory  Relations  of  Certain  Abdominal 
Affections.) 

In  palpating  tumors  or  iKithologic  resistances  we  should  carefully 
heed  their  position,  their  form,  their  size,  the  possibility  of  outlining 
their  boundaries,  their  consistence  (solid,  hard,  compact,  elastic,  fluc- 
tuating),^ the  character  of  their  surface  (smooth,  nodular),  and  their 
sensitiveness  to  pressure.  We  should  then  determine  from  what  organ 
the  tumor  arises ;  whether  it  is  covered  by  the  stomach  or  by  the 
intestines,  etc.  Artificial  distention  of  the  stomach  or  colon  will  often 
clear  up  this  part  of  the  examination.  The  stomach  can  be  distended 
either  by  means  of  an  effervescing  powder  or  by  inflation  through  a 
stomach  tube.  (See  Gastric  Examination.)  The  colon  is  most  con- 
veniently inflated  by  means  of  an  ordinary  Davidson  syringe.^  Infla- 
tion will  conceal  from  inspection,  percussion,  and  palpation  tumors 
which  are  situated  behind  the  stomach  or  colon  or  in  their  posterior  wall. 

In  determining  sensitiveness  to  pressure  very  gentle  palpation  is  first 
employed.  If  this  produces  no  pain,  more  force  is  used.  We  should 
then  determine  whether  there  is  sensitiveness  to  quiet  and  regular 
pressure  or  only  to  a  sudden  blow,  for  in  many  cases  the  sensitiveness 
is  produced  only  by  a  blow,  not  by  mere  pressure.  This  is  frequently 
the  case  in  peritonitis.  After  we  have  demonstrated  the  existence 
of  a  sensitiveness  to  pressure,  we  should  always  attempt  to  difieren- 
tiate  at  what  depth  it  is  situated.  By  pinching  up  the  skin  or  the 
entire  abdominal  wall  in  a  fold  we  can  readily  prove  whether  it  is 
merely  a  sensitiveness  of  the  abdominal  wall  and  of  the  skin  or 
whether  it  arises  from  the  abdominal  cavity.  If  ^^'e  can  determine  a 
hyperalgesia  of  the  unaltered  skin,  even  to  light  touch  or  to  pin  prick, 
over  the  painful  area  in  any  doubtful  painful  affection  of  the  abdominal 

^  There  is  a  special  sort  of  fluctuation,  the  so-called  "  hydatid  thrill,"  -which  is  some- 
times appreciated  over  echinococcus  cysts  by  striking  a  blow  upon  one  spot  of  the  tumor. 
The  thrill  proceeds  from  the  impact  of  the  daughter  bladders. 

^  It  is  frequently  necessary  beforehand  to  cleanse  and  empty  the  rectum  thoroughly 
with  a  copious  enema  of  water. 


PALPATION  OF  THE  ABDOMEN. 


307 


contents,  very  probably  the  pain  in  question  is  not  alone  peripheral  (or- 
ganic pain),  but  is  either  increased  or  exclusively  caused  by  central  stimu- 
lation ;  in  other  words,  the  patient's  suifering  depends  upon  more  than  an 
anatomic  change  limited  to  the  abdominal  contents.  Cutaneous  hyper- 
algesia plays  an  important  role  in  the  diagnosis  of  pseudoperityphlitis. 
This  is  a  painful  condition  of  the  iliocecal  region  which  often  arises 
psychically,  especially  since  public  attention  has  been  more  and  more 
attracted  to  the  vermiform  appendix.  (See  Examination  of  the  Nervous 
System;  Hyperalgesic  Zones  of  the  Skin  in  Diseases  of  Deep-lying 
Organs,  p.  774.)  Such  psychical  iliocecal  pain  is  frequently  responsible 
for  an  unnecessary  operation. 

SOURCES  OF  ERROR  IN  PALPATING  THE  ABDOMEN. 

The  abdominal  walls  frequently  resist  palpation  with  a  vigorous 
reflex  tension  which  no  device  can  control,  even  under  perfectly  physio- 
logic conditions.  The  individual  parts  of  the  abdominal  wall,  espe- 
cially the  muscular  bellies  and  tendinous  bands   of   the  recti,   vary 


Fig.  108.— Abdominal  aneurism.    (Specimen  from  an  autopsy  at  the  New  York  City  Hospital.) 


considerably  both  in  their  tension  and  in  their  resistance,  so  that  they 
sometimes  produce  the  impression  of  circumscribed  tumors  or,  at  least, 
of  pathologic  resistances.  This  is  even  more  striking  when  the  sec- 
tion of  the  abdominal  muscles  lying  directly  over  the  affected  parts 
becomes  reflexly  contracted  and  more  tense.  Abdominal  pressure  will 
facilitate  the  recognition  of  such  tense  muscle  bellies — e.  g.,  coughing 


308  INSPECTION  AND  PALPATION  OF  THE  ABDOMEN 

will  make  their  contour  still  plainer.  Examination  during  coughing  or 
during  increased  abdominal  pressure  is  an  especially  useful  means  of 
differentiating  whether  tumors  or  resistances  are  situated  beneath  or 
within  the  abdominal  wall.  Tension  of  the  abdominal  muscles  from 
coughing  will  cause  the  resistance  to  disappear  if  beneath  the  abdominal 
wall.  If  situated  in  the  wall  itself,  a  tumor  or  resistance  either  be- 
comes more  distinct  or,  at  least,  remains  just  as  plain  during  coughing. 
The  lobules  of  fat  of  the  panniculus  adiposus  may  simulate  a  nodular 
growth  within  the  abdomen.  The  same  methods  may  be  used  to  pre- 
vent this  source  of  error.  Contracted  intestinal  coils  are  often  plainly 
felt  through  thin  abdominal  walls,  as  if  they  were  cords  (see  p.  306). 
The  string-like  contracted  transverse  colon  running  across  the  abdomen 
is  often  mistaken  for  a  tubercular  degenerated  and  contracted  omentum. 
The  characteristic  mobility  of  the  transverse  colon,  which  we  can  ordi- 
narily roll  under  the  palpating  finger,  the  palpable  recognition  of  the 
haustra,  and  finally  the  results  gained  by  the  distention  of  the  colon 
from  the  rectum  (p.  306),  will  generally  prevent  a  mistake. 

Fecal  tumors  frequently  cause  an  error  in  diagnosis.  These  are  col- 
lection of  feces  in  the  colon,  sometimes  in  the  form  of  large  compact 
masses,  sometimes  in  that  of  smaller  tumors  arranged  in  a  row,  like 
a  string  of  beads.  Constipation  usually  accompanies  such  phenom- 
ena ;  but  fecal  tumors  are  sometimes  observed  even  in  patients  whose 
bowels  move  daily.  They  present  a  peculiar,  somewhat  doughy  con- 
sistence ;  they  can  frequently  be  crumbled  into  smaller  pieces ;  they 
are  often  arranged  characteristically,  like  a  string  of  beads ;  their  posi- 
tion in  the  course  of  the  colon  and  the  sigmoid  flexure  is  suggestive. 
The  coincidence  of  constipation,  the  lack  of  serious  symptoms,  and  the 
disappearance  of  the  masses  after  purgatives  or  enemata  should  prevent 
an  error  in  diagnosis.  Epigastric  or  aortic  pulsations  may  sometimes 
simulate  an  aneurism  or  a  tumor  (p.  300).  If  such  a  pulsation  is 
transmitted  to  a  tumor,  the  latter  might  be  taken  for  a  pulsating  tumor. 
Remembering  this  should  be  sufficient  to  prevent  the  mistake. 

SPECIAL   RESULTS   OF  PALPATION   IN   CERTAIN  AFFECTIONS  OF 
THE  ABDOMEN  AND    ITS  ORGANS. 

Inflammatory  exudations  are  appreciated  by  the  examiner  as  imperfectly  or  per- 
fectly circumscribed  tumor-like  resistances.  They  are  almost  always  passive  and 
immovable  with  respiration.  Perityphlitic  exudations  are  inflammatory  exudations 
characterized  by  their  peculiar  location  about  the  cecum.  In  spite  of  the  presence 
of  pus — i.  e. ,  appendicular  perforation  and  abscess — they  may  exhibit  a  very  firm 
consistence.  A  distinct  palpatory  differentiation  between  the  resistance  of  puru- 
lent and  of  non-purulent  appendicitis  has  often  been  attempted,  but  the  differ- 
ences are  only  those  of  degree.^  The  firm  resistance  which  has  been  claimed  to  be 
characteristic  of  the  so-called  stercoral  form  of  typhlitis  does  not,  as  was  supposed, 
depend  upon  feces,  but  is  caused  by  the  inflammatory  exudate  and  phlegmonous 
infiltration  of  the  tissues.  A  firm  tumor  (as  contrasted  with  a  diffused  resistance) 
is  very  likely  due  to  the  formation  of  thick  adhesions  and  localized  infiltration 
and  exudation.     Such  forms  are  also  frequently  perforative,  despite  their  gener- 

^  See  the  writei-'s  paper  upon  "The  Pathology  and  Treatment  of  Typlilitis,"  der 
Verhandlungen  des  XIII.  Cong./,  inn.  Med.  in  Miinchen,  1895,  Bergmann,  Wiesbaden. 


PALPATION  OF  THE  ABDOMEN. 


309 


ally  favorable  outcome.  The  long-continued  persistence  of  such  a  tumor,  des- 
pite the  lack  of  all  serious  appearances,  is  one  of  the  most  trustworthy  signs  of 
an  abscess  which  for  the  time  being  remains  quiescent.  Wherever,  despite  the 
most  serious  symptoms,  the  resistance  remains  merely  diffuse .  a  grave  state  of 
affairs  ordinarily  exists,  and,  frequently  enough,  primary  diffuse  perforative  peri- 
tonitis. Roux  considers  as  an  especially  characteristic  sign  of  pus  formation  the 
doughy  edematous  infiltration  of  the  cecal-wall,  appreciable  to  palpation  (like  thick 
blotting  paper).  Even  large  perityphlitic  abscesses  do  not  furnish  any  fluctuation 
until  very  late  in  their  course.  The  abdomen  itself,  on  account  of  its  air  con- 
tents, frequently  fluctuates  to  a  certain  extent.  A  perityphlitic  abscess  lies  in 
the  depths  and  is  surrounded  by  yield- 
ing walls ;  hence  fluctuation  is  absent  or 
indistinct.  If  the  walls  should  be  firm, 
the  resistance  from  the  infiltration  would 
prevent  the  appreciation  of  fluctuation. 
Not  infrequently  we  can  palpate  a  sort 
of  swashing,  gurgling,  or  splashing  over 
a  perforated  perityphlitic  abscess,  be- 
cause it  contains  gas  and  fluid.  But 
intestinal  coils  which  contain  air  and 
fluid  will  furnish  the  same  sign,  so  that 
it  is  not  diagnostic  of  a  gas-containing 
abscess  unless  it  is  very  striking  over 
an  area  where  the  presence  of  a  large, 
firm,  and  superficial  tumor  makes  the 
supposition  of  a  normal  intestinal  coil 
improbable.  A  cylindric,  rope-like 
body,  corresponding  in  its  form  and 
its  position  to  an  enlarged  appendix — 
i.  e.,  inside  and  below  the  cecum,  at 
the  edge  of  the  true  pelvis — will,  es- 
pecially if  it  is  sensitive  to  pressure, 
support  the  diagnosis  of  a  previous  at- 
tack of  appendicitis,  and  sometimes 
will  furnish  a  strong  argument  for  an 
interval  operation.  A  contracted  in- 
testinal coil  might  cause  confusion. 

In  the  anatomico-pathologic  sense 
of  the  word  a  tumor  is  appreciated  as  a 
firm,  often  hard,  and  lumpy  mass.  Tu- 
mors of  the  intestine  (those  of  the 
colon  are  much  the  commonest)  are 
best  characterized  by  the  resulting  in- 
testinal stenosis  and  by  their  mobility, 
which  latter,  unless  adhesions  occur, 
is  frequently  very  pronounced,  much 
more  so  than  with  any  other  abdomi- 
nal   organ.     Tumors   of    the    stomach 

are  generally  recognized  with  ease,  both  by  their  position  and  by  the  accompany- 
ing gastric  symptoms.  They  are  most  frequently  situated  at  the  pylorus.  Despite 
a  very  widespread  opinion,  they  should  not  be  searched  for  much  to  the  right  of 
the  median  line,  because,  as  a  result  of  the  loop  form  of  the  stomach,  the  pylorus 
reaches  only  slightly  to  the  right  (see  Fig.  74).  Moreover,  tumors  of  the  stomach 
frequently  lead  to  gastric  dilatation,  and  therefore  to  alterations  of  its  position. 
Hence  they  may  be  found  very  low  in  the  abdomen  and  quite  exceptionally  even 
in  the  pelvis.  The  best  way  to  determine  the  relations  of  a  gastric  tumor  is  to 
examine  the  stomach  both  when  empty  and  when  distended  with  gas.  (See  Ex- 
amination of  the  Stomach,  p.  854.)  Gastric  tumors  are  generally  but  slightly- 
movable  with  respiration ;  but  there  are  countless  exceptions. 


Fig.  109. — Sarcoma  of  the  kidney,  with  the- 
descending  colon  pushed  to  one  side  and  for- 
ward. 


310  INSPECTION  AND  PALPATION  OF  THE  ABDOMEN 

Renal  tumors,  wMch  grow  from  the  loins,  can  scarcely  be  pushed  forward  by 
the  posterior  palpating  hand.  Besides,  while  growing  forward,  they  still  remain 
covered  by  the  hepatic  or  splenic  flexures  of  the  colon.  This  covering  can  be 
plainly  demonstrated  to  jjercussion,  palpation,  and  inspection  (Fig.  109),  by  infla- 
ting the  colon  with  gas  (inserting  an  ordinary  Davidson  syringe  in  the  rectum). 
If  we  inflate  by  jerks,  inspection  and  palpation  will  probably  show  the  anterior 
position  of  the  colon  most  distinctly.  Eenal  tumors  sometimes,  but  not  neces- 
sarily, move  with  respiration.  Hydronephrosis  gives  rise  to  a  renal  tumor  which 
is  characterized  by  an  elastic  consistence,  and  sometimes  also  by  a  change  in 
size  coinciding  with  the  alterations  in  the  amount  of  urine. 

Tumors  of  the  liver  and  of  the  spleen  are  characterized  by  their  position  and 
by  their  relation  to  organ  boundaries,  which  we  can  definitely  palpate  and  percuss, 
and  also  by  their  marked  mobility  with  respiration. 

Tumors  of  the  mesenteric  and  retroperitoneal  glands  are  characterized  chiefly 
by  their  multiplicity ;  by  the  rounded  contour  of  the  individual  tumors  ;  by  their 
deep  position  underneath  the  intestines,  recognized  by  percussion  as  well  as  by 
palpation  ;  and  by  their  etiology,  for  they  are  generally  metastatic.  Tuberculous 
retroperitoneal  and  mesenteric  glands  j^resent  similar  conditions.  Tuberculous 
tumors  of  the  peritoneum  are  palpated  as  nodular  or  irregularly-defined  resistances. 
The  tubercular  infiltrated  and  retracted  omentum  presents  a  very  characteristic  pic- 
ture. It  can  be  felt  as  a  knobbed  cord  between  the  xiphoid  process  and  the  navel, 
running  horizontally  and  superficially.  It  may  sometimes  closely  simulate  an  en- 
larged and  uneven  liver.  Tumors  of  the  bladder  and  tumors  grotoing  out  from  the 
pelvis  are  charactei'ized  by  their  position,  which  can  be  more  accurately  established 
by  means  of  a  rectal  or  vaginal  examination. 

Diffuse  enlargements  or  low  position  of  the  liver  are  recognized  quite  easily  by  the 
shape  of  the  resistance  ;  the  determination  of  the  sharp  hepatic  edge ;  and  the  res- 
piratory mobility.  The  diminution  in  the  size  of  the  liver  in  acute  yellow  atrophy  and 
in  cirrhosis  can  safely  be  diagnosed  by  palpation  and  percussion  only  where  the 
previous  position  of  the  liver  edge  has  been  known,  The  normal  liver  is,  however, 
not  always  palpable,  depending  upon  the  thickness  of  the  abdominal  covering  and 
upon  the  extent  of  the  respiratory  excursions.  In  palpating  the  liver  border  it  is 
often  very  important  to  recognize  the  normal  notch  at  the  insertion  of  the  ligamen- 
tum  teres.  Enlargement  of  the  gall-bladder  from  biliary  stasis,  gall-stones  or 
empyema  may  be  characteristically  localized  by  palpating  just  to  the  right  of  this 
notch,  where  we  can  frequently  very  plainly  follow  the  sharp  edge  of  the  liver 
above  the  rounded  or  gourd-shaped  tumor,  the  gall-bladder.  Occasionally  we  can 
feel  one  very  large  or  countless  small  gall-stones  enclosed  in  the  enlarged  gall- 
"bladder  of  a  gall-stone  affection.  Any  hard  places  are  usually  caused  by  an 
inflammatory  thickening  of  the  wall  or  by  carcinomatous  infiltration,  which  so 
frequently  follows  old  cases  of  cholelithiasis.  '^ Dipping'' — i.  e.,  jerky  palpation 
— over  the  enlarged  gall-bladder  will  sometimes  bring  out  a  crepitating  or  grating 
of  the  gall-stones  upon  each  other.  If  we  cannot  feel  the  enlarged  gall-bladder 
in  cholelithiasis,  we  frequently  can  feel  a  peculiar  tongue-like  projection  of  the 
liver  drawn  out  by  the  enlargement  of  the  gall-bladder  and  situated  directly  above 
it  (Eiedel)  (Fig.  ilO).  A  similar  or  even  larger  projection  can  be  determined  over 
the  corset  liver  (Fig.  111).  Alterations  in  the  liver  consistence — e.  g.,  the  char- 
acteristic induration  of  cirrhosis — can  bo  easily  recognized  at  the  thin  sharp  liver 
edge,  provided  the  patient  has  thin  and  relaxed  abdominal  coverings.  The  large 
lumps  or  nodules  of  the  lobulated  syphilitic  or  carcinomatous  liver  are  still  easier 
to  feel. 

It  is  generally  easy  to  palpate  a  dislocated  or  movable  kidney,  especially  if  the 
dislocation  is  marked  {true  floating  kidnei/).  It  is  commoner  upon  the  right  side. 
The  best  method  of  palpation  in  difiicuit  cases  is  with  the  left  hand  behind  the 
loin  to  push  against  the  right  hand  palpating  the  organ  from  in  front  with  the 
abdominal  walls  as  relaxed  as  possible.  A  movable  kidney  can  then  be  recognized 
as  a  bean-shaped,  vertically  placed  body  between  the  two  palpating  hands.  At 
times  it  is  somewhat  sensitive  to  pressure.  At  the  height  of  inspiration  it  may  be 
partially  grasped  between  the  two  hands.     The  deep  location,  the  verification  of 


PALPATION  OF  THE  ABDOMEN. 


311 


the  upper  bluntly  rounded  end  of  the  kidney,  the  lack  of  any  sharp  edge  which 
could  correspond  to  the  liver  border,  should  prevent  confusion  with  a  corset  liver. 
Sometimes  the  hilus  and  the  pulsating  renal  artery  on  the  concave  side  of  the 


Fig.  110.— Riedel's  projection  of  the  liver  in  cholelithiasis. 

kidney  can  be  felt.  With  this  condition  the  abdominal  walls  are  frequently  much 
relaxed,  so  that  it  is  sometimes  possible  to  feel  a  dislocated  kidney  better  in  the 
standing  or  sitting,  than  in  the  recumbent,  posture.    If  the  walls  are  very  relaxed, 


Fig.  111.— Corset  liver  (Frerichs). 


the  lower  end  of  even  a  normally  placed  kidney  may  be  felt.     A  disregard  of  this 
fact  has  led  to  the  diagnosis  of  entirely  too  many  "wandering  kidneys." 

Diffuse   e7ilargement  of  the  spleen,   acute  splenic  swelling,  passive  congestion  of 


312  INSPECTION  AND  PALPATION  OF  THE  ABDOMEN. 

the  spleen,  the  spleen  of  leukemia,  of  pseudoleukemia,  and  of  intermittent  fever  are 
all  very  easily  palpated  and  determined  by  their  position,  shape,  and  mobility 
with  respiration.  The  very  large  splenic  tumor  of  leukemia  and  malaria  often 
shows  one  or  more  horizontal  notches  on  the  anterior  edge  (Fig.  112),  and  its 
anterior  surface  is  smooth  and  reaches  some  distance  below  the  navel.  Acute 
splenic  swelling  in  typhoid  fever  and  other  infectious  diseases  can  sometimes  be  de- 
monstrated only  at  the  height  of  inspiration  when  its  inferior  edge  is  felt  just 
below  the  costal  margin.  This  is  of  far  greater  diagnostic  import  than  the  results 
of  splenic  percussion,  which,  as  we  have  seen,  are  frequently  untrustworthy.  In 
adults  a  spleen  of  normal  size  can  only  very  exceptionally  be  palpated  beneath 
the  rib  margin  even  with  deep  inspiration,  and  then  the  abdominal  walls  are  gen- 
erally very  lax  or  the  organs  are  dislocated  (floating  spleen,  enteroptosis).  In 
young  children,  however,  this  is  frequently  possible,  and  therefore  with  them 
one  must  be  rather  cautious  in  diagnosing  splenic  enlargement.  To  recognize  a 
moderate  grade  of  splenic  enlargement  by  palpation  we  should  examine  both  in 


Fig.  112.— Splenic  tumor  of  leukemia. 

the  dorsal  decubitus  and  in  the  right  semilateral  position  (diagonal  position). 
Sometimes  one  and  sometimes  the  other  position  ftirnishes  better  results.  In 
palpating  the  spleen,  stand,  if  possible,  upon  the  right  side  of  the  sick-bed,  place 
the  palpating  right  hand  as  flat  as  possible  upon  the  left  hypochondrium,  with 
the  fingers  at  the  costal  margin,  and  with  each  expiration  gradually  exert 
slightly  more  pressure  and  attempt  to  feel  the  edge  of  the  spleen  during  deep 
inspiration.  Especially  in  typhoid  fever  a  splenic  enlargement  can  be  felt  only 
at  the  end  of  deep  inspiration.  In  very  sick  cases  the  best  method  is  from  time 
to  time  to  encourage  one  or  two  deep  inspirations,  because  frequently  repeated 
respiratory  efforts  tire  the  patient  and  his  breathing  becomes  very  superficial. 
Trying  to  feel  the  spleen  with  the  fingers  hooked  in  under  the  rib  margin  from 
above  ordinarily  produces  such  vigorous  reflex  abdominal  contraction  that  nothing 
else  can  be  felt.  Correct  splenic  palpation  requires  much  practice.  It  is  a  good 
preparation  for  abdominal  palpation. 

Large  left-sided  pleural  effusions  sometimes,  though  exceptionally,  dislocate 


PALPATION  OF  THE  ABDOMEN.  31S 

the  spleen  sufficiently  for  it  to  be  palpable.  Ferber  explains  this  peculiarity  (his 
opinion  is  supported  by  postmortem  researches)  in  this  way:  Such  effiisions  push 
the  spleen  so  that  the  posterosuperior  end  reaches  forward,  the  inferior  end, 
backward  ;  hence  the  long  axis  of  the  spleen  assumes  at  first  a  vertical  position, 
and  finally  a  direction  from  in  front  and  above  backward  and  downward.  In  other 
cases  the  upper  edge  of  the  spleen  is  turned  so  toward  the  interior  by  the  dia- 
phragm, bowing  convexly  downward,  that  the  splenic  surface  lies  no  longer  verti- 
cally, but  horizontally.  Both  results  are  thoroughly  unfavorable  for  palpation, 
and,  besides,  the  respiratory  mobility  is  lost,  because  the  diaphragm  on  that  side 
is  almost  stationary.  What  we  often  mistake  for  the  sjjleen  in  these  cases  is  the 
bulging  of  the  depressed  diaphragm  running  parallel  to  the  costal  border  (see  Fig. 
97,  /.,  206). 

(Compare  the  section  on  Examination  of  the  Stomach  in  regard  to  the 
palpability  of  the  spleen  in  certain  cases  of  gastric  dilatation.) 

A  distended  bladder  is  easy  enough  to  recognize  after  it  has  once  been  felt. 
It  may  be  confused  with  the  jjregnant  uterus,  with  other  enlai'gements  of  the 
uterus,  with  ovarian  tumors,  and  with  inflammatory  exudations.  To  differentiate 
we  must  utilize  other  methods  of  examination — e.  g.,  by  vagina,  and  especially 
examination  after  catheterization. 

A  peritoneal  friction  rub  may  be  appreciable  to  palpation  over  the  different 
organs  or  over  tumors  of  the  abdomen.  The  friction  can  be  felt  as  a  rough  gra- 
ting with  the  respiratory  and  palpatory  moving  of  the  parts.  It  may  also  be 
appreciated  by  auscultation  (see  p.  286).  These  friction  murmurs  can  be  produced 
by  any  uneven  surface  (tumor  surface),  but  in  most  of  the  cases  they  are  caused 
by  inflammatory  deposition  of  fibrin.  Splenic  enlargement  (in  leukemia)  frequently 
leads  to  perisplenic,  and  cholelithiasis  to  periheiDatic,  friction  murmurs. 

Peristaltic  intestinal  noises  can  also  be  appreciated  by  palpation.  (See  Section 
on  Auscultation  of  the  Abdomen,  p.  286.) 

' '  Dipping ' '  over  the  abdomen  will  elicit  a  splashing  wherever  both  fluid  and 
gas  are  present  in  the  digestive  tract  or  in  the  peritoneal  cavity.  We  can  feel 
splashing  over  the  stomach  and  over  the  region  of  the  small  intestine  normally. 
Over  the  large  intestine,  splashing  signifies  that  a  diarrhea  is  either  already 
present  or  impending.  Splashing  over  the  sigmoid  region  frequently  depends  upon 
the  overlying  small  intestine,  and  cannot  be  trusted  for  diagnosis.  Over  the  cecal 
region,  splashing  may  generally  be  considered  pathologic,  and  might  suggest  the 
possibility  of  typhoid  fever.  Concerning  the  splashing  and  swashing  in  perityph- 
litis, see  page  309.  Concerning  the  splashing  of  the  stomach,  see  Stomach  Ex- 
amination (p.  354).  Shaking  noises  of  the  abdomen  (p.  286),  which  appear  when 
patients  move,  can  ordinarily  be  felt  as  well  as  heard. 


314  DIAGNOSIS  OF  INDIVIDUAL   VALVULAR  LESIONS. 

DIAGNOSIS  OF  INDIVIDUAL  VALVULAR  LESIONS,  OF 
AORTIC  ANEURISMS,  AND  OF  PERICARDITIS. 

To  appreciate  this  section  the  reader  should  first  study  the  sections 
upon  Cardiac  Percussion  and  Auscultation,  and  upon  Palpation  and 
Inspection  of  the  Cardiac  Region. 

FOUNDATIONS  OF  THE  PATHOLOGIC  PHYSIOLOGY  OF 
VALVULAR  LESIONS. 

EFFECT  OF  VALVULAR  LESIONS  UPON  THE  CIRCULATION;  ME- 
CHANICS OF  COMPENSATION ;  LAWS  GOVERNING  THE  ALTER- 
ATIONS OF  SIZE  OF  THE  INDIVIDUAL  HEART  CHAMBERS  IN 
VALVULAR  LESIONS. 

To  understand  the  symptom-complex  of  any  valvular  lesion  we  must 
appreciate  :  the  fundamental  factors  of  physical  diagnosis  (outlined  in 
the  preceding  sections),  the  effect  of  each  individual  valvular  defect 
upon  the  circulation,  and  the  anatomic  changes  and  the  modifications  of 
the  functions  of  the  individual  heart  chambers  which  are  produced  by 
the  wonderful  efforts  of  compensation.  In  the  following  introduction 
we  give,  to  avoid  repetition,  the  fundamental  factors  of  the  pathologic 
physiology  of  valvular  lesions  : 

Any  valvular  lesion,  whether  a  stenosis  or  an  insufficiency,  from  the 
moment  of  its  origin  leads  to  certain  alterations  in  the  distribution  of 
pressure  upon  each  side  of  the  affected  valve.  If  the  body  and  the 
heart  itself  did  not  possess  a  series  of  powerful  compensatory  aids  to 
improve  this  relation  of  altered  pressure,  then  every  serious  lesion  at  its 
very  inception  would  not  only  cause  serious  general  disturbances  of  cir- 
culation, but  very  soon  prove  fatal.  Experience  shows  that  neither  is 
the  case.  Without  compensation  the  blood  in  every  valvular  lesion 
would  be  collected  behind  the  diseased  valve,  and  peripherally  the 
blood-mass  and  arterial  pressure  would  gradually  diminish  more  and 
more.  The  heart's  reserve  power  prevents  to  a  certain  extent  such  a 
dangerous  condition  ;  the  sections  of  the  heart  lying  behind  the  injured 
valve  work  harder,  diminish  the  blood-stasis,  furnish  enough  blood  to 
the  peripheral  arteries,  and  so  prevent  a  dangerous  fall  of  the  arterial 
pressure.  The  reserve  power  is  utilized  in  stenosis  to  overcome  the 
■  obstacle  ;  whereas  in  insufficiency  it  must  force  more  blood  forward 
during  the  succeeding  phase  through  the  injured  valve.  Rosenbach  and 
Cohnheim  produced  artificial  valvular  lesions  in  animals,  and  proved 
that  immediately  after  the  onset  of  a  lesion  an  increase  of  cardiac  work 
prevented  any  serious  consequences  to  the  circulation.  To  effect  this 
increased  work  permanently,  anatomic  changes  in  the  heart  are  bound 
to  ensue  within  a  short  time.  These  consist  in  hypertrophies  and  dilata- 
tions of  the  different  chambers. 

Under  the  head  of  Compensation  we   include  the  entire  complex, 


PATHOLOGIC  PHYSIOLOGY  OF   VALVULAR  LESIONS.        315 

increased  filling  and  increased  work  of  certain  heart  chambers  with 
their  resulting  dilatation  and  hypertrophy — i.  e.,  the  sum  of  all  those 
functional  and  anatomic  changes  which,  in  spite  of  serious  lesions  of 
the  valvular  apparatus,  correct  the  fault  up  to  a  certain  point,  render 
life  possible,  and  also  warrant  a  condition  of  circulation  subjectively 
endurable  to  the  patient.  Compensation,  however,  does  not  make  the 
circulation  normal,  because  the  pressure  behind  the  valve  must  be  kept 
abnormally  high,  so  that  despite  the  resistance  the  essentials  for  the  cir- 
culation may  be  preserved.  What  compensation  accomplishes  is  only 
to  keep  the  pressure  in  the  systemic  arteries,  capillaries,  and  vejns  within 
the  physiologic  limits,  so  that  the  current  rapidity  and  volume  of  the 
circulation  is  approximately  normal,  and  so  that  in  consequence  the  most 
essential  bodily  functions  can  be  performed  without  the  patient  feeling 
very  sick.  To  fulfil  all  these  requirements,  the  compensatory  changes 
must  naturally  prevent  the  increase  of  pressure  from  working  backward 
behind  the  next  valve.  Therefore,  in  mitral  lesions  the  most  perfect 
compensation  will  not  change  the  increase  of  blood-pressure  and  volume 
within  the  pulmonary  circulation.  Such  patients  suffer  from  dyspnea 
in  case  of  any  unusual  demands  upon  the  respiration  (see  p.  86). 

This  conception  of  compensation  is  only  a  relative  one.  In  this  connection 
another  point  should  be  mentioned.  In  stenoses  of  the  auriculoventricular 
valves  and  in  all  insufficiencies  ^  compensation  does  not  prevent  a  stasis  in  the 
chambers  situated  behind  the  obstacle.  The  general  circulation  in  these  valvular 
lesions  therefore  suffers  from  a  poverty  of  blood,  because  the  mass  of  blood  which 
permanently  distends  these  congested  chambers  is  of  no  avail  to  the  circulation. 
We  do  not  yet  know  whether  in  these  cases  the  circulation  adapts  itself  to  such  a 
condition  by  narrowing  the  remaining  vascular  system,  or  whether,  in  order  to 
make  up  for  the  deficit,  the  blood-mass  gradually  increases.  Unless  the  latter  is 
the  case,  the  deficit  in  the  circulation  would  act  something  like  a  venesection  and 
be  essentially  equalized  by  a  narrowing  of  that  part  of  the  vascular  system  which 
is  not  dammed. 

Dilatations  and  hypertrophies  of  separate  heart  chambers  follow 
very  simple  physiologic  laws,  and  from  them  the  cardiac  condition  in 
any  valvular  lesion  can  be  determined. 

These  laws  are  as  follows  : 

.1.  Any  heart  chamber  which  suffers  an  increase  of  pressure  only 
during  systole  hypertrophies — i.  e.,  corresponding  to  the  greater  amount 
of  work,  its  muscle  increases  in  thickness,  without  an  increase  in  the 
size  of  the  cavity  (primary  hypertrophy).^ 

^  The  stenoses  of  the  arterial  orifices  behave  differently,  because  they  are  the  only 
valvular  lesions  where,  during  the  stage  of  compensation,  there  exists  no  increase  of 
diastolic  pressure  above  the  obstacle ;  in  other  words,  the  pressure  during  systole  is 
increased,  but  their  is  no  damming  behind. 

^  The  pathologists  designate  this  kind  of  hypertrophy  of  the  cardiac  wall  in  which 
the  included  cavity  is  not  enlarged  as  simple  hypertrophy,  in  contrast  to  the  so-called 
eccentric  hypertrophy,  in  which  wall  thickness  and  cavity  both  increase  (see  the  following 
note).  It  does  not  seem  easy  to  explain  why  an  enlargement  of  the  cardiac  cavity  does 
not  always  result  as  a  consequence  of  the  growth  of  the  muscular  elements,  but  since  an 
enlargement  of  a  heart  cavity  would  increase  the  amount  of  work,  it  is  clear  how  very 
injurious  to  the  progress  of  compensation  such  an  enlargement  would  be.  As  a  matter 
of  fact  it  can  be  proved  mathematically,  as  well  as  demonstrated  experimentally,  that 
the  cavity  must  increase  in  size  coincident  with  the  increase  in  size  of  its  walls.     For 


316  niAGXOSIS  OF  INDIVIDUAL   VALVULAR  LESIONS. 

2.  Every  heart  chamber  which  suffers  an  increase  of  pressure  during- 
diastole — /.  e.,  which  is  filled  over  normal — becomes  enlarged  {prinmry 
dilatation,  dilatation  from  increased  diastole,  compensatory  dilatation).  In 
order  that  the  circulation  shall  be  well  preserved,  it  is  necessary  for 
the  resulting  dilated  chamber  to  contract  completely  or  very  nearly  so. 
Therefore  it  must  accomplish  more  work,  because,  as  is  well  known,  the 
work  done  during  systole  equals  the  product  of  the  svstolic  volume  by 
the  pressure  to  be  overcome.  As  a  result  of  this  increase  of  cardiac 
work  incumbent  upon  such  a  heart  chamber,  its  walls  must  eventually 
hypertrophy  [secondary  hypjertrophy).  This  hypertrophy  is  apparent 
either  in  an  increase  of  thickness  of  the  walls  or  (perhaps  more  prob- 
ably) in  a  preservation  of  their  normal  thickness  despite  the  dilatation.^ 

3.  Where  the  conditions  for  primary  hypertrophy  and  primary  dila- 
tation occur  coincidentally,  hypertrophy  and  dilatation  of  the  heart 
chamber  in  question  may  take  place  entirely  independently  of  each 
other. 

4.  In  addition  to  the  pyrimary  dilatation  mentioned  above  (Law  2), 
a  so-called  secondary  dilatation  may  arise.  The  latter,  for  the  same 
reasons  as  under  Law  2,  occurs  if  a  heart  chamber  without  any  primary 
increase  in  its  blood-supply  is  not  able  to  contract  fully,  and  so  during 
diastole  suffers  an  increased  pressure,  because  the  blood  entering  finds 
a  certain  amount  of  blood  left  there  from  the  preceding  diastole.  This 
type  of  dilatation  depending  upon  an  incomplete  systole  is  called  a 
secondary  or  pjaralytic  dilatation.  It  has  no  compensatory  significance, 
as  contrasted  with  the  type  of  dilatation  described  under  Law  2,  which 
is  (as  we  shall  see  from  examples)  of  decided  value  to  the  circulation, 
and  therefore  fittingly  called  a  compensatory  dilatation. 

Dilatations  due  to  incomplete  systole  are  most  frequently  met  with, 
in  the  so-called  compensatory  disturbances  of  heart  lesions  (see  below). 
Here,  despite  the  variation  in  their  causation,  they  all  possess  this 
common  attribute,  they  all  depend  upon  cardiac  weakness,  with  the 
result  that  systole  becomes  weaker  and  the  systemic  arteries  are  less 
completely  filled  than  during  compensation.  By  the  appearance  of 
secondary  or  paralytic  dilatations  these  disturbances  of  compensa- 
tion can  alter  the  primary  picture  of  compensated  valvular  lesions  in 
manifold  ways.  Such  secondary  alterations  may  disappear  when  the 
heart  has  regained  its  complete  power,  or  they  may  remain  permanent 

example,  suppose  we  place  one  of  the  writei-'s  glutoid  capsules  (Deutsch.  med.  Woch., 
1897,  Xo.  1),  filled  -(vith  some  oily  substance,  in  a"  2  per  cent,  solution  of  muriatic  acid 
and  let  it  stand  at  an  incubator  temperature.  The  capsule-wall  will  gi-adually  swell,  and, 
since  there  can  be  no  increase  in  the  internal  contents,  the  surface  will  become  indented, 
the  wall  sinking-  in  to  fill  up  the  space  gained.  Now,  how  can  we  explain  the  difl'erent 
behavior  in  the  growth  of  the  heart-wall  so  that  there  results  a  pure  simple^  hyper- 
trophy without  any  dilatation?  Perhaps  it  is  because  a  growth  of  muscular-  fibers  in 
the  layei-s  of  the  nivocardium  surrounding  the  cavity  is  made  mechanically  impossible 
by  the  maximum  svstolic  compression.  This  compression  pei-sists  as  long  as  a  ventricle 
for  which  the  requirements  for  a  pure  hypertrophy  are  present— ('.  e.,  increased  resist- 
ance to  the  systole — is  able  by  means  of  the  reserve  power  at  its  disposal  to  conti-act 
itself  completelv. 

^  "Wliat  the  writer  has  called  secondary  hypertrophy  is  the  same  condition  pathologists. 
designate  as  eccentric  hypertrophy. 


PATHOLOGIC  PHYSIOLOGY  OF  VALVULAR  LESIONS.        317 

■despite  the  cure  of  the  compensatory  disturbance — e.  g.,  the  secondary 
dilatation  of  the  hypertrophied  right  ventricle  in  mitral  insufficiency. 
The  persistence  of  such  secondary  alterations  may  perhaps  be  explained 
by  the  fact  that,  if  a  heart  chamber  has  once  been  enlarged  by  a  para- 
lytic dilatation,  its  recovery  is  rendered  difficult,  because  the  opposition 
to  systolic  contraction  increases  in  proportion  to  the  increase  in  its  con- 
tents (since  the  work  of  a  heart  chamber  in  contracting  is  equal  to  the 
product  of  its  systolic  volume  by  the  opposed  pressure).  If  this  opposi- 
tion to  systole  caused  by  the  dilatation  reaches  such  a  grade  that  the 
secondary  hypertrophy  of  the  cardiac  muscle  is  no  longer  able  to 
equalize  the  dilatation,  but  is  limited  to  propelling  the  normal  volume 
of  blood  from  the  diastolic  position,  then  the  heart  chamber  in  question 
will  finally  to  a  certain  extent  become  decidedly  dilated.  In  this  way 
a  paralytic  dilatation  will  persist  anatomically  fixed  notwithstanding  the 
fact  that  the  compensatory  disturbance  has  receded. 

Even  without  the  previous  appearance  of  a  distinct  disturbance  in 
compensation,  similar  dilatations  sometimes  affect  those  chambers  of  the 
heart  which,  according  to  Law  1,  should  be  purely  hypertrophied,  be- 
cause they  have  been  subjected  not  to  greater  filling,  but  merely  to 
increased  systolic  pressure.  The  most  frequent  instance  is  again  the 
dilatation  of  the  right  ventricle  in  mitral  insufficiency,  which  may 
occur  even  without  any  disturbance  in  compensation.  Such  dilatations 
are  in  a  measure  related  to  the  paralytic  dilatations  after  a  compensatory 
disturbance  which  are  described  above  as  anatomically  fixed.  The  fact 
that  such  a  disturbance  in  compensation  does  not  precede  can  probably 
be  explained  by  assuming  that  the  dilatation  in  these  cases  begins  quite 
gradually,  not  from  an  acute  loss  of  cardiac  power,  but  in  consequence 
of  a  slow  increase  in  the  obstacle,  which  has  gone  too  far  to  permit  the 
persistence  of  a  complete  systole,  and  by  further  assuming  that  this  dila- 
tation is  rendered  comparatively  harmless  by  the  hypertrophy  which 
develops  step  by  step  and  becomes  at  the  same  time  fixed. 

Another  conception  of  such  primary  dilatation  of  certain  chambers  of  the 
heart  which  are  simply  under  higher  pressure  during  the  systole  and  have  not 
been  subjected  to  greater  filling  (as  in  aortic  and  pulmonic  stenosis)  is  that  it  is 
a  compensatory  phenomenon.  The  ventricle  subjected  to  an  excessive  systolic 
pressure  reaches  a  greater  degree  of  efficiency  when  its  musculature  is  distended, 
just  as  a  skeletal  muscle  gains  in  power  with  an  increase  in  the  distance  between 
its  two  extremities.  Nevertheless,  the  writer  would  not  venture  to  claim  that  in  this 
respect  the  heart  acts  in  an  analogous  manner  to  the  skeletal  muscles,  nor  that 
this  explanation  is  a  better  one  than  the  preceding. 

After  we  have  reviewed  these  latter  observations  Ave  find  that  we 
must  modify  Law  1,  for  an  increased  resistance  to  the  systole  of  a 
heart  chamber  ^  can  produce  a  pure  hypertrophy  of  its  wall  only  so 
long  as  this  resistance  does  not  overstep  a  certain  degree,  but  as  soon 
as  this  point  is  passed  incomplete  systole,  dilatation,  and  finally  second- 
ary hypertrophy  of  the  dilated  heart  chamber  occur.  Perhaps  this  will 
explain  the  peculiarity  that  in  some  cases  of  clironic  nephritis  we  find 
a  pure  hypertrophy,  and  in  other  cases  a  hypertrophy  with  dilatation  of 
the  heart. 


318  DIAGNOSIS  OF  INDIVIDUAL   VALVULAR  LESIONS. 

It  has  often  been  questioned  whether  such  heart  chambers,  enlarged  by  par- 
alytic dilatation  and  later  anatomically  fixed  in  their  dilatation,  ever  contract 
again  completely  in  sjiite  of  their  increased  contents,  or  whether  they  permanently 
produce  incomplete  systoles.  An  objection  to  the  former  of  these  two  possibilities 
is  that  if  no  stasis  occurs,  provided  a  circulation  is  permanently  possible,  the  other 
heart  chambers  will  be  more  extensively  dilated  during  diastole  in  order  to  receive 
the  excess  of  the  propelled  blood,  and  so  they  will  be  obliged  to  accomplish  cor- 
respondingly more  work  during  systole,  and  for  this  purpose  they  must  naturally 
be  permanently  dilated  and  at  the  same  time  hj^ertrophied.  This  would  finally 
result  in  an  entirely  purposeless  enlargement  of  and  in  excessive  work  for  the 
entire  heart,  and  besides  in  a  purposeless  increase  in  the  circulation  (excessive 
compensation).  It  is  not  possible  to  defiiiitely  and  absolutely  decide  whether  such 
conditions  of  the  circulation  can  really  occur.  They  are  quite  opposed  to  the 
teleologic  conception  of  the  jn-ocess  of  compensation.  If  so,  these  permanent  ex- 
cessive burdens  of  the  heart  which  increase  ^ith  each  disturbance  in  compensation 
will  furnish  an  explanation  for  the  fact  that  practically  every  heart  lesion  leads, 
sooner  or  later,  to  a  definite  cardiac  insufficiency,  although  the  causal  vahoilar 
lesion  does  not  grow. 

To  decide  whether  such  a  heart  chamber  with  fixed  paralytic  dilatation 
always  contracts  incompletely  depends  \ery  closely  upon  another  question : 
Does  the  systole  of  the  heart,  under  physiologic  conditions,  always  contract 
completely,  or  is  it  sometimes  also  incomplete?  This  latter  question  must, 
it  seems  to  the  writer,  according  to  our  present  knowledge,  be  answered  in  the 
following  way  :  The  ventricle  contracts  completely  or  almost  completely  if  the 
obstacles  opposed  to  its  systole  are  normal.  It  should  act  in  the  same  way  so  long 
as  the  obstacles  to  its  emptying  are  only  slightly  increased.  Aside  fi-om  the  teleo- 
logic significance  which  the  latter  condition  possesses  for  the  preservation  of  the 
circulation  even  under  somewhat  more  difiicult  conditions,  the  writer  sees  a  clinical 
demonstration  in  proof  of  it  in  the  fundamental  Law  No.  2 — i.  e. ,  with  a  mere  sys- 
tolic increase  of  work  a  ventricle  will  ordinarily  merely  hypertrophy  without  any 
dilatation.  As  soon  as  the  slightest  increase  in  opposition  prevents  the  ventricle 
from  contracting  completely,  it  must  always  dilate — e.  g.,  a  dilatation  of  the  right 
ventricle  must  therefore  always  occur  in  mitral  insufficiency.  With  more_  pro- 
nounced opposition  to  its  emptying,  the  heart  seems  to  react  with  a  diminished 
systole  (concurred  in  by  Marey,''  breser,^  Tigerstedt  and  Johansson, ^  and  O. 
Frank  *).  The  question  resolves  itself,  then,  into  whether  we  are  to  consider  this 
latter  phenomenon  as  a  physiologic  reaction  or  as  a  consequence  of  a  pathologic 
condition — a  paralysis  of  the  heart.  Personally,  in  agreement  with  O.  Frank  and 
Moritz,=  the  writeV  considers  it  a  physiologic  reaction.  His  reasons  are  :  the 
skeletal  muscles  behave  quite  analogously  ;  the  phenomenon  is  frequently  of  great 
teleologic  significance  for  assisting  the  heart  and  the  arteries  with  high  blood- 
pressure  ;  and  it  has  been  experimentally  demonstrated  that  such  a  heart,  as  soon 
as  the  opposition  has  been  removed,  recovers  itself  immediately  and  contracts 
again  completely.  If  we  believe  that  incomplete  systoles  occur  physiologically,  it 
seems  perfectly' conceivable  and  entirely  within  physiologic  facts  that  a  cardiac 
chamber  enlarged  by  paralytic  dilatation  permanently  contracts  incompletely. 

A  certain  number  of  autopsies  upon  patients  with  valvular  lesions 
seem  to  argue  against  the  above-mentioned  laws.  AVe  must  remember, 
however,  that  the  relations  of  size  of  the  chambers  in  the  heart  of  the 
cadaver  differ  essentially  from  those  in  the  living  heart,  because  the 
phase  in  which  each  cardiac  chamber  is  paralyzed  (systolic,  diastolic 
immobility)  is  of  especial  significance.  The  degree  of  rigor  mortis  of 
the  heart  is  very  rarely  heeded  at  autopsy,  although  it  would  lie  a  valu- 

1  La  circulation  du  Savg.,  1881.  ^  Arch.  f.  exp.  Path.  u.  Pharm.,  vol.  xxiv. 

3  Skandinav.  Arch.f.  Physiol.,  yoI  l,  1889.        ^  Zeit.  f.  Biol,  vol.  xxxii. 
^  D.  Arch.f,  klin.  Med.,  vol.  Ixvi. 


PATHOLOGIC  PHYSIOLOGY  OF  VALVULAR  LESIONS.        319 

able  study  to  determine  the  time  of  onset  of  the  heart-muscle  rigor  and 
its  influence  upon  the  size  of  the  heart  chamber.  Moreover,  we  have  no 
rio-ht  to  compare  the  relations  of  the  heart  of  valvular  disease  at  autopsy 
with  the  relations  of  the  compensated  valvular  lesion,  because  disturb- 
ances of  compensation  usually  affect  patients  with  valvular  disease  some 
little  time  before  their  death,  and  so  the  relations  of  the  size  of  the 
heart  may  be  very  different.  We  will  mention  this  again  in  the  special 
description  of  individual  valvular  lesions. 

In  reality,  therefore,  in  order  to  determine  the  relations  of  size  of  the  individual 
heart  chambers  during  good  comj^ensation  we  should  utilize  only  autopsies  upon 
patients  with  vah-ular  lesions  v\-ho  have  died  suddenly  from  some  intercurrent 
trouble,  and  not  those  upon  patients  whose  death  is  directly  dependent  upon  their 
heart  lesion.  Even  in  the  former  the  autopsy  finding  is  not  actually  and  necessarily 
the  same  as  during  life. 

It  is  rather  doubtful  whether  the  Eontgen  rays  will  furnish  us  more  trustworthy 
results  about  these  relationships. 

Compensatory  anatomic  alterations  of  the  heart  are  usually  perma- 
nent, because  the  valvular  lesion  itself  rarely  improves,  and  because  life 
depends  upon  the  maintenance  of  compensation.  Compensatory  changes 
are  more  apt  to  increase  in  the  course  of  years,  because  most  valvular 
lesions  are  progressive.  Where  the  valvular  lesion  itself  is  capable  of 
retrogression,  the  compensatory  changes,  too,  may  retrograde  to  a  slight 
extent  or  even  completely  disappear.  These  are  extremely  rare  cases. 
Dilatations  and  hypertrophies  proceed  in  accordance  with  the  necessity 
which  occurs,  and  this  necessity  can  be  perfectly  explained  by  studying 
the  above-mentioned  laws. 

COMPENSATORY  DISTURBANCES. 

A  valvular  lesion,  thanks  to  the  so-called  compensatory  changes, 
the  hypertrophy  and  dilatation  of  individual  heart  chambers,  may  for 
years  produce  no  marked  symptoms,  but  sooner  or  later  the  gen- 
eral circulation  will  be  affected  more  or  less  decidedly,  because  com- 
pensatory contrivances  fail.  We  then  speak  of  "  disturbances  in  com- 
pensation." The  causes  of  these  disturbances  may  be,  on  the  one 
hand,  an  increase  in  the  opposition  to  the  circulation  produced  by  the 
valvular  lesion,  or  the  appearance  of  new  circulatory  obstacles  (arterio- 
sclerosis, nephritis) ;  or,  on  the  other  hand,  an  injury  to  the  heart 
muscle,  which  recent  investigations  have  taught  us  not  infrec(uently 
depends  upon  inflammatory  alterations  of  the  heart  muscle,  and  which 
in  valvular  lesions  is  frequently  produced  quite  gradually.  The  same 
process  goes  on  quite  similarly  in  other  circulatory  obstructions  which 
do  not  depend  upon  an  injured  valve.  For  a  long  time  they  also  may 
remain  compensated  by  the  hypertrophy  of  certain  heart  chambers, 
until  finally  disturbances  in  compensation  ensue.  All  cases  of  compen- 
satory disturbance  depend  upon  a  disturbance  in  the  favorable  rela- 
tion between  the  circulatory  obstacles  and  the  cardiac  power,  either 
an  absolute  diminution  of  cardiac  power  or  a  relative  diminution  of 
the  latter  in  proportion  to  an  increasing  obstacle.     This  condition  is 


320  DIAGNOSIS  OF  INDIVIDUAL    VALVULAR  LESIONS. 

exhibited  by  a  diminution  of  the  systoles  of  all  or  of  individual  heart 
chambers.  The  heart  begins  to  work  with  an  increasing  amount  of 
residual  blood  in  all  or  in  a  certain  one  of  its  chambers.  We  will  men- 
tion under  Individual  Valvular  Lesions  how  the  relation  of  the  size 
of  the  heart  is  affected  by  secondary  or  paralytic  dilatations.  Gen- 
eral stasis  ensues  in  consequence  of  diminished  systoles.  If  the  weak- 
ened condition  affects  the  right  heart  more  than  the  left,  the  stasis  will 
be  localized  more  in  the  systemic  than  in  the  pulmonary  circulation,  and 
vice  versa.  Thus,  the  clinical  picture  will  vary.  Compensatory  dis- 
turbances have,  however,  considerable  uniformity  despite  the  most 
varied  obstacles  to  the  circulation,  and  they  are  equally  significant 
whether  the  diminution  of  heart  power  proceeds  from  the  left  or  from 
the  right  heart.  Only  in  rare  individual  cases  do  these  disturbances 
vary  decidedly.  This  uniformity  probably  depends  upon  the  fact  that 
the  coronary  arteries  are  injured  as  much  in  paralysis  of  the  right  as  in 
paralysis  of  the  left  heart,  so  that  the  entire  heart  finally  shares  in  the 
paralysis.  This  usually  uniform  clinical  picture  of  compensatory  dis- 
turbance may  be  described  as  follows  :  The  filling  of  the  systemic  capil- 
laries diminishes.  The  distention  of  the  veins  and  the  venous  pressure 
increase.  The  circulation  is  slow^ed  by  diminution  in  the  blood-supply. 
Cyanosis  and  dyspnea  ensue.  Edema  and  other  dropsical  accumula- 
tions are  added.  The  urinary  excretion  is  diminished  and  the  urine 
frequently  contains  albumin.  The  causes  of  these  appearances  are  dis- 
<^ussed  in  the  sections  on  edema,  dyspnea,  cyanosis,  amount  of  urea,  and 
albuminuria.  The  pulse  frequently  varies  ;  it  is  very  often  accelerated, 
as  if  the  heart  attempted  to  overcome  to  some  extent  its  fault  of  incom- 
plete contraction  by  great  frequency  of  contraction.  The  heart  action 
is  frequently  very  irregular  and  produces  the  impression  of  overstimu- 
lation. Very  pronounced  irregularity  has  been  designated  quite  prop- 
erly delirium  cordis.  Neither  great  rapidity  nor  irregularity  of  the 
pulse  necessarily  accompanies  compensatory  disturbances.  Like  the 
other  symptoms,  one  or  the  other  of  them  may  be  lacking  or  very 
much  less  pronounced.  The  single  constant  factor  in  compensatory  dis- 
turbances is  the  diminished  cardiac  power  and  the  insuflficieut  systole. 
Quite  an  important  diagnostic  sign  of  disturbed  compensation  in  a  val- 
vular lesion  with  an  audible  murmur  is  that  this  murmur  becomes 
fainter  and  perhaps  inaudible  on  account  of  the  diminution  in  the  cur- 
rent rapidity  within  the  heart.  On  the  other  hand,  a  dilatation  of  the 
ventricle  caused  by  the  disturbed  compensation  may  produce  a  murmur 
where  one  was  not  audible  before,  or  bring  one  out  very  much  more 
distinctly,  due  to  a  relative  insufficiency  of  the  auriculoventricular  valve 
(p.  264  et  seq.),  which  is  superimposed  upon  the  original  lesion.  This 
subject  has  already  been  discussed  under  Cardiac  Murmurs.  From  evi- 
dent reasons,  the  heart  tones  are  frequently  weaker  in  disturbed  com- 
pensation. In  patients  with  disturbed  compensation  we  sometimes  find 
a  relatively  tense  pulse — i.  e.,  high  arterial  pressure — which  would  seem 
to  argue  against  our  explanation  that  compensatory  disturbances  depend 
essentially  upon  insufficient  cardiac  power.     As  a  matter  of  fact,  the 


INDIVIDUAL    VALVULAR  LESIONS.  321 

difficulty  vanishes  when  we  remember  that  the  left  ventricular  work  does 
not  depend  merely  upon  the  arterial  pressure,  but  is  measured  bv  the 
product  of  the  arterial  pressure  by  the  volume  of  blood  emptied  durino- 
systole,  and  that  with  marked  arterial  resistance  even  a  very  weak  svstole 
may  produce  high  arterial  pressure.  The  writer  calls  such  conditions 
"  high-pressure  stases,"  in  contrast  with  the  more  frequent  "  low-pressure 
stases,"  where  arterial  pressure  is  diminished  by  the  disturbed  compen- 
sation. "  High-pressure  stases  "  occur  in  circulatory  disturbances  asso- 
ciated with  arteriosclerosis  or  chronic  nej^hritis. 

INDIVIDUAL  VALVULAR   LESIONS. 

The  alterations  in  size  of  the  different  heart  chambers  (dilatations 
and  hypertrophies)  which  occur  in  individual  valvular  lesions  will  be 
explained  perfectly  by  a  thorough  comprehension  of  the  laws  which 
have  been  discussed  in  the  preceding  pages  concerning  the  origin  of 
compensation  and  compensatory  disturbances.  For  the  sake  of  brevitv 
only  the  number  of  the  law  which  explains  the  h}-pertrophy  or  dilata- 
tion will  be  mentioned  in  the  text  (see  p.  315  et  seq.).  The  reader  will 
find  that  his  comprehension  of  these  laws  will  be  facilitated  by  study- 
ing the  hydraulic  diagram  given  at  the  beginning  of  each  description. 
He  will  find  represented  there  the  alterations  in  pressure  which  the  val- 
vular lesion  produces  upon  each  heart  cliamber.  The  explanation  of 
the  signs  employed  in  these  diagrams  is  given  with  Fig.  113,  The 
reader  should  consult  pages  244  to  274  in  order  to  understand  the  dia- 
grams representing  the  results  of  physical  examination  in  each  valvular 
lesion,  and  he  should  recall  (p.  164  e^  seq.)  that  the  blue  represents  the 
superficial,  the  red  the  deep  cardiac,  dulness.  A  cross  ( X )  is  used  to 
designate  the  point  upon  the  skeleton  for  the  percussed  boundaries.  The 
shaded  wedges  represent  the  murmurs,  and  their  thickness  the  intensity 
of  the  murmur.  Xear  the  blunt  end  of  the  wedge  the  sign  >  represents 
a  decrescendo  murmur ;  the  sign  <  represents  a  crescendo  murmur. 
The  tones  at  the  apex  of  the  heart  and  over  the  tricuspid  valve  are  rep- 
resented by  the  signs  1  _. ;  M'hile  over  the  base  of  the  heart  (over  the 
great  vessels)  the  tones  are  represented  by  the  signs  ^  1 .  The  phase 
of  the  murmur  is  determined  by  its  position,  as  compared  with  the  tones. 
Accentuation  of  the  tone  is  represented  by  an  accentuation  of  the  sign. 

VALVULAR  LESIONS  OF  THE  LEFT  HEART. 
The  valvular  lesions  of  the  left  heart  are  much  the  most  frequent. 
(Congenital  heart  disease  is  not  included.)  In  any  given  case  therefore 
the  diagnosis  will  l^e  facilitated  by  the  rule  that  wherever  a  valvular 
lesion  appears  after  birth,  as  a  result  of  joint  rheumatism  or  arterio- 
sclerosis, we  shoukl  think  first  of  a  left-sided  lesion.  On  the  contrary, 
in  congenital  cardiac  disease  we  think  first  of  right-sided  valvular  lesions. 

MITRAL  INSUFFICIENCY. 

The  essential  fault  in  mitral  insufficiency  (Figs.  113  and  114)  consists 
in  a  systolic  regurgitation  of  blood  into  the  left  auricle.     This  regur- 

21 


322  DIAGNOSIS  OF  INDIVIDUAL    VALVULAR  LESIONS. 

gitation  depends  upon  the  imperfect  closure  of  the  mitral  valve  and  gives 
rise  to  a  systolic  murmur.  It  is  the  most  frequent  of  all  valvular 
lesions.  The  regurgitation  increases  the  pressure  in  the  auricle  enough 
to  dilate  its  walls.  The  increased  pressure  in  the  auricle  is  transmitted 
back  through  the  entire  pulmonary  circulation.  The  pulmonary  semi- 
lunar valves,  however,  are  shut  during  diastole,  so  that  the  right  ven- 
tricle does  not  suffer  from  the  raised  pressure  at  this  stage.  But  the 
increased  pulmonary  pressure  acting  to  augment  the  work  of  the  right 
ventricle  during  systole  necessitates  its  hypertrophy  (primary  hyper- 
trophy) (Law  1).  Dilatation  of  the  left  auricle  is  responsible  for  its 
own  secondary  hypertrophy  (Law  2).  But  there  is  another  especially 
important  element.  The  left  ventricle  receives  more  blood  during  its 
diastole  than  normally  because  the  left  auricle  is  overfilled ;  hence  it 


(.vvlation 


'^^^einic  ciTeu\a^^° 


Fig.  113. — Hydraulic  diagram  of  mitral  insufficiency  :  +,  Increased  pressure;  +  s,  increased  sys- 
tolic pressure ;  +  d,  increased  diastolic  pressure ;  +  ds,  increased  systolic  and  diastolic  pressure 
in  the  heart  chambers  within  which  the  signs  appear.  Hence,  aheart  chamber  marked  with 
-r  f  hypertrophies  primarily ;  one  with  +  d  dilates  primarily ;  and  one  with  +  ds  both  dilates 
and  hypertrophies  primarily. 

becomes  primarily  dilated  (Law  2)  because  the  pressure  within  it  is 
increased  during  diastole.  This  dilatation  leads  in  turn  (Law  2)  to  a 
secondary  hypertrophy  of  the  left  ventricle.  The  reason  for  the  left 
ventricular  dilatation  is  plainly  compensatory  ;  because  despite  the  fact 
that  a  part  of  its  blood  is  regurgitated  into  the  auricle,  its  increased 
capacity  enables  the  arterial  system  to  be  completely  filled.^ 

In  a  well-compen.sated  mitral  insufficiency  the  systemic  circulation 
is  practically  normal.  The  pulse  is  not  at  all  small,  as  has  often  been 
stated,  and  the  only  striking  disturbance  which  persists  during  compen- 
sation even  of  a  severe  case  of  mitral  insufficiency  is  a  more  or  less 
pronounced  dyspnea,  which  ensues  because  the  lungs  are  overfilled  with 
blood. 

^  Theoretically,  a  very  slight  deficit  in  the  arterial  filling  must  neces.sarily  ensue, 
because  an  extra  amount  of  blood  is  required  for  the  increased  filling  of  the  pulmonary 
circulation,  of  the  left  auricle,  and  of  the  left  ventricle. 


INDIVIDUAL    VALVULAR  LESIONS. 


323 


With  this  the  series  of  compensatory  changes  in  mitral  insufficiency 
is  complete.  Clinically  (Fig.  114)  the  lesion  is  recognized  by  a  sys- 
tolic murmur,  generally  heard  most  clearly  and  loudly  at  the  apex  of 
the  heart,  but  under  certain  circumstances  (see  p.  269  et  seq.'j  with  its 
maximum  at  the  base.  This  murmur  may  even  overpower  or  obliter- 
ate the  systolic  mitral  tone.  Sometimes  we  can  feel  it  as  a  thrill  as 
well  as  hear  it.  The  primary  dilatation  of  the  left  ventricle  and  left 
auricle  can  be  demonstrated  by  percussion  (frequently  by  palpation). 
Simple  or  pure  hypertrophy  of  the  right  ventricle  cannot  ordinarily  be 
appreciated  by  percussion  (p.  182);  but  the  increased  pressure  in  the 
pulmonary  circulation  which  produces  this  hypertrophy  of  the  right 
ventricle  is  generally  evident  from  an  accentuation  of  the  second  pul- 


FiG.  11-).— Diagnostic  diagram  of  mitral  insufficiency.    (The  signs  are  described  upon  p.  321.) 


monic  tone  (p.  251),  sometimes  from  the  increased  pulsation,  or  shock, 
of  the  pulmonary  valve  closure,  visible  or  palpable  in  the  region  of  the 
pulmonary  artery  (p.  300).  The  diagnostic  significance  of  the  pul- 
monary second  accentuation  is,  however,  frequently  overestimated.  Not 
infrequently  it  fails  to  appear,  and  again  there  are  many  cases  where 
the  compensatory  power  of  the  right  ventricle  is  not  sufficient  to  pro- 
duce it — e.  g.,  cases  of  a  mild  degree  of  insufficiency,  where  the 
increased  pressure  is  slight ;  and  finally  cases  where,  before  the  appear- 
ance of  the  mitral  insufficiency,  the  ])ulraonic  second  was  physiologi- 
cally weaker  than  the  aortic  second.  In  contradistinction  to  the  diastolic 
murmur  of  aortic  insufficiency  (see  p.  330),  it  is  worth  remembering 
that  the  murmur  of  mitral  insufficiency   is  heard  with  less  intensity 


324  DIAOXOSIS  OF  lyDIVIDUAL    VALVULAB  LESIOXS. 

when  the  patient  is  standing  than  when  lying  down.  This  is  very 
likely  due  to  the  action  of  gravity.  In  fact,  a  taint  mitral  insufficiency 
murmur  can  Irecjuently  be  heard  only  in  the  recumbent  posture. 

The  above-mentioned  signs  are  ordinarily  noted  in  a  well-compen- 
sated case  of  mitral  insufficiency.  Sooner  or  later,  however,  disturb- 
ances of  compensation  are  botiud  to  appear.  They  ordinarilv  be^in  in 
this  way  :  The  right  ventricle  can  no  longer  completely  contract,  and 
therefore  dilates  (paralytic  dilatation,  Law  4)  ;  as  a  consequence  the 
accentuation  of  the  second  pulmonic  disappears,  the  left  auricle  and  the 
left  ventricle  in  turn  receive  less  blood,  and  the  fillino-  of  the  svstemic 
arteries  and  capillaries  diminishes.  This  last  danger  signal  is  still  more 
marked  when  from  the  same  cause  the  left  ventricle  begins  to  weaken. 
All  the  other  ap]H\irances  of  disturbed  compensation  described  above 
can  be  added  to  the  lack  of  arterial  filling  until,  under  the  influence  of 
rest  or  cardiac  tonics,  compensation  is  ag-ain  established.  The  heart 
power  then  increases.  The  right  ventricle  again  empties  itself  com- 
pletely and  returns  to  its  condition  of  ptire  or  simple  hypertrophy. 
But  orciinarily  during  the  course  of  re-establishing  compensation  the 
right  ventricular  dilatation  becomes  anatomically  fixed  by  the  develop- 
ment of  a  secondary  hypertrophy — /.  t.,  by  the  addition  of  layers  of 
new  muscular  tissue  {]).  317).  This  is  permanent  and  can  be  demon- 
strated by  percussion.  (See  p.  ooO  in  reference  to  the  completeness  of 
the  contraction  of  this  permanently  dilated  right  ventricle.)  AVith  the 
re-establishmeut  of  compensation  the  severe  circulatory  disturbances 
completely  disappear. 

The  right  ventricle  may  become  dilated  and  hypertrophied  in  a  sim- 
ilar way  even  without  compensation  being  disturbed,  depending  upon 
the  conditions  described  upon  p.  317. 

The  dilatation  of  the  right  ventricle  in  mitral  insufficiency  is  in 
reahty  (see  p.  316)  a  secondary  one — /.  t..  a  result  of  incomplete  sys- 
tole— and  should  be  sharply  distinguished  from  the  left  ventricular  dila- 
tation.     The  latter  has  a  compensatory  significance. 

(See  p.  132  in  reg-ard  to  the  characteristics  of  the  pulse  in  mitral 
insufficiency  ;  p.  288.  in  regard  to  the  presence  of  a  pulmonary  pulse  ; 
p.  176.  in  reg-ard  to  the  depth  of  the  king  borders  from  pulmonary 
stasis:  p.  86.  in  regard  to  the  character  of  the  respiration;  p.  253, 
in  regard  to  the  disappearance  of  the  mitral  tone,  or  both  tones  to  the 
left  heart  :  p.  270.  in  regard  to  the  difierence  between  a  mitral  and 
an  aortic  systolic  murmur  ;  }>.  270.  in  reg-ard  to  the  occurrence  of  a 
prediastolic  murmur,  and  p.  2-36.  in  regard  to  a  splitting  or  doubling 
of  the  second  tone.) 

MITRAL  STENOSIS. 

In  mitral  insufficiency  the  obstacle  to  the  circulation  is  effective 
during  systole  :  Init  in  mitral  stenosis,  a  comparatively  frequent  valvular 
lesion,  the  obstacle  acts  during  diastole  of  the  left  ventricle.  To  under- 
stand what  follows  we  should  remember  that  the  ventricular  diastole 
can  be  subdivided  into  two  intervals  in  relation  to  the  auricle.      Purino^ 


INDIVIDUAL   VALVULAR  LESIONS. 


325 


the  first  part  of  the  ventricular  diastole  the  auricle  is  passive ;  the 
blood,  under  the  influence  of  a  moderate  pressure  from  its  course  through 
the  pulmonary  circulation,  flows  into  the  left  ventricle  without  the  aid 
of  the  auricle.  In  mitral  stenosis,  however,  an  obstacle  prevents  this 
emptying  of  the  auricle;  thedeft  auricular  pressure  increases,  and,  the 
blood  collecting,  distends  the  auricular  walls,  which  are  ordinarily 
relaxed  at  this  period.  The  first  result  of  mitral  stenosis  upon  the 
heart  (I^aw  2)  is  therefore  the  dilatation  of  the  left  auricle.  During 
the  second  part  of  ventricular  diastole  the  auricular  systole  comes  into 
action,  and  on  account  of  the  stasis  behind  the  stenosed  mitral  valve  it 
has  to  propel  an  increased  amount  of  blood,  and  in  addition  overcome 
the  obstacle  at  the  mitral  valve.  As  a  result  (Laws  1  and  2)  a  hyper- 
trophy of  the  dilated  left  auricle  supervenes.  We  might  imagine  that 
(without  help  from  the  right  ventricle)  the  increased  power  of  the  left 
auricle  could  eflFect  the  compensation.     But  experience  has  shown  us 


ilation 


Systemic  ^^^ 


Fig.  115.— Hydraulic  diagram  of  mitral  stenosis.    (See  Fig.  113  for  the  explanation  of  the 

signs.) 


that  this  is  not  the  case,  because  hypertrophy  of  the  right  ventricle 
belongs  as  much  to  mitral  stenosis  as  to  mitral  insufliciency,  so  that, 
despite  the  increased  work  of  the  left  auricle,  there  remains  an  increased 
task  for  the  right  ventricle.  The  explanation  is  probably  that  the  left 
auricle  does  not  grow  to  be  strong  enough  both  to  expel  completely  its 
increased  content  and  to  overcome  the  mechanical  obstacle  of  the  nar- 
rowed mitral  valve.^  This  is  not  to  be  wondered  at  when  we  consider 
the  slight  muscular  power  of  the  auricle ;  as  a  matter  of  fact,  autop- 
sies show  no  very  striking  hypertrophies  of  the  auricle.  Assuming, 
then,  that  in  mitral  stenosis  the  left  auricle  cannot  completely  empty 
itself,  and  so  is  continually  laboring  with  residual  blood,  it  happens, 
naturally,  that  during  auricular  diastole  the  blood  from  the  lungs  does 
not  flow  into  an  empty,  but  into  an  already  partially  filled,  left  auricle. 

I  Perhaps  the  same  laws  in  regard  to  the  completeness  and  incompleteness  of  con- 
traction apply  here  as  to  the  ventricle  (see  p.  318). 


326 


DIAGNOSIS  OF  INDIVIDUAL    VALVULAR  LESIONS. 


This  is  of  equal  significauce  to  an  increased  resistance  to  the  pulmo- 
nary circulation  present  during  auricular  diastole  or  ventricular  systole. 
There  are  no  valves  at  the  outlet  of  the  pulmonary  veins ;  hence  it  is 
easy  enough  to  understand  that  the  contraction  of  the  left  auricle  must 
drive  back  a  part  of  the  blood  stagnating  in  the  auricular  chamber  into 
the  lungs  and  part  through  the  narrowed  mitral  valve/  The  increased 
resistance  in  the  pulmonary  circulation  persists  until  the  ventricular 
systole  occurs,  and  can  be  overcome  only  by  the  hypertrophy  (primary) 
of  the  right  ventricle  (Law  1).  Thus,  the  hypertrophy  of  the  right 
ventricle  in  mitral  stenosis  enables  compensation  to  be  effected  by  pro- 
ducing a  continuous  diastolic  flow  through  the  stenosed  mitral  valve. 
It  presupposes  an  elastic  tension  of  the  pulmonary  vessels,  so  that  the 


/  (o) 

Fig.  116.— Diagnostic  diagram  of  mitral  stenosis.    (See  p.  321  for  the  explanation  of  the  signs.) 

systolic  power  of  the  right  ventricle  is  transmitted  through  the  lung 
into  the  left  auricle.  Despite  its  complexity,  this  supposition  alone 
seems  to  explain  that  the  systole  of  the  right  ventricle  aids  in  producing 
compensation,  although  the  obstacle  is  diastolic.^  The  conditions  are 
much  simpler  in  mitral  insufficiency ;  for  here,  as  a  direct  result  of  the 
regurgitation,  both  ventricles  are  working  directly  at  variance,  making 
it  perfectly  clear  why  the  right  ventricle  must  do  more  work. 

^  The  fact  that  a  considerable  portion  of  the  blood  is  driven  backward  instead  of 
forward  by  the  auricular  contraction  also  explains  the  absence  of  dilatation  of  the  left 
ventricle,  in  spite  of  the  increase  in  the  pulse  volume  of  the  left  auricle. 

^  This  passive  elastic  function,  in  which  the  propelling  force  is  traced  back  to  the 
right  ventricle,  is  in  reality  a  normal  function  of  the  left  auricle  and  the  pulmonary 
vessels,  since  during  the  first  part  of  the  ventricular  diastole  the_  blood  flows  into  the 
left  ventricle  mainly  on  account  of  the  excess  of  pressure  which  is  left  over  from  the 
lungs. 


INDIVIDUAL   VALVULAR  LESIONS.  327 

There  is  no  question  of  a  primary  dilatation  of  the  right  ventricle 
in  mitral  stenosis  any  more  than  in  mitral  insufficiency,  because  in 
either  case,  so  long  as  the  pulmonary  semilunar  valves  close  perfectly, 
there  is  no  increase  of  right  ventricular  pressure  except  during  systole 
(Law  1).  Stenosis  of  the  mitral  valve  evidently  furnishes  no  reason 
for  any  change  in  the  left  ventricle.  In  a  well-compensated  mitral 
stenosis  the  left  ventricle  does  not  show  concentric  atrophy,  as  is  some- 
times contended,  because  our  conception  of  good  compensation  is  not 
compatible  with  the  supposition,  necessarily  included  in  such  a  conten- 
tion,  that  the  diminished  left  ventricle  forces  decidedly  less  blood  than 
normally  into  the  systemic  arteries/ 

We  not  infrequently  see  at  the  autopsy  table  a  case  of  mitral  stenosis 
with  a  large  right  and  a  small  left  ventricle.  The  reason  is  either  that 
the  lesion  could  not  be  compensated,  on  account  of  the  extreme  degree 
of  the  obstruction  (essential  obstruction  ^),  or  that  the  patient  died  dur- 
ing a  disturbed  compensation,  in  which  the  incomplete  systole  of  the 
right  ventricle  occasioned  a  paralytic  dilatation  of  its  own  chamber,  and 
consequently  an  imperfect  filling  of  the  left  ventricular  cavity. 

This  paralytic  dilatation  of  the  right  ventricle  may  remain  fixed 
even  after  the  disturbed  compensation  has  been  adjusted,  and  an  en- 
larged and  hypertrophied  right  ventricle  may  result  permanently,  just  as 
in  mitral  insufficiency.  Even  without  actual  disturbance  of  compensa- 
tion the  same  result  may,  under  some  circumstances,  be  accomplished 
by  the  causes  mentioned  upon  p.  317.  Whether  such  a  dilated  and 
hypertrophied  right  ventricle  is  then  completely  or  incompletely  con- 
tracted is  not  certain  (see  p.  318).  This  must  have  some  efiect  upon 
the  other  heart  cavities,  for  the  left  auricle  and  the  left  ventricle  would 
then  contain  much  more  blood  than  normally  and  the  left  ventricle 
would  also  be  dilated.  In  this  way  we  might  explain  cases  of  pure 
mitral  stenosis  which  show  a  dilatation  of  the  right,  as  well  as  of  the 
left,  ventricle.  But  such  a  supposition  cannot  be  accepted  Avithout 
hesitation,  because  it  supposes  that  the  diseased  mitral  stenotic  heart 
would  finally  perform  a  greater  systolic  effiort  than  the  healthy  heart. 
And  this  is  not  only  a  priori  improbable,  but  it  is  not  in  any  way  sup- 
ported by  the  character  of  the  pulse.  So  in  mitral  stenosis,  where  we 
meet  with  a  dilatation  of  the  left  ventricle,  we  assume  that  either  a  simple 
paralytic  dilatation  from  a  final  paralysis  of  the  left  heart,  or,  with  a 
coincident  hypertrophy  of  the  left  ventricle,  a  complication  with  mitral 
insufficiency  exists.  This  may  escape  anatomic  demonstration  and,  if 
there  is  no  systolic  murmur,  even  clinical  confirmation. 

Mitral  stenosis  will  produce  a  dilatation  of  the  left  auricle  (see  pp.  184, 
185),  which  can  be  demonstrated  by  percussion  ;  but  the  hypertrophy 

'  The  deficit  which  the  systemic  circulation  suffefs  in  consequence  of  the  collection 
of  blood  in  the  left  auricle  and  in  the  lungs  is  of  little  importance  to  the  left  ventricle 
during  the  stage  of  compensation,  because  the  vessels  of  tiie  greater  circulation  possess 
a  capacity  of  adapting  themselves  to  varying  degrees  of  fulness.  Perhaps  the  deficit  is 
cared  for  by  an  increase  of  the  blood-mass  (see  p.  315). 

■^  The  reader  is  referred  to  the  author's  paper :  "  Herzmittel  und  Vasomotoren- 
mittel"  (Cardiac  and  Vasomotor  Remedies),  Concj.f.  inn.  Med.  at  Berlin,  1901. 


328  DIAGNOSIS  OF  INDIVIDUAL    VALVULAR  LESIONS. 

of  the  right  ventricle,  unless  associated  with  dilatation,  ordinarily  escapes 
such  clinical  demonstration.  In  later  stages  mitral  stenosis  may  be  asso- 
ciated with  an  appreciable  increase  of  the  heart  dulness  to  the  right  as 
well  as  to  the  left.  The  enlargement  to  the  left  may  in  exceptional 
cases  (see  above)  be  due  to  a  true  dilatation  of  the  left  ventricle ;  but 
ordinarily  it  is  the  dilatation  of  the  right  ventricle  which  pushes  the 
heart  and  the  apex  beat  to  the  left  (see  pp.  182,  291  et  seq.). 

In  a  case  of  mitral  stenosis  we  generally  hear  a  diastolic  murmur 
with  a  presystolic  accentuation  or  merely  a  presystolic  murmur  at  the 
apex  ;  frequently  we  can  also  feel  it  as  a  presystolic  thrill.  (In  regard 
to  the  mode  of  production  of  this  murmur  and  its  significance  see 
p.  269  et  seq. ;  in  regard  to  the  details  of  its  localization  see  p.  266 ; 
in  regard  to  the  presystolic  mitral  murmur  of  aortic  insufficiency  see 
p.  331).  The  second  pulmonic  tone  is  generally  accentuated  in  mitral 
stenosis  in  consequence  of  the  increased  pressure  in  the  pulmonary 
circulation  and  the  hypertrophy  of  the  right  ventricle.  The  value  of 
this  sign  for  the  diagnosis  of  mitral  stenosis  has,  however,  often  been 
overestimated  (see  p.  251).  If  compensation  is  disturbed  the  accentua- 
tion may  disappear.  The  normal  second  pulmonic  tone  is  often  (if  not 
generally)  weaker  than  the  normal  second  aortic  tone,  so  that  a  patho- 
logic accentuation  of  the  former  is  frequently  not  apparent  to  the 
examiner.  And,  finally,  with  a  mild  degree  of  mitral  stenosis  the 
increase  of  pressure  in  the  pulmonary  circulation  may  be  insufficient  to 
produce  a  plain  accentuation  of  the  second  pulmonic. 

We  frequently  hear  a  splitting  or  doubling  of  the  second  tone  (see 
p.  255  et  seq.),  and  occasionally  a  presystolic  or  diastolic  tone  due  to  an 
imperfectly  opened  mitral  valve  (see  p.  257  et  seq.). 

During  quiet  cardiac  action  sometimes  the  only  auscultatory  sign  of 
mitral  stenosis  is  a  triple  rhythm,  the  third  tone  of  which  is  furnished 
by  the  presystolic  tone.  Besides,  it  is  well  to  remember  that  mitral 
stenosis  is  more  liable  than  any  of  the  other  valvular  lesions  to  run  its 
course  without  giving  rise  to  a  murmur  (see  p.  264). 

(In  regard  to  the  character  of  the  pulse  of  mitral  stenosis  see  p.  132  ; 
in  regard  to  the  character  of  the  respiration  see  pp.  109  and  315  ;  in 
regard  to  the  presence  of  a  pulmonary  pulse  see  p.  288  ;  in  regard  to 
the  deep  position  of  the  lung  borders  on  account  of  pulmonary  stasis 
see  p.  177  et  seq.). 

AORTIC   INSUFFICIENCY. 

Aortic  insufficiency — imperfect  closure  of  the  aortic  valve  (Figs. 
117  and  118) — is,  next  to  mitral  insufficiency,  the  most  common  valvular 
lesion.  Its  mechanism  is  the  one  most  readily  comprehended  by  the 
beginner.  The  fault  is  that  during  diastole  (Fig.  117)  the  blood  rushes 
back  into  the  left  ventricle  through  the  imperfectly  closed  semilunar 
valves,  and  so  gives  rise  to  the  characteristic  diastolic  murmur  (see 
below).  Without  compensation  the  mechanical  effect  upon  the^  circula- 
tion would  be  that  the  aorta,  deprived  of  part  of  its  blood  during  dias- 
tole, could  not  fill  the  arteries  and  keep  up  the  pressure.     Compensa- 


INDIVIDUAL   VALVULAR  LESIONS. 


329 


tion  prevents  such  a  result  in  the  following  way  :  The  regurgitating  blood 
enters  the  diastolic  relaxed  left  ventricle.     This  chamber  is  at  the  same 


.s,«»^'"°°' 


Fig.  117.— Hydraulic  diagram  of  aortic  insufficiency.    (Compare  Fig.  113  for  explanation.) 

time  receiving  blood  through  the  mitral  valve.  Its  walls  have  there- 
fore to  endure  an  increased  pressure  during  diastole,  and  hence  become 
dilated  (p.  31 6  et  seq.,  Law  2).  In  virtue  of  its  reserve  power  the  left 
ventricle  still  contracts  itself  completely,  and   naturally  sends  an  in- 


FiQ.  118.— Diagnostic  diagram  of  aortic  insufficiency.   (Compare  p.  321  for  an  explanation  of  the 

signs.) 

creased  volume  of  blood  into  the  aorta.     But  it  cannot  continually  per- 
form this  extra  work  without  hypertrophy  (Law  2).     As  soon  as  hyper- 


330  DIAGNOSIS  OF  INDIVIDUAL   VALVULAR  LESIONS. 

trophy  takes  place  the  valvular  lesion  is  compensated,  and  for  the  time 
being  harmless.  Then  at  every  systole  the  aorta  receives  more  blood 
than  normally,  and  the  loss  through  regurgitation  is  not  significant.  So 
one  sees  in  this  lesion,  as  in  mitral  insufficiency,  that  the  dilatation  of  the 
left  ventricle  is  primary,  and  that  it  is  essential  to  the  accomplishment 
of  compensation.  Therefore  primary  dilatation  and  secondary  hyper- 
trophy of  the  left  ventricle  are  an  essential  result  of  aortic  insufficiency 
(Fig.  118).  Frequently  a  diffuse  dilatation  of  the  aorta,  which  depends 
upon  its  being  stretched  by  the  increased  power  of  the  systole,  goes 
hand  in  hand  with  the  dilatation  of  the  left  ventricle.  This  aortic 
dilatation  may  become  evident  in  the  appearance  of  an  exceptional 
pulsation  and  an  increased  dulness  in  the  upper  intercostal  spaces  to  the 
right  of  the  sternum  (Fig.  92).  It  is  liable  to  be  confused  with  a  real 
sacculated  aortic  aneurism  (see  p.  345).  Thus  far  the  right  ventricle 
takes  no  part  in  compensating  an  aortic  insufficiency.  But  as  soon  as 
disturbance  in  compensation  arises,  as  soon  as  the  left  ventricle  is  unable 
to  perform  its  increased  work  perfectly,  so  that  during  systole  it  is  in- 
completely emptied,  then  the  residual  blood  within  its  cavity  prevents  a 
complete  emptying  of  the  left  auricle,  and,  just  as  in  mitral  stenosis,  this 
reacts  upon  the  pulmonary  circulation  and  the  right  ventricle.  If  such 
a  paralysis  of  the  left  ventricle  occasions  a  considerable  dilatation  of  its 
walls,  a  relative  mitral  insufficiency  will  also  appear  and,  in  the  well- 
known  way,  react  upon  the  pulmonary  circulation  and  the  right  ven- 
tricle. This  reactionary  effect  upon  the  pulmonary  circulation,  which, 
according  to  our  discussion  above,  does  not  depend  entirely  upon  the 
occurrence  of  a  relative  mitral  insufficiency,  but  which  can  sometimes 
be  caused  by  the  residual  blood  in  the  left  ventricle,  explains  how 
failure  of  the  left  ventricular  power  in  aortic  insufficiency  finally  pro- 
duces the  ordinary  picture  of  disturbance  of  compensation,  with  cyanosis, 
dyspnea,  edema,  etc.,  just  as  in  the  mitral  lesions.  The  disturbance  of 
compensation  may  be  repaired  ;  and  then,  depending  upon  the  individ- 
ual peculiarities  of  the  case,  the  right  ventricle  either  regains  its  normal 
size,  or  else,  if  a  relative  mitral  insufficiency  (see  p.  317  ei  seq.)  persists 
on  account  of  the  hypertrophied  left  ventricle,  may  remain  permanently 
hypertrophied,  or  both  hypertrophied  and  dilated.  Such  a  permanent 
dilatation  of  the  right  ventricle,  supposing  it  contracted  itself  completely, 
would  produce  secondarily  a  further  enlargement  of  the  left  auricle  and 
ventricle  (excessive  compensation?)  (see  p.  318). 

The  most  important  of  the  physical  signs  of  this  valvular  lesion  is 
(Fig.  118)  a  diastolic  murmur  audible  at  the  aortic  area  and  over  the 
sternum  (see  p.  266,  2).  The  murmur  is  sometimes  plainly  transmitted 
into  the  carotids,  and  is  usually  more  distinctly  heard  in  the  standing 
than  in  the  recumbent  posture,  because  gravity  favors  the  regurgitation. 
A  weak  murmur  of  aortic  insufficiency  (contrasted  with  that  of  a  mitral 
insufficiency,  p.  323)  is  oftentimes  audible  only  while  the  patient  is 
standing.^     The  second  aortic  sound  may  be  absent ;  again,  it  may  be 

['  A  very  faint  murmur  of  aortic  insufficiency  can  sometimes  be  appreciated  by  the 
ear  against  the  chest  when  it  is  not  audible  through  tlie  stethoscope. — Ed.] 


INDIVIDUAL   VALVULAR  LESIONS.  331 

unaffected  if  the  aortic  valves  are  not  much  diseased,  or  it  may  even  be 
accentuated,  in  consequence  of  the  increased  systolic  filling  of  the  aorta  ; 
but  more  frequently,  on  account  of  the  changes  of  the  aortic  valves,  it 
is  diminished  or  even  disappears.  In  most  cases  of  aortic  insufficiency 
a  systolic  murmur  can  also  be  heard  over  the  aorta.  According  to  one 
hypothesis,  this  systolic  murmur  depends  upon  a  roughness  at  the  aortic 
valves,  due  to  endocarditis  or  atheroma,  which  affects  the  blood-cur- 
rent during  systole,  although  there  is  no  actual  stenosis.  According 
to  another  hypothesis,  the  systolic  murmur  results  from  the  diastolic 
regurgitating  stream  clashing  with  the  systolic  stream  (p.  262),  a  real 
stenosis).  According  to  a  third  hypothesis,  it  is  the  result  of  the 
increased  rapidity  of  expulsion  of  the  blood  from  the  more  powerful 
systole  (p.  261).  However  this  may  be,  it  is  well  to  be  cautious  in 
making  a  diagnosis  of  aortic  stenosis  from  the  presence  of  a  systolic 
murmur  heard  over  the  aorta  in  a  case  of  aortic  insufficiency  unless 
there  are  other  signs  of  its  presence.  An  especially  rough  or  musical 
murmur  speaks  with  some  probability  for  the  existence  of  an  aortic 
stenosis  ;  but  the  deciding  point  is  the  character  of  the  pulse.  If  there 
is  an  actual  aortic  stenosis — that  is,  one  caused  mechanically — the  pulse 
will  possess  more  or  less  plainly  the  characteristics  of  the  jmlsus  tardus 
(see  p.  105  et  seq.,  p.  127).  See  p.  274  in  regard  to  the  presence  of  a 
doubled  maximum  diastolic  and  systolic  murmur — i.  e.,  one  heard  very 
plainly  both  oyer  the  aorta  and  at  the  apex.  A  complicating  mitral 
insufficiency  or  stenosis  is  often  wrongly  diagnosticated  from  such  signs. 

Austin  Flint  i  described  in  aortic  insufficiency  a  presystolic  murmur  audible 
over  the  auscultation  area  of  the  mitral  valve.  He  explained  it  in  this  way: 
The  regurgitating  stream  from  the  aorta  spreads  out  the  curtain  of  the  mitral 
valve  just  as  the  presystolic  stream  from  the  left  auricle  is  passing  through  this 
valve  into  the  left  ventricle.  Hence  the  mitral  curtain  cannot  be  perfectly  opened, 
and  a  sort  of  functional  mitral  stenosis  results.  This  produces  the  presystolic 
murmur.  This  explanation  does  not  seem  to  the  writer  sufficiently  proved  by  the 
postmortem  findings  ;  nevertheless  it  deserves  diagnostic  attention.  A  certain 
differentiation  of  this  condition  from  the  combination  of  an  aortic  insufficiency 
with  an  organic  mitral  stenosis  must  be  very  difficult.  Certainly  such  a  functional 
origin  of  a  pronounced  presystolic  murmur  is  rare,  so  that  the  diagnosis  of  a  mitral 
stenosis  complicated  with  aortic  insufficiency  is  not  so  difficult. 

Further  important  diagnostic  signs  of  aortic  insufficiency  are  :  the 
pulsus  celer  (pp.  105  and  127)  and  a  series  of  signs  depending  upon  it, 
which  have  been  explained  above  ;  a  capiUary  pulse  (p.  144  et  seq.) ;  the 
single  and  double  arterial  tones  (p.  282) ;  the  Duroziez  double  murmur  (p. 
282  et  seq.)  ;  the  rare  appearance  of  the  penetrating  venous  puke  (p.  152 
et  seq.)  ;  and  the  rare  arterial  liver  pulse  (p.  300).  All  these  signs  are, 
of  course,  most  plainly  marked  during  good  compensation  ;  less  plainly 
during  disturbed  compensation.     They  are  not  all  equally  plain. 

During  disturbance  of  compensation  in  aortic  insufficiency  the 
character  of  the  pulse  still  seems  exceptionally  well  preserved  despite 
the  poor  circulation.     This  depends  in  the  first  instance  upon  the  fact 

^  Flint's  3Iurmur,  first  described  in  Manual  of  Auscultation  and  Percussion,  Austin 
Flint,  3d  ed.,  1883,  p.  231. 


332  DIAGNOSIS  OF  INDIVIDUAL   VALVULAR  LESIONS. 

that  even  with  poor  filling  of  the  arteries  the  pulse  does  not  lose  its 
character  of  pulsus  celer,  which  would  naturally  produce  the  impression 
of  an  exceptionally  good  pulse.  Besides,  measurements  of  the  direct 
pressure  by  means  of  the  v.  Basch  sphygmomanometer  show  that  with 
this  valvular  lesion  the  systolic  pressure  (see  pp.  107  and  135  et  seq.) 
can  be  high  despite  disturbance  in  compensation.  This  only  apparently 
contradicts  our  statement  above  in  regard  to  the  characteristics  of  dis- 
turbance of  compensation.  For  even  if  we  neglect  the  arguments 
against  the  v.  Basch  principles  of  pressure-measuring  which  were  stated 
above  (stasis  of  the  wave,  action  of  the  blow),  we  must  not  forget  that 
the  systolic  pressure  in  this  valvular  lesion  should  be  considered  a  much 
less  exact  measure  of  the  mean  arterial  pressure  than  under  ordinary 
circumstances,  because  a  considerable  portion  of  the  systolic  pressure  is 
of  no  use  to  the  circulation  on  account  of  the  regurgitation.  And  so  it 
happens  that  an  abnormally  high  systolic  pressure  for  perfect  compensa- 
tion in  aortic  insufficiency  is  in  reality  essential  to  establish  a  mean 
normal  pressure  in  the  capillaries.  And  then  even  in  disturbed  com- 
pensation the  absolute  systolic  pressure  will  almost  always  be  normal  or 
above  normal.  Moreover,  inconsequence  of  the  quick  and  high  ascent 
of  the  pulse  wave,  the  pulse  will  be  felt  a  longer  time  than  normal  on 
the  other  side  of  the  pelotte  of  v.  Basch's  instrument,  and  thereby 
cause  an  overestimation  of  the  systolic  pressure.  Finally,  even  if  com- 
bined with  marked  arterial  resistance,  disturbances  of  compensation  are 
not  necessarily  associated  with  a  low  blood-pressure  (see  p.  321). 

AORTIC    STENOSIS. 

Aortic  stenosis  (Figs.  119  and  120)  causes  an  obstacle  to  the  left  ven- 
tricular systole.  The  left  ventricle  overcomes  this  obstacle  at  first  by 
means  of  its  reserve  power,  and  later  by  the  hypertrophy  of  its  walls — 


-SysteT 
Fig.  n9.— Hydraulic  diagram  of  aortic  stenosis.    (Compare  Fig.  113  for  explanation.) 

ordinarily  a  pure  primary  hypertrophy  without  dilatation  (p.  315, 
Law  1).  The  hypertrophy  of  the  left  ventricle  may  not  be  demon- 
strable clinically,  or  it  may  only  exhibit  an  accentuation  of  the  apex 


INDIVIDUAL    VALVULAR  LESIONS. 


333 


beat  (see  p.  293  et  seq.)  without  any  cardiac  enlargement  evident  to  per- 
cussion (see  p.  183).  Sooner  or  later,  however,  disturbances  in  com- 
pensation do  occur  and  a  secondary  dilatation  of  the  left  ventricle  is 
added  to  the  hypertrophy  (Law  4).  This  dilatation  either  disappears 
when  compensation  is  restored,  or  may  persist  anatomically  established 
(see  p.  316  et  seq.).  Such  a  permanent  dilatation  (p.  317)  sometimes 
develops  without  being  preceded  by  a  real  disturbance  in  compensation. 
(See  p.  318  et  seq.  in  regard  to  the  completeness  or  incompleteness  of 
contraction  of  such  a  permanently,  secondarily  dilated  and  hypertrophied 
ventricle.)  The  dilatation  of  the  left  ventricle  in  aortic  stenosis  should 
be  sharply  distinguished  from  its  dilatation  in  mitral  and  in  aortic 
insufficiency.     It  is  not  in  any  sense  compensatory ;  it  may  be  absent  in 


Fig.  120.— Diagnostic  plan  of  aortic  stenosis.   (For  explanation  of  the  signs  see  p.  321.) 

fresh  lesions,  but  in  older  lesions  it  is  frequently  to  be  found.  It  need 
scarcely  be  mentioned  that,  through  disturbances  in  the  compensation,  an 
aortic  stenosis  may  produce  the  same  effect  upon  the  pulmonary  circu- 
lation and  the  right  heart  (p.  330  et  seq.)  as  aortic  insufficiency. 

The  physical  signs  of  aortic  stenosis  are  pictured  in  Fig.  120.  Aus- 
cultation reveals  a  systolic  murmur  audible  over  the  aortic  area  in 
the  second  right  intercostal  s])ace,  transmitted  upward  to  the  vessels  of 
the  neck,  and  sometimes  audible  over  tlie  entire  left  ventricle.  The 
murmur  is  also  ])alpable  at  times,  and  may  even  be  heard  at  a  distance. 
The  murmurs  are,  in  fact,  so  constantly  loud  that  the  demonstration  of 
a  loud  systolic  murmur  argues  in  favor  of  aortic  stenosis  and  against 
accidental  murmurs.  The  conditions  for  murmur  formation  (groat  rapidity 
of  the  current,  large  volume  of  the  stream)  are  more  favorable  in  aortic 


334  DIAGNOSIS  OF  INDIVIDUAL   VALVULAR  LESIONS. 

stenosis  than  in  almost  any  other  valvular  lesion.  The  murmur  may 
possess  two  maximum  points  (over  the  aorta  and  at  the  apex)  (see  p. 
274).  The  most  essential  sign  of  aortic  stenosis  is  the  pulsus  tardus,  the 
presence  and  peculiarity  of  which  have  been  explained  (see  pp.  105  d 
seq.,  and  127).  The  tension  of  this  deliberate  and  tardy  pulse  wave 
during  the  stage  of  compensation  is  not  necessarily  low.  Frequently  it 
is  not  only  delayed,  but  also  slowed — that  is,  less  frequent  than  normaL 
Evidently  the  tardiness  and  slowness  essentially  lessen  the  heart's  work. 
In  a  high  grade  of  aortic  stenosis  this  slowing  of  the  cardiac  action  is  an 
important  condition  for  the  preservation  of  complete  compensation,  and 
is  therefore  of  especial  diagnostic  significance.  Despite  the  hypertrophy 
of  the  left  ventricle,  the  apex  beat  is  said  to  be  frequently  weakened  ;  but 
this  is  certainly  not  always  the  case.  Where  such  a  weakened  apex  beat 
does  appear,  Gutbrod-Skoda's  theory  that  it  is  due  to  a  loss  of  recoil 
depending  upon  slowness  of  cardiac  emptying  will  not  satisfy  the  con- 
ditions. For  we  know  that  the  apex  beat  coincides  with  the  closure  time 
of  the  heart.  Hence  we  must  acknowledge  that  the  recoil  theory  of  the 
heart  beat  has  been  finally  disproved.  Rosenstein's  explanation  seems 
more  plausible.  He  claims  that  the  hypertrophy  of  the  left  ventricle 
produces  a  more  rounded  shape,  and  that  it  is  more  difficult  for  such  a 
rounded  apex  to  reach  between  the  ribs,  and  so  the  apex  beat  is  weak- 
ened. Many  cases  of  aortic  stenosis  exhibit  the  strong,  slow,  heaving 
beat  described  upon  p.  293  et  seq.  If  the  moderate  force  of  the  apex 
beat  prevents  it  from  readily  pushing  through  the  intercostal  space,  the 
slowness  of  the  heaving  would  render  its  appreciation  more  difficult. 

There  is  nothing  characteristic  about  the  tones  in  aortic  stenosis. 
Ordinarily  they  persist.  Under  some  circumstances  decided  weakness 
of  the  tones  over  the  entire  left  heart  makes  it  probable  that  a  mitral 
insufficiency  complicates  the  aortic  stenosis  (see  p.  253  et  seq.).  In  this 
lesion  the  shape  of  the  cardiac  dulness  as  outlined  by  percussion  may 
be  normal ;  hence  the  probability  of  confusion  between  the  systolic 
murmur  of  an  aortic  stenosis  and  an  accidental  murmur  from  atheroma 
or  roughness  of  the  aortic  intima.  The  pulse  should  distinguish  the 
two  conditions.  Other  kinds  of  accidental  murmurs  (anemia,  fever)  are 
less  difficult  to  diagnose,  because  their  maximum  is  not  usually  over 
the  aorta.  The  author  has  already  emphasized  (p.  331)  the  frequent 
error  of  diagnosing  an  aortic  stenosis  because  a  systolic  murmur  is 
heard  over  the  aorta  in  addition  to  the  diastolic  murmur  in  aortic  insuf- 
ficiency. The  presence  or  absence  of  the  pulsus  tardus  should  be  dis- 
tinctive in  this  case  as  well.  To  distinguish  the  murmur  of  aortic 
stenosis  from  that  of  mitral  insufficiency  we  should  carefully  locate  its 
maximum  intensity  and  notice  the  characteristic,  although  slight,  differ- 
ence of  phase  (p.  271  et  seq.). 

VALVULAR   LESIONS  OF    THE   RIGHT    HEART. 

In  the  diagnosis  of  valvular  lesions  of  the  right  side  of  the  heart  it 
is  important  to    remember   that   they  are  most  frequently   congenital 


INDIVIDUAL    VALVULAR  LESIONS. 


335 


lesions,  and  that  they  rarely  originate  during  extra-uterine  life  ;  this  is 
exactly  the  reverse  of  left-sided  lesions.  Nevertheless,  acquired  right- 
sided  valvular  lesions  are  not  quite  as  rare  as  is  sometimes  claimed. 
When  they  do  originate  after  birth  they  are  most  frequently  complica- 
tions of  coexistent  left-sided  lesions. 

TRICUSPID  INSUFFICIENCY  (Figs,  121  and  122). 

As  a  relative  insufficiency  complicating  left-sided  valvular  lesions, 
this  lesion  occurs  quite  frequently ;  but  as  a  true  anatomic  valvular 
change,  it  is  rare  except  in  congenital  heart  disease.  The  weak  right 
auricle  is  all  that  exists  behind  the  tricuspid  valve  to  compensate  the 
disturbance.  Its  compensatory  power  is  naturally  limited,  so  that  the 
disturbance  to  the  circulation  is  more  serious  than  in  mitral  insuffi- 
ciency.    The  first  result  of  a  tricuspid  insufficiency  (see  the  hydraulic 


,^\atioB 


Systemic 


Fig.  121.— Hydraulic  diagram  of  tricuspid  insufficiency.   (For  explanation  see  Fig.  113.) 

scheme,  Fig.  121)  is  a  dilatation  of  the  right  auricle,  because  the 
regurgitating  blood  distends  this  chamber  during  its  diastole  (p.  316, 
Law  2).  The  dilated  auricle,  having  more  blood  to  propel,  necessarily 
hypertrophies  (Law  2).  It  must  then  force  an  increased  mass  of  blood 
into  the  right  ventricle ;  the  latter  chamber  therefore  dilates  and 
hypertrophies  (Law  2),  and  the  lesion  is  compensated  in  so  far  as  it  is 
possible.  The  right  ventricle,  in  virtue  of  its  dilatation  and  in  spite  of 
the  blood  leaking  through  the  tricuspid  orifice,  is  then  able  to  propel 
sufficient  blood  with  each  systole  into  the  pulmonary  circulation.  Prac- 
tically this  compensation  has  very  narrow  limits,  because  the  systole 
of  the  dilated  and  hypertrophied  right  auricle  is  not  sufficiently  power- 
ful to  satisfy  the  right  ventricle,  and  because  the  inherent  muscular 
weakness  of  the  right  auricle  does  not  permit  of  enough  hypertrophy 
to  overcome  the  defect ;  hence  blood  is  also  dammed  back  into  the 
veins.  When  such  a  result  is  produced,  the  amount  of  venous  blood 
which  enters  the  right  heart  will  depend  upon  the  venous  pressure,  upon 


336  DIAGNOSIS  OF  INDIVIDUAL    VALVULAR  LESIONS. 

the  elastic  tension  of  the  right  auricular  walls,  and  upon  the  aspiration 
power  of  the  thorax.  Increasing  insufficiency  of  the  tricuspid  valve 
will  then  soon  produce  the  signs  of  severe  stasis,  and,  ordinarily,  the 
circulation  will  stop  on  account  of  an  increasing  distention  of  the  venous 
system.  The  prognosis  of  tricuspid  insufficiency  is  therefore  much  more 
serious  than  that  of  mitral  insufficiency  unless  the  tricuspid  insufficiency 
is  a  relative  one,  depending  upon  back  pressure. 

In  this  lesion  a  dilatation  of  the  right  auricle  and  right  ventricle  can 
be  made  out  by  percussion  and  sometimes  by  palpation  (see  Figs.  122 
and  91).  Auscultation  discloses  a  systolic  murmur  over  the  tricuspid 
area  (p.  267).  This  murmur  can  be  differentiated  from  the  murmurs 
of  pulmonary  and  aortic  stenosis  by  a  slight  difference  in  phase  (p.  271). 
During   compensation    the    second    pulmonic    may    retain    its    normal 


Fig.  122. — Diagnostic  diagram  of  tricuspid  insufficiency.    (For  explanation  of  the  signs  see 

Fig.  90  an.d  p.  321.) 

strength ;  during  disturbance  of  compensation  it  may  be  diminished. 
The  heart  tones  over  the  right  ventricle  may  remain  normal  if  the 
insufficiency  is  slight,  or  be  weakened  if  the  insufficiency  is  marked,  just 
as  in  mitral  insufficiency  (see  p.  252).  Much  the  most  important  and  sug- 
gestive symptom  of  tricuspid  insufficiency  is  the  regurgitating  or  positive 
venous  pulse  (p.  150  et  seq.)  visible  in  the  jugular  veins,  often  visible 
as  a  liver  pulse,  and  visible  sometimes  even  in  the  small  cutaneous  veins 
of  the  body.  The  positive  venous  pulse  in  the  jugular  veins  is,  under 
some  circumstances,  accompanied  by  a  systolic  tone  over  the  jugular 
vein,  depending  upon  the  systolic  tension  of  the  vein-wall  and  of  the 
valve  at  the  bulb  (p.  284).  The  positive  venous  pulse  is  present  both 
during  effective  compensation  and  during  disturbed  compensation.  The 
arterial  pulse  remains  normal  during  perfect  compensation  ;  but  good 


INDIVIDUAL   VALVULAR  LESIONS. 


337 


compensation  is  possible  only  with  slight  degrees  of  tricuspid  insuffi- 
ciency. During  disturbed  compensation  it  very  quickly  assumes  a 
dansrerous  diminution  of  volume  and  tension. 

TRICUSPID  STENOSIS. 

This  valvular  lesion,  fortunately,  is  very  rare,  both  in  the  congenital 
and  the  acquired  forms  (Figs.  123  and  124).  Like  tricuspid  insuffi- 
ciency, it  can  be  compensated  with  difficulty,  and  then  generally  for  a 
short  time  only.  (See  the  hydraulic  scheme.  Fig.  123.)  Compensation 
takes  place  in  this  way.:  The  right  auricle,  in  consequence  of  the 
obstruction  to  the  entrance  of  the  blood  into  the  right  ventricle, 
becomes  dilated  during  the  first  period  of  the  ventricular  diastole,  when 
the  auricle  is  relaxed  (p.  316,  Law  2).  To  overcome  the  difficulty  of 
emptying  its  increased  contents  through  the  narrow  tricuspid  opening 
by   its  systole,   it  must    hypertrophy   (Laws    1  and   2).     Should  this 


(Aation 


"Systemic  cW^"^ 
Fig.  123. — Hydraulic  diagram  of  tricuspid  stenosis.    (For  explanation  see  Fig.  113.) 

hypertrophy  succeed  in  emptying  the  auricle  completely,  the  lesion  is 
compensated.  But,  just  as  with  tricuspid  insufficiency,  the  hypertrophy 
of  so  weak  a  muscular  organ  as  the  right  auricle  has  very  narrow  lim- 
its. Besides,  the  increased  contraction  only  partially  helps  the  ven- 
tricle, because  some  of  the  blood  is  regurgitated  into  the  veins.  Mild 
degrees  of  stenosis  may  therefore  attain  an  approximate  compensation, 
but  usually  the  auricle  is  quickly  paralyzed.  There  is  this  essential 
difference  between  mitral  and  tricuspid  stenosis  :  The  latter  must  be 
compensated  by  the  aid  of  the  auricle  alone,  whereas  the  former  has 
the  additional  help  of  the  right  ventricle.  In  tricuspid  stenosis  no 
reason  exists  for  a  dilatation  or  a  hypertrophy  of  any  other  heart  cham- 
ber except  the  right  auricle.  The  dilatation  of  the  right  ventricle, 
which  is  sometimes  found,  probably  always  depends  upon  a  coincident 
insufficiency  of  the  tricuspid. 

The  physical  signs  (Fig.  124)  ars  a  dilatation  of  the  right  auricle, 
demonstrable  by  percussion  or  palpation,  and  a  diastolic,  a  presystolic- 

22 


338 


BIAONOSIS  OF  INDIVIDUAL    VALVULAR  LESIONS. 


ally  accentuated,  or  a  pure  presystolic  murmur,  audible  over  the  tricus- 
pid area  (p.  269  et  seq.).  If  compensation  is  well  maintained  the 
second  pulmonary  tone  may  be  of  normal  intensity ;  with  disturb- 
ance of  compensation  it  becomes  very  faint.  The  tricuspid  tones,  like 
the  other  tones,  may  retain  their  normal  character  during  compensa- 
tion. 

Under  some  circumstances  a  presystolic  or  diastolic  tricuspid  tone 
may  be  of  some  diagnostic  service.  It  is  analogous  to  the  presystolic 
or  diastolic  mitral  tone  (p.  258  et  seq.). 

PULMONARY  INSUFFICIENCY. ^ 

Pulmonary  insufficiency,  an  inability  of  the  pulmonary  semilunar 
valves  to  close  perfectly,  is  an  exceptional  valvular  lesion  and  usually 
congenital  (Figs.  125  and  126).     Its  eflPect  upon  the  lesser  circulation  is 


Fig.  124.— Diagnostic  diagram  of  tricuspid  stenosis.    (For  explanation  of  the  signs  see  p.  321.) 


analogous  to  the  action  of  an  aortic  insufficiency  upon  the  greater. 
Compensation  (see  the  hydraulic  scheme.  Fig.  125)  M'ill  be  understood 
by  referring  to  that  lesion.  In  this  case  it  depends  upon  dilatation  and 
hypertrophy  of  the  right  ventricle. 

The  diagnostic  signs  consist  essentially  in  a  diastolic  murmur  heard 
over  the  pulmonic  area  (Fig.  126)  and  transmitted  downward  (p.  268), 
and  in  the  demonstrable  dilatation  of  the  right  ventricle.  The  diastolic 
murmur,  unlike  that  of  aortic  insufficiency,  is  not  transmitted  to  the 

'  See  Gerhardt,  "  Ueber  Schlussunfiihigkeit  der  Lungenarierienklappen,"  Ver- 
handl.  des  IL  Cong./,  inn.  Med.,  1892,  p.  290. 


INDIVIDUAL   VALVULAR  LESIONS. 


339 


neck  vessels.      The  tones  are  generally  normal,  just  as  in  aortic  insuffi- 
ciency.    The  pulsus  celer  belongs  to  the  pulmonary  circulation,  and,  so, 


Fig.  125.— Hydraulic  diagram  of  pulmonary  insufaciency.    (For  explanation  see  Fig.  113.) 

naturally  escapes  notice,  or  at  most  betrays  itself  only  by  an  exceptional 
pulsation  of  the  pulmonary  area,  provided  the  latter  is  not  covered  by 
lung  tissue  (analogous  to  the  increased  aortic  pulsation  in  aortic  insuffi- 


FiG.  126.— Diagnostic  diagram  of  pulmonary  insufficiency.    (For  an  explanation  of  the  signs' 

see  p.  321.) 


ciency,  p.  299  et  seq.).     The  lack  of  a  pulsus  celer  in  the  peripheral 
arteries  aids  in  distinguishing  pulmonary  from  aortic  insufficiency. 


340  DIAGNOSIS  OF  INDIVIDUAL    VALVULAR  LESIONS. 

Gerliardt  ^  has  called  attention  to  the  occurrence  of  a  double  tone  audible 
over  the  lung  at  some  distance  from  the  heart — i.  e.,  outside  of  the  right  scapula 
(analogous  to  the  crural  double  tone  of  aortic  insufficiency,  p.  282)  ;  also  of  a 
cog-wheel  or  jerky  respiratory  murmur  synchronous  with  the  pulse  and  heard  at 
some  distance  from  the  heart.  He  attributes  the  latter  phenomenon  to  the 
vigorous  systolic  distention  of  the  lung  vessels  by  the  pulmonary  pulsus  celer. 
Both  signs  are  to  a  certain  extent  the  audible  evidences  of  a  pulsus  celer  of  the 
pulmonary  artery. 

Pawinski  ^  has  called  attention  to  the  appearance  of  a  relative  insufficiency 
of  the  pulmonary  artery  in  mitral  stenosis  from  the  mechanical  dilatation  of 
this  artery. 

PULMONARY  STENOSIS. 

Pulmonary  stenosis  (Figs.  127  and  128)  is  the  most  frequent  of  all 
congenital  valvular  lesions,  and  therefore  has  considerable  practical 
importance.  Hypertrophy  of  the  right  ventricle  (see  hydraulic  scheme, 
Fig.  127)  is  essential  for  its  compensation  (Law  1)  ;  and  to  this  hyper- 


0^^ 

'Systemic  ci-c^^' 
Fig.  127.— Hydraulic  diagram  of  pulmonary  stenosis.    (For  explanation  see  Fig.  113.) 

trophy  dilatation  is  added  secondarily  by  disturbances  in  the  compensa- 
tion, or  sometimes  without  (Law  4). 

The  essential  physical  sign  is  the  systolic  murmur  audible  over  the 
pulmonic  area  and  the  right  ventricle,  and  often  over  the  entire  lung 
corresponding  to  the  branches  of  the  pulmonary  artery.  In  distinc- 
tion to  the  systolic  aortic  murmur,  the  murmur  of  pulmonary  stenosis 
is  not  transmitted  into  the  vessels  of  the  neck.  Sometimes  it  may  be 
differentiated  from  the  systolic  auriculoventricular  murmur  by  a  slight 
diiference  in  phase  (p.  271).  There  is  generally  nothing  characteristic 
about  the  tones.  We  may  not  be  able  to  demonstrate  a  dilatation  of 
the  right  ventricle,  because  its  hypertrophy  takes  place  only  primarily. 
But  ordinarily  a  ])aralytic  dilatation  (Law  4)  soon  occurs  and  becomes 
anatomically  fixed. 

This  lesion  is  almcst  exclusively  congenital,  and  is  frequently  com- 
bined with  pulmonary  phthisis  and  clubbed  fingers  (p.  59). 

*  Loc.  cit.  "^  Deutsch.  Arch.f.  klin.  Med.,  1894,  vol.  lii. 


INDIVIDUAL    VALVULAR  LESIONS. 


341 


DIAGNOSIS   OF  COMBINED  VALVULAR   LESIONS. 

The  diagnosis  of  single  valvular  lesions  generally  seems  compara- 
tively simple ;  but  it  is  sometimes  no  easy  task  to  distinguish  correctly, 
when,  as  so  frequently  happens,  several  lesions  are  present  at  the  same 
time.  The  relations  become  complicated,  because  one  valvular  lesion 
influences  the  other  in  regard  to  the  changes  of  pressure  within  the 
heart.  This  influence  may  be  expressed  by  alterations  in  the  strength 
of  the  heart  tones,  by  the  presence  of  dilatation  and  hypertrophy  of  indi- 
vidual chambers,  and  by  the  peculiarity  of  the  pulse.  With  combined 
valvular  lesions  the  clinician's  task  assumes  a  special  difficulty,  because 
he  must  analyze  complex  murmurs  into  several  individual  ones,  deter- 


FiG.  128.— Diagnostic  diagram  of  pulmonary  stenosis.   (For  an  explanation  of  the  signs  see  p.  321.) 


mining  their  origins,  and  decide  which  are  systolic  and  which  are  dias- 
tolic. 

The  most  important  rule  for  the  diagnosis  of  such  complicated  cases 
is  to  heed  only  those  physical  signs  which  are  characteristic  of  one 
definite  valvular  lesion  ;  then,  starting  with  the  supposition  that  this 
lesion  is  actually  present,  to  analyze  the  other  symptoms  and  determine 
whether  any  symptom  disproves  this  supposition,  and,  further,  to  decide 
whether  all  the  signs  can  be  explained  by  this  one  hypothesis.  If  one 
lesion  is  not  sufficient  to  explain  all  the  signs,  those  not  yet  explained 
should  be  considered  further.  In  this  way,  step  by  step,  we  can  com- 
plete the  diagnosis  of  combined  valvular  lesions.  The  taj>k  may  be 
lightened  by  first  considering  the  more  frequent  valvular  lesions ;  and, 
in  case  there  is  no  question  of  a  congenital  disease,  in  neglecting  the 
more  unusual  lesions  of  the  right  heart,  unless,  of  course,  some  signs 


342 


DIAGNOSIS  OF  INDIVIDUAL    VALVULAR  LESIONS. 


persist  which  cannot  be  explained  by  the  supposition  of  only  left-sided 
changes.  For  illustration  :  suppose,  in  a  case  with  several  murmurs,  a 
plain  presystolic  murmur  can  be  heard  at  the  apex.  This  murmur  is  in 
all  probability  due  to  a  mitral  stenosis,  because  tricuspid  stenosis  is  so 
rare.  We  then  try  to  see  if  this  hypothesis  will  explain  all  the  signs. 
If  a  systolic  murmur  can  also  be  heard  we  must  search  for  some 
other  cause.  We  estimate  its  maximum  point,  its  relations  of  trans- 
mission, its  exact  phase  (p.  270  et  seg.),  and  under  some  circumstances 
the  peculiarity  of  the  pulse,  and  soon  decide  whether  this  systolic  mur- 
mur arises  at  the  aortic  or  at  the  mitral  orifice.  We  then  diagnose 
two  lesions — a  mitral  stenosis  and  insufficiency — and  review  the  clinical 
picture  to  determine  whether   all  the  signs  are  satisfied,  or  whether. 


Fig.  129.— Diagnostic  diagram  of  a  complicated  valvular  lesion:  Mitral  insufficiency  and 
stenosis  and  aortic  insuflSciency,  possibly  an  aortic  stenosis  as  well.  The  last  cannot  be  diag- 
nosed from  the  cardiac  signs  alone.  The  pulse  must  first  be  carefully  examined.  (For  an  explana- 
tion of  the  signs  see  p.  321  et  seq.) 

perhaps,  we  need  to  assume  a  third  lesion.  And  so,  step  by  step,  we 
arrive  at  a  complete  diagnosis. 

To  distinguish  whether  a  murmur  audible  over  a  large  area  of  the 
heart  arises  at  one  or  more  places — in  other  words,  whether  it  is  com- 
posed of  several  diiferent  murmurs — we  should  construct  a  figure  of  the 
minimum  points,  according  to  the  rule  of  p.  272  et  seq.  This  method 
is  very  important  in  diagnosing  combined  valvular  lesions. 

A  careful  attention  to  the  evidences  in  the  vessels  (peculiarity  of  the 
pulse,  degree  of  the  cyanosis,  venous  pulse,  arterial  tones,  etc.)  will  give 
just  as  important  information  for  the  diagnosis  of  combined  as  of 
single  lesions. 

In  general,  here  as  well  as  everywhere  else,  the  systematic  analysis 


INDIVIDUAL    VALVULAR  LESIONS.  343 

of  a  clinical  picture  can  only  be  acquired  by  considerable  practice,  and 
even  then  only  after  thorough  reflection. 

Figure  129  illustrates  such  a  combined  valvular  lesion. 

CONGENITAL  VALVULAR  LESIONS;   ABNORMAL  COMMUNICATION 
OF  THE  HEART  CAVITIES;    ADMIXTURE  CYANOSIS. 

Experience  has  taught  us  that  in  making  diagnoses  of  acquired  valvular 
lesions  we  can  narrow  the  possibilities  to  those  of  the  left  heart,  excepting  the 
possibility  of  the  rather  rare  tricuspid  insufficiency.  In  congenital  lesions  we 
can  confine  our  attention  mostly  to  the  right  heart.  Perhaps  the  reason  is  that 
during  intra-uterine  life  the  right  side  of  the  heart  has  much  more  work  to  do 
than  during  extra-uterine  life,  because  the  right  ventricle  supplies  blood  not  only 
to  the  pulmonary  circulation  by  means  of  the  pulmonary  artery,  but  also  to 
part  of  the  systemic  circulation  by  means  of  the  ductus  Botalli. 

The  great  difficulty  in  the  diagnosis  of  congenital  heart  disease  is  that,  besides 
the  valvular  lesions  which  depend  ujjon  endocarditis,  there  are  very  often  developed 
obstructions,  malformations,  abnormal  communications  between  heart  cavities,  etc. , 
and  all  these  are  mutually  influenced,  etiologically  and  clinically,  in  a  very  com- 
plicated way. 

The  most  frequent  and  practically  important  conditions  of  malformation  and 
obstruction  to  be  considered  in  the  diagnosis  of  congenital  lesions  are:  a  patent 
foramen  ovale,  ventricular  septum,  or  ductus  Botalli ;  origin  of  the  aorta  from  both 
ventricles,  connection  of  the  pulmonary  artery,  closed  at  its  origin,  with  the  aorta 
through  the  ductus  Botalli  (the  right  heart  must  then  communicate  with  the  left 
through  the  foramen  ovale,  or  through  an  opening  in  the  ventricular  septum); 
transposition  of  the  great  vessels,  so  that  the  aorta  comes  from  the  right,  the  pul- 
monary artery  from  the  left,  ventricle  ;  obliteration  of  the  aorta  at  the  mouth  of  the 
ductus  Botalli  (life  is  then  preserved  by  the  formation  of  a  collateral  circulation 
between  the  upper  and  the  lower  part  of  the  aorta).  It  need  not  be  said  how 
difficult  it  is  to  recognize  these  conditions,  whether  they  appear  isolated  or  as 
complications  of  fetal  valvular  defects.  Only  a  few  hints  can  be  given  in  the 
present  state  of  modern  diagnosis. 

Much  stress  is  ordinarily  laid  upon  the  exceptionally  pronounced  cyanosis 
which  appears  so  frequently  in  congenital  heart  disease,  and  which  is  often  attrib- 
uted to  the  admixture  of  venous  with  arterial  blood  through  some  communication. 
The  conditions  are,  however,  especially  favox'able  for  a  high  grade  of  cyanosis  in 
right-sided  valvular  lesions  without  supposing  the  admixture  of  arterial  and  venous 
blood,  because,  on  the  one  hand,  compensation  is  here  either  very  poor  or  soon 
disturbed  (e.  g.,  tricuspid  lesions),  and  because,  on  the  other  hand,  in  all  right- 
sided,  even  in  pulmonary,  lesions,  as  soon  as  there  is  a  disturbance  in  compensa- 
tion, .the  stasis  must  be  concentrated  in  a  most  direct  and  intense  way  upon  the 
systemic  veins.  Therefore,  in  congenital  cardiac  disease  it  is  incorrect  to  make  a 
diagnosis  of  an  abnormal  communication  and  consequent  admixture  of  arterial 
and  venous  blood  simply  from  marked  cyanosis.  Many  authors  even  go  so  far  as 
to  deny  the  possibility  of  such  admixture  cyanosis,  on  account  of  certain  mechan- 
ical considerations.  They  are  supported  with  some  reason  by  the  fact  that  com- 
munications between  the  ventricles  and  between  the  auricles  have  sometimes  been 
found  at  autopsies  without  any  signs  during  life  of  such  a  cyanosis.  And  they 
contend  that  this  lack  of  admixture  cyanosis  (despite  the  communication)  is  not 
surprising,  because  the  two  abnormally  communicating  heart  cavities  contract 
coincidentally,  so  that  no  blood  need  be  sent  from  one  to  the  other.  Certainly, 
every  abnormal  communication  of  the  cardiac  cavities  does  not  cause  admixture 
cyanosis;  but  it  is  probable  that  under  certain  conditions  venous  blood  may  be 
mixed  with  arterial.     The  following  examples  may  be  cited  in  evidence : 

A  mere  defect  in  the  septum  between  the  auricles  and  the  ventricles  ordi- 
narily causes  no  admixture  cyanosis ;  yet  it  is  perfectly  easy  to  understand  that  such 
an  effect  may  result  if  at  the  same  time  a  right-sided  valvular  lesion  is  also  present. 


344  DIAGNOSIS  OF  INDIVIDUAL    VALVULAR  LESIONS. 

With  tricuspid  insufficiency,  for  example,  and  an  open  foramen  ovale,  the  ven- 
tricular systole  may  force  the  venous  blood  out  of  the  right  ventricle  not  only  into 
the  right,  but  also,  in  consequence  of  the  increase  of  pressure,  into  the  left 
auricle.  With  tricuspid  stenosis,  during  ventricular  diastole  the  blood  from  the 
right  auricle  may  partly  flow  in  the  direction  of  least  resistance  through  the  foramen 
ovale  into  the  left  auricle  and  ventricle.  Just  so  it  is  conceivable  that  in  pul- 
monary stenosis  during  diastole  the  blood  from  the  right  ventricle  is  forced  into  the 
left  ventricle  through  a  patent  ventricular  septum,  the  presumption  being  that  the 
right  ventricle  has  become  so  strongly  hypertrophied  that  it  overbalances  the  aortic 
pressure  which  acts  upon  the  other  side  of  the  communicating  orifice. 

The  plainest  and,  perhaps,  also  most  frequent  example  of  admixture  cyanosis  is- 
"straddling"  of  the  aorta — i.  e.,  its  origin  from  both  ventricles  and  insertion 
above  the  defect  in  the  ventricular  septum.  Here,  of  course,  the  aorta  must  con- 
tain mixed  blood.     We  observe  this  appearance  in  congenital  pulmonary  stenosis. 

Patency  of  the  ductus  Botalli  alone  can  hardly  occasion  admixture  cyanosis, 
because  the  aortic  pressure,  if  no  other  anomaly  is  present,  is  always  higher  than 
that  of  the  pulmonary  artery,  so  that  the  blood  could  pass  through  the  aorta  into- 
the  pulmonary  artery,  but  not  in  the  reverse  direction.  But  mixed  blood  must  flow 
into  the  aorta  if  the  ductus  Botalli  is  the  only  outlet  of  the  pulmonary  artery,  which 
is  completely  closed  at  its  opening  into  the  right  ventricle,  because  the  aorta  must 
obtain  its  blood  fi-om  the  opening  in  the  ventricular  septum — i.  e. ,  from  the  right 
ventricle. 

In  congenital  valvular  lesions,  therefore,  it  is  reasonable  to  assume  the  possibility 
of  admixture  cyanosis,  and  to  be  fairly  certain  of  its  presence,  if  the  cyanosis  is 
very  pronounced  while  the  veins  are  very  little  dilated  (marked  cyanosis  with  slight 
stasis). 

In  any  given  case,  however,  the  cause  of  the  admixture  cyanosis  is  not  so  easily 
determined.  In  tricuspid  lesions  we  should  naturally  first  suppose  an  open  foramen 
ovale;  whereas,  in  pulmonary  stenosis  a  patent  ventricular  septum,  with  or  without 
a  straddling  aorta,  would  be  more  probable.  Under  some  circumstances  a  systolic 
murmur  at  the  cardiac  apex  may  be  a  positive  sign  of  a  ventricular  septum  defect. 
This  sign  is,  however,  of  very  little  practical  .value,  because  in  pulmonary  steno- 
sis just  where  a  patent  ventricular  septum  is  to  be  taken  into  consideration  the  sys- 
tolic murmur  is  frequently  very  plainly  audible  over  the  entire  heart,  because  it 
proceeds  from  the  entire  right  ventricle  (p.  267  et  seq.). 

It  is  difficult  to  diagnosticate  patency  of  the  ductus  Botalli.  We  should  re- 
member that  this  anomaly  very  often  accompanies  congenital  pulmonary  stenosis. 
Zinn  and  Hermann  Miiller  ^  have  called  attention  to  a  band-like  dulness  reaching 
upward  and  to  the  left  of  the  upper  part  of  the  sternum.  An  accentuation  of  the 
second  pulmonic  has  been  repeatedly  stated  to  be  a  result  of  a  patent  ductus 
Botalli,  because  with  this  abnormality  the  pulmonary  arteries  are  affected  by  the 
aortic  pressure.  Miiller  attributes  diagnostic  significance  to  the  systolic  and  dias- 
tolic murmurs  which  appear  over  the  great  vessels,  and  states  that  they  sometimes 
merge  into  a  practically  continuous  murmur.  The  systolic  murmur  depends  upon 
the  systolic  passage  of  blood  from  the  aorta  through  the  narrow  ductus  Botalli  into 
the  pulmonary  aorta  ;  the  diastolic  murmur,  upon  the  diastolic  continuation  of  this 
current.  The  congenital  obliteration  of  the  aorta  at  the  place  of  origin  of  the 
ductus  Botalli  is,  on  the  contrary,  very  easy  to  diagnose,  whether  it  is  associated 
with  congenital  valvular  lesions  or  isolated.  The  collateral  circulation  by  which 
the  blood  flows  from  the  peripheral  arteries  of  the  upper  part  of  the  body 
(subclavian,  etc.)  to  the  lower  part  of  the  aorta  becomes  visible  under  the  skin  and 
makes  the  diagnosis  clear.  Such  an  obliteration  may  exist  without  any  disturb- 
ances of  the  circulation. 

There  are  many  questions  in  the  pathology  and  diagnosis  of  congenital  heart, 
lesions  which  still  lack  solution. 

1  Corresp.-Bl.  f.  schw.  Aerzle,  1899,  p.  449. 


ANEURISM  OF  THE  AORTA. 


345 


ANEURISM   OF  THE   AORTA.       • 

Aortic  aneurisms  are  most  frequently  situated  upon  the  ascending  aorta  or  upon 
the  arch  of  the  aorta.  When  an  aneurism  reaches  a  certain  size  Ave  can  detect  a 
prominence  in  the  upper  intercostal  spaces  to  the  right  of  the  sternum  ;  and  appre- 
ciate it  by  palpation  as  well.  Small  aneurisms  may  not  exhibit  any  prominence,  but 
the  pulsation  can  generally  be  appreciated  by  palpation.  If  the  aneurism  reaches 
to  the  surface,  j^ercussion  will  show  a  decided  dulness,  which  generally  merges 
with  the  cardiac  dulness.  If  a  layer  of  lung  remains  in  front  of  the  aneurism,  the 
dulness  may  be  either  entirely  absent  or  there  may  be  only  a  moderate,  deep  dul- 
ness, demonstrable  by  strong  percussion.  Here,  too,  the  pulsation  may  be  trans- 
mitted through  the  overlying  layers  of  lung  up  to  the  surface.  Auscultation  very 
frequently  reveals  a  systolic  murmur,  which  may  sometimes  be  appreciated  by 
palpation.  The  entrance  of  the  blood  into  the  aneurismal  sac  produces  this  mur- 
mur because  there  is  a  widening  of  lumen  in  the  blood-path  (p.  261  et  seq.    See 


Fig.  130.— Large  aneurism  of  ascending  and  transverse  arch  of  aorta  (New  York  City  Hospital). 


Fig.  103,  III.).  This  murmur,  like  that  of  aortic  stenosis,  is  transmitted  most 
distinctly  in  the  direction  of  the  aortic  current — i.  e. ,  to  the  neck  vessels.  Dias- 
tolic murmurs  are,  however,  sometimes  due  to  aneurisms.  If  there  is  no  com- 
plicating aortic  insufficiency,  such  a  murmur  arises  from  the  regurgitation  of 
blood  into  the  sac,  which  is  stretched  during  diastole.  Similar  murmurs  may  be 
heard  over  the  abdominal  aorta.  ^  Under  such  circumstances  a  diastolic  murmur 
may  be  one  of  the  earliest  signs  of  an  aortic  aneurism,  and  may  readily  lead  to 
a  confusion  with  aortic  insufficiency  unless  the  aiieurism  is  evident  to  inspection, 
palpation,  and  percussion.  Frequently,  however,  the  diastolic  murmur  over  an 
aortic  aneurism,  depends  upon  a  combination  of  the  aneurism  with  an  aortic  in- 
sufficiency. For  the  sac,  continually  increasing  in  size,  gradually  produces  a 
dilatation  of  the  aortic  orifice,  and  so  a  relative  insufficiency,  or  else  the  endar- 
teritis, which  is  always  present  in  an  aneurismal  aorta,  attacks  the  valves  as  well. 
Unless  an  aortic  aneurism  is  combined  with  a  valvular  lesion,  the  heart  need  not 
be  hypertrophied  nor  dilated,  because  an  aneurismal  dilatation  of  the  aorta  by 
itself  offers  no  considerable  obstacle  to  the  circulation.     Large  aneurisms,  on  the 

'  V.  Leyden,  Deuisch.  med.  Woch.,  ,1900,  No.  23,  p.  365  et  seq. 


346  DIAGNOSIS  OF  INDIVIDUAL    VALVULAR  LESIONS. 

contrary,  generally  crowd  the  heart  somewhat  to  the  left,  so  that  the  apex  beat 
lies  farther  outside  than  normally.  To  determine  the  exact  seat  of  the  aneurism 
in  relation  to  the  origin  of  the  innominate  and  of  the  left  carotid  and  subclavian 
arteries,  we  should  accurately  compare  the  exact  time  and  strength  of  the  carotid 
and  radial  pulses  on  the  two  sides.  The  aneurismal  dilatation  frequently  delays 
the  pulse  in  those  arteries  which  arise  from  the  aorta  beyond  the  aneurism,  because 
a  sort  of  pump  action  retards  the  pulse  wave.  In  other  cases  the  delay  is  due  to 
the  fact  that  some  of  the  arteries  arise  from  the  sac  itself,  and  are  narrowed  at 
their  origin.  The  pulse  may  then  be  also  abnormally  small.  In  many  cases  ceitain 
accompanying  signs  are  important  in  confirming  the  diagnosis  of  aneurism.  They 
are  to  be  attributed  to  the  pressure  of  the  aneurism  upon  the  trachea,  with  dyspnea  ; 
upon  the  esophagus,  with  difficulty  in  swallowing  ;  upon  the  left  bronchus,  with 
a  diminished  respiratory  murmur  over  the  left  lung  ;  upon  the  left,  rarely  upon 
the  right,  recurrent  laryngeal,  with  a  unilaterial  vocal  paralysis.     A  venous  col- 


FiG.  131. — Aneurism  of  the  descending  arch  of  the  aorta  (Dr.  Cutler,  Massachusetts  General 

Hospital)  (see  x-ray). 

lateral  circulation  visible  in  the  skin  over  the  chest  is  of  the  same  diagnostic 
importance  for  an  aneurism  as  for  other  intrathoracic  tumors  (p.  55etseq.).  It 
results  from  the  pressure  of  the  aneurism  upon  the  great  veins  inside  the  thorax. 
Mention  should  be  made  of  the  Oliver- Car darelli  sign  (tracheal  tug)  (p.  299). 
The  symptoms  of  the  rare  aortic  aneurisms  which  are  situated  at  some  distance 
from  the  great  vessels  of  the  heart  (thoracic  and  abdominal  aorta)  can  be  readily 
deduced. 

In  consequence  of  the  increased  systole  of  the  left  ventricle,  an  aortic  insuffi- 
ciency may  cause  a  considerable  diffuse  dilatation  of  the  ascending  aorta  and 
produce  an  abnormal  pulsation  and  increased  dulness  over  the  upjjer  intercostal 
spaces  to  the  right  of  the  heart  (see  Fig.  92).  Pain  is  a  prominent  s^Tiiptom  in 
this  condition  as  well  as  in  aortic  aneurism,  so  there  may  be  some  difficulty  in 
the  differential  diagnosis.  The  most  important  criteria  for  diagnosing  a  sacular 
aneurism  are  the  exhibition  of  comjjression  signs  (recurrent  paralysis,  etc.),  of  the 


PERICARDITIS. 


347 


Oliver-Cardarelli  phenomenon,  and  of  difference  in  the  pulses.  If  an  aneurism 
forms  a  circumscribed,  prominent  tumor,  dull  to  percussion,  there  will  be  no 
possibility  of  confusion. 

Recently  the  Eontgen  rays  have  been  repeatedly  employed  in  the  diagnosis  of 
aortic  aneurism.  They  allow  of  certain  conclusions,  however,  only  when  the 
aneurism  is  in  the  form  of  a  pulsating  tumor  which  is  distinctly  separated  from 
the  heart.  These  are  cases  in  which  other  methods  of  examination  usually  deter- 
mine the  diagnosis.  In  contrast  to  these  cases,  there  are  many  others  in  which 
the  Eontgen  examination  will  not  certainly  diflerentiate  an  aortic  aneurism  from 
a  diffuse  dilatation  of  the  aorta  due  to  aortic  regurgitation,  or  even  from  a  dilated 
right  ventricle.  For  the  details  of  the  Eontgen  examination  the  reader  is  referred 
to  the  special  works  upon  the  subject. 

PERICARDITIS. 

Physical  examination  generally  reveals  a  dry  pericarditis  by  a  char- 
acteristic rubbing  friction  sound  (see  p.  279  et  seq.).  So  long  as  the 
layers  of  the  pericardium  are  not  separated  from  one  another  by  a  fluid 
exudation  throughout  their  entire  extent,  exudative  pericarditis  will  also 


Fig.  132.— Diagnostic 


im  of  an  exudative  pericarditis  (see  pp.  279  and  321  for  an  explana- 
tion of  the  signs). 


cause  a  pericardial  friction  rub,  because  there  is  always  a  deposition  of 
exuded  fibrin  in  addition  to  the  fluid  (p.  280).  The  cardinal  sign  of 
exudative  pericarditis  is,  however,  a  characteristic  cardiac  dulness  which 
is  increased  upward.  It  ordinarily  assumes  the  form  of  a  blunt  triangle 
with  its  base  below  (p.  187  et  seq.).  The  width  of  this  duhiess  is  in- 
creased in  the  sitting  or  erect  posture  (p.  187  etseq.),  the  apex  beat  is 
weakened  (p.  294),  and  the  heart  tones  are  also  enfeebled  (p.  250), 
especially  in  the  outer  portions,  on  account  of  the  interposed  exudation. 
In  some  cases  the  apex  beat  lies  within  the  borders  of  superficial  cardiac 


348  GRAPHIC  EXPRESSIONS  IN  PULMONARY  CASES. 

dulness  (p.  295  et  seq.),  and  frequently  there  is  a  visible  prominence  of 
the  precordia  (p.  34).  Beyond  these  features  the  diagram  (Fig.  132) 
will  illustrate  the  entire  clinical  picture  of  exudative  pericarditis.  Such 
a  border  of  deep  cardiac  dulness  does  not  always  occur  (see  p.  185  et 
seq.),  and  the  heart  is  apparently  laid  bare  by  the  crowding  back  of  the 
lungs,  causing  only  a  very  large  superficial  dulness. 


GRAPHIC  EXPRESSIONS  FOR  THE  PHYSICAL  SIGNS 
IN   PULMONARY  CASES. 

In  the  sections  upon  Percussion,  Auscultation,  Inspection  and  Palpa- 
tion we  have  described  and  explained  the  individual  physical  signs  of 
pulmonary  and  pleural  affections,  and  so  now  we  need  only  add  a  con- 
cise abstract  of  our  method  of  combining  these  signs  in  order  to  make 
a  general  picture  in  any  given  case.  For  the  sake  of  simplicity  and 
brevity  we  employ  graphic  expressions  to  describe  the  lung  conditions. 
These  have  been  found,  in  the  Clinic  at  Bern,  both  practical  and  com- 
prehensive. 

The  rules  for  such  graphic  expression  are  simple  and  easily  mem- 
orized. We  represent  the  respiratory  murmur  audible  over  a  certain 
area  of  the  lung  by  a  small  right  angle,  and  mark  it  at  the  correspond- 
ing spot  upon  a  chest  diagram.  This  sign  may  be  modified  in  various 
ways,  according  to  the  modification  of  quality  of  the  respiratory  mur- 
mur. The  vertical  limb  of  the  angle  represents  the  inspiratory  murmur  j 
the  horizontal,  the  expiratory  murmur ;  the  length  of  the  limb  shows 
its  duration ;  the  thickness,  its  intensity.  A  simple,  smooth,  straight 
line  signifies  normal  vesicular  breathing ;  a  dotted  line,  cog-wheel  breath- 
ing ;  a  toothed  line,  rough  vesicular  breathing.  A  small  cross-line 
on  the  limb  signifies  mixed  breathing ;  two  cross-lines,  pure  bronchial 
breathing.     From  these  rules  we  can  readily  understand  the  following  : 

L  Vesicular  breathing. 

L  Weak  vesicular  breathing  (diminished). 

L  Coarse  vesicular  breathing. 

L  Coarse  vesicular  breathing  with  prolonged  expiration. 

|_  Rough  vesicular  breathing  with  prolonged  expiration. 

=fcj^  Bronchial  breathing. 

4^  Mixed  (bronchovesicular)  inspiration  with  bronchial  expiration. 

[f^  Vesicular  inspiration  with  bronchial  expiration. 

■L_  Mixed  (bronchovesicular)  inspiration  with  prolonged  expiration. 

L...  Cog-wheel  vesicular  breathing. 

Lf^  Cog-wheel  inspiration  with  bronchial  expiration. 

Li  Indistinct  (feeble)  breathing,  etc. 


GRAPHIC  EXPRESSIONS  IN  PULMONARY  CASES.  349 

The  rales  are  designated  thus  : 

Dry  rales  : 
i^T'    Sonorous  and  sibilant. 
A      Crackling  (creaking). 

Moist  rales  : 

(a)  Non-consonating  or  non-resonant. 

qOq     Large,  coarse,  ^ 

o°o      Small,  fine, 

Moist  or  bubbling. 


-as 


Medium, 
Mixed, 


(6)  Consonating  or  resonant. 


*      Large,  coarse,  ^ 


•  • 


)■  Moist  or  bubbling. 


,:.      Small,  fine, 
•%      Medium, 

•  :•     Mixed, 

Inspiratory  rales  are  designated  by  prefixing  the  letter  "  i "  ;  expira- 
tory, by  prefixing  "  e  "  ;  e.  g., 

Inspiratory,  non-consonating,  mixed  moist  or  bubbling  rales,  "  /o?o  •" 

Inspiratory  and  expiratory  sonorous  and  sibilant,  le  nO^  • 

Crepitant  rales  or  crepitation  are  designated  by  prefixing  Kn. 

A  pleuritic  or  a  pericardial  rub  is  designated  by  the  sign:  /vMaa, 

yvMM.     If  it  is  possible  to  confuse  a  pleuritic  with  a  pericardial  rub, 

"  pi "  or  "  pe  "  should  be  prefixed. 

Tone  phenomena  are  expressed  as  words,  or  abbreviations  may  be 
used,  as : 

ty  =  tympanitic  note, 
hty  =  high  tympanitic  note. 
Ity  =  low  tympanitic  note. 

'In  recapitulation  we  may  mention  (see  p.  1 64)  that  a  blue  surface 
corresponds  to  the  superficial  dulness — i.  e.,  with  light  percussion — 
the  red,  to  the  deep  dulness.  A  mixed  color  is  employed  for  a  dul- 
ness which  can  be  demonstrated  as  well  by  deep  as  by  superficial  per- 
cussion. The  intensity  of  the  color  represents  the  intensity  of  the 
dulness.  Palpable  borders  are  represented  in  black.  The  border  lines 
are  generally  so  drawn  that  the  form  of  the  dulness  and  the  direction 
of  the  lines  correspond  as  nearly  as  possible  to  the  reality. 


J50 


GRAPHIC  EXPRESSIONS  IN  PULMONARY  CASES. 


Fig.  133.— Physical  signs  in  riglit  pleurisy  with  efFusions. 


Fig.  134.— Physical  examination  in  left  pyopneumothorax  (see  Fig.  98.) 


GRAPHIC  EXPRESSIONS  IN  PULMONARY  CASES.  351 


-  Transmitted. 


Fig.  135.— Physical  examination  in  left  croupous  pneumonia. 


Ketraction  of  the  pul- 

T  monary  border. 


Fig.  136.— Physical  signs  in  pulmonary  phthisis  :  Marked  change  on  the  right;  beginning 

on  the  left. 


352  GRAPHIC  EXPRESSIONS  IN  PULMONARY  CASES. 


Fig.  137— Physical  signs  in  catarrhal  pneumonias,  infarcts,  etc. 


Fig.  138.— Physical  examination  in  diflfnse  bronchitis. 


EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS.    353 


Fig.  139.— Physical  examination  iu  capillary  bronchitis  or  miliary  tuberculosis. 


EXAMINATION    OF  THE  STOMACH    AND   STOMACH 

CONTENTS. 

Under  the  examination  of  the  stomach  we  shall  consider  not  only 
the  estimation  of  its  size  and  position,  and  whatever  other  results  may 
be  determined  by  palpation  (pain,  demonstration  of  tumors,  etc.),  but 
more  particularly  the  methods  of  testing  its  specific  functions.  Purely 
physical  methods  of  examination  furnish  such  meagre  results  that  we 
have  to  depend  upon  the  last-named  methods  for  most  of  the  diagnostic 
points.  Therefore  the  bulk  of  the  following  section  will  be  devoted  to 
the  functional  examination  of  the  stomach,  and  especially  to  the  study 
of  its  secretion  relations.  Under  the  examination  of  air-containing 
abdominal  viscera  we  have  already  alluded  to  many  points  in  physical 
diagnosis  (compare  pp.  196  et  seq.,  215  etseq.,  and  301  et  seq.).  We  have 
intentionally  postponed  until  now  any  more  minute  consideration  of  the 
physical  methods  of  examining  the  stomach,  because  such  methods  reveal 
but  isolated  symptoms  which  are  of  no  value  excejit  in  connection  with 
others.  Many  of  the  cases  require  the  employment  of  the  stomach 
tube,  although  its  use  is  attended  with  certain  discomfoi'ts,  and  at  times 
even  with  injuries,  to  the  patient.  Still,  quite  a  number  of  important 
diagnostic  points  may,  of  course,  be  obtained  without  using  the  tube, 
so  that  it  is  advisable  to  employ  first  the  other  methods  of  examination. 

23 


354    EXAMIXATIOy  OF  THE  STOMACH  ANB  STOMACH  CONTENTS. 


METHODS    OF    EXAMINATION    WITHOUT   EMPLOYING 
THE  STOMACH  TUBE. 

The  subjective  symptoms  in  the  diagnosis  of  stomach  disorders 
play  an  important  part — i.  e.,  the  complaints,  the  kind  of  pain  or  vomit- 
ing, when  the  latter  occurs,  the  character  of  the  stools,  etc. — in  short, 
the  history  in  the  broadest  sense  of  the  word.  But  all  this  belongs 
rather  to  special  pathology. 

For  the  objective  examination,  which  chiefly  concerns  us,  we  refer 
to  the  sections  upon  Inspection,  Palpation,  and  Percussion  of  the 
Abdomen.     But  a  few  special  points  must  be  taken  up  here. 

THE  DETERMINATION  OF  THE  SIZE,  POSITION,  AND  SHAPE  OF 
THE  STOMACH,  THE  SaCALLED  SPLASHING  SOUNDS  OF  THE 
STOMACH. 

It  is  difficult  to  estimate  the  size  of  the  stomach  by  percussion  im- 
mediately, but,  if  the  abdominal  walls  are  lax,  inspection  will  often  show 
the  outlines  of  the  stomach,  the  greater  and  sometimes  the  lesser  curva- 
ture as  well.  Palpation  will  sometimes  permit  a  difPerentiation  of  the 
tense  stomach  from  the  less  tense  intestines.  If  these  methods  of  ex- 
amination afford  no  definite  result,  as  is  frequently  the  case,  we  may  fill 
the  stomach  either  with  gas  or  fluid.  The  former  may  be  accomplished 
bv  giving  the  patient  a  teaspoonful  of  sodium  bicarbonate,  and  imme- 
diately afterward  the  same  amount  of  tartaric  acid,  each  salt  dissolved 
in  a  half-glassful  of  water.  The  alkaline  solution  should  always  be 
swallowed  first,  because  the  acid  solution  might  cause  pain  if  the  mucous- 
membrane  is  sensitive,  and  especially  if  a  gastric  ulcer  is  present.  The 
admixture  of  the  two  solutions  produces  carbonic  acid  gas,  which  dilates 
the  stomach  like  an  air  cushion,  so  that  its  outlines  can  be  easily  defined 
by  inspection,  palpation,  and  percussion.  If  this  test  is  successful,  per- 
cussion is  hardly  necessary.  The  experiment  is,  however,  not  always 
successful,  for  the  stomach  may  rapidly  expel  the  gas,  either  upward  or 
downward.  Again,  a  large  dilated  stomach  might  recjuire  the  develop- 
ment of  more  gas,  and  so  we  should  have  to  repeat  the  attempt  with  a 
second  and  larger  dose  of  effervescing  powder.  It  is  not  advisable  to 
use  too  great  an  amount  at  first,  because  it  may  distend  the  stomach 
too  much  and  cause  pain.  Inflating  the  stomach  with  air  by  means  of 
an  ordinary  Davidson  syringe  is  free  from  all  these  disadvantages  and 
the  amount  of  air  can  easily  be  controlled. 

A  reasonably  accurate  estimate  of  the  size  of  the  stomach  can  be 
reached  in  some  cases  by  noting  the  change  in  percussion  which  ensues 
when  the  patient  while  erect  swallows  water  little  by  little.  It  is  best 
to  commence  mth  the  fasting  stomach,  which  is  usually  retracted  and 
entirely  covered  by  intestine.  After  one  or  two  glassfuls  of  warm  v.'ater 
have  been  swallowed,  the  fundus  will  be  dropped  downward  and 
forward,  and  light  percussion  will  bring  out  an  approximately 
half-moon-shaped  dulness  in  the  region  of  the  greater  curvature  (Fig. 


EXAMINATION  WITHOUT  EMPLOYING   THE  STOMACH  TUBE.  355 

140,  a).  It  is  perfectly  easy  to  see  that  this  dulness  corresponds  to  the 
liquid  within  the  stomach,  for  if  the  patient  swallows  more  water  the 
size  of  the  dull  area  will  be  increased  upward,  provided  the  stomach- 
wall  is  of  normal  resistance  (6)  ;  but  wnth  a  lax  wall  or  with  a  patho- 
logic dilatation  of  the  stomach,  the  weight  of  the  fluid  will  depress  the 
greater  curvature  (c).  This  method  is  generally  less  valuable  than 
inflation  with  gas  ;  besides,  it  is  annoying  and  sometimes  distressing  to 
the  patient,  especially  so  unless  moderately  warm  water  is  employed. 

The  dislocation  of  the  spleen  in  association  with  gastric  dilatation 
should  always  be  borne  in  mind.  The  enlarging  stomach  draws  it 
downward,  hj  means  of  the  gastrosplenic  ligament,  until  it  can  be 
readily  palpated. 


Fig.  140.— Dulness  due  to  liquid  in  the  stomach,  percussion  in  the  erect  posture:  a,  With  a 
small  amount ;  6  and  c,  with  larger  amounts  ;  b,  with  normal  gastric  tone  ;  c,  with  relaxed  gastric 
tone—/,  e.,  stretching  of  the  greater  curvature  by  the  weight  of  the  fluid. 

The  normal  position  of  the  greater  curvature  should  not  be  lower 
than  perhaps  two  finger-breadths  above  the  navel  (compare  Fig.  74). 
But  in  estimating  the  size  of  the  stomach  we  must  remember  that  the 
greater  curvature  is  always  depressed  in  gastroptosis,  either  in  the  con- 
genital form  or  especially  in  that  resulting  from  enteroptosis,  and  also 
in  the  anomalous  loop-shaped  type ;  and  yet  in  both  these  instances  the 
stomach  need  not  be  really  dilated  and  its  functions  may  still  be  normal. 
Therefore  it  is  advi.^able  to  map  out  the  position  of  the  lesser  as  well 
as  of  the  greater  curvature,  and  both  can  be  best  accomplished  by 
inflating  with  gas. 

The  capacity  of  the  stomach  varies  considerably  even  under  physio- 
logic conditions.     This  variation  depends  largely  upon  the  diet — e.  g.,  a 


356    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

person  who  lives  chiefly  upon  vegetables,  such  as  potatoes,  exhibits  a  very- 
large  stomach,  although  it  need  by  no  means  be  diseased.  Increased 
capacity  then  signifies  only  an  enlargement  of  the  stomach.  Before  a 
stomach  can  justly  be  called  a  dilated  stomach,  or  "  stauungsmagen,"  we 
must  be  sure  that  the  enlargement  is  accompanied  by  a  loss  of  motility 
— i.  e.,  by  motor  insufficiency. 

Splashing  sounds  in  the  gastric  region  (see  later  section  upon  Gas- 
tric Motility)  elicited  by  so-called  "  dipping  "  percussion  depend  upon 
the  presence  of  air  and  fluid.  For  this  purpose  the  patient  is  best 
examined  in  the  dorsal  decubitus.  With  the  left  hand  placed  flat  upon 
the  epigastrium  for  palpation,  and  the  ear  near  the  body,  the  examiner 
strikes  gently  with  the  right  hand  in  the  left  hypochondrium,  or  upon  the 
lower  left  ribs.  The  splashing  may  then  be  felt  as  well  as  heard.  Splash- 
ing sounds  do  not  necessarily  mean  a  dilatation  or  a  stomach  with 
insufficient  motor  power  unless  they  are  elicited  when  the  stomach  should 
be  empty — e.  g.,  in  the  morning  before  breakfast,  or  more  than  seven 
hours  after  an  ordinary  meal.  If  heard  or  felt  under  such  circumstances 
the  sign  means  motor  insufficiency  of  the  stomach,  which  is  most  com- 
mon in  pathologic  dilatation  of  the  stomach.  Again,  if  the  splashing 
can  be  obtained  over  an  area  larger  than  the  normal  (see  above),  then 
we  may  consider  the  organ  enlarged. 

A  very  decided  splashing  sound  elicited  by  quite  gentle  tapping 
over  the  stomach  area  suggests,  however,  a  gastric  atony,  even  if 
obtained  within  the  time  limits  mentioned  above.  We  might  call  this 
"superficial  splashing,"  in  contrast  to  "deep  splashing"  elicited  by 
vigorous  blows.  This  superficial  splashing  merely  shows  that  the 
stomach-walls  are  relaxed  (gastric  atony),  but  does  not  necessarily  mean 
that  the  stomach  is  dilated  (gastric  dilatation).  On  the  other  hand,  a 
pathologically  dilated  stomach,  or  "stauungsmagen,"  need  not  show 
any  decided  signs  of  atony — i.  e.,  it  need  not  furnish  any  superficial 
splashing,  especially  when  the  gastric  dilatation  is  due  to  stenosis  of  the 
pylorus. 

A  pathologic  dilatation  of  the  stomach  which  does  not  lead  to  a 
superficial  splashing,  and  that  condition  which  does  lead  to  a  superficial 
splashing — i.  e.,  atony — are  two  fundamentally  different  lesions,  and 
should  be  distinguished  properly  one  from  the  other.  The  foregoing 
explanation  of  the  significance  of  superficial  splashing  should  not  be 
misconstrued,  as  it  has  been.^  For  the  author  does  not  invariably  make 
a  diagnosis  of  motor  insufficiency  of  the  stomach  merely  from  the  demon- 
stration of  a  superficial  splashing.  Nor  does  he  regard  motor  insuffi- 
ciency and  atony  as  identical  conditions.  By  atony  he  understands 
merely  a  diminished  tension.  Many  such  gastric  atonies  are  never  com- 
plicated by  any  other  symptoms,  and  he  especially  wishes  to  insist  that 
the  presence  of  food  in  the  stomach  need  not  be  in  any  way  prolonged 
by  mere  atony.  He  considers  "  atony  "  diagnostically  significant,  not 
as  a  name  of  a  disease,  but  merely  as  a  name  of  the  physical  condition 
of  the  stomach,  with  which,  of  course,  diseased  conditions  of  the  gastric 
1  Eisner,  Berlin,  klin.  Woch.,  1901,  No.  16. 


EXAMINATION  WITHOUT  EMPLOYING   THE  STOMACH  TUBE.  357 

function  may  under  some  circimistances  be  combined.  So  far  as  the 
significance  of  "  superficial  splashing  "  is  concerned,  it  should  be  noted 
that  even  relaxed  abdominal  walls  may  favor  the  origin  of  "  superficial 
splashing,"  because  the  tension  upon  the  abdominal  contents  equals  the 
sum  of  the  pressure  of  the  abdominal  wall  and  of  the  gastric  muscula- 
ture, and  because  a  superficial  blow  naturally  has  a  stronger  action  the 
less  the  tension  of  the  abdominal  walls.  From  perfectly  evident  rea- 
sons "  superficial  splashing  "  will  be  favored  by  a  low  position  of  the 
stomach  (gastroptosis),  quite  independent  of  the  usual  association  of 
this  position  with  gastric  atony.  It  may  still  further  be  noted  that  the 
atony  of  the  gastric  muscularis  may  be  entirely  concealed  by  pronounced 
passive  tension  of  the  gastric  wall  due  to  an  abundant  meal.  Then, 
despite  the  atony,  the  full  stomach,  up  to  a  certain  time,  will  not  furnish 
any  "superficial  splashing." 

Sometimes  a  splashing  may  be  wrongly  referred  to  the  stomach 
when  it  really  proceeds  from  the  colon  filled  with  liquid  feces  and  gas, 
as  in  some  cases  of  diarrhea.  The  existence  of  diarrhea  and  the  demon- 
stration of  a  similar  splashing  along  the  ascending  and  descending  colon 
will  usually  prevent  any  confusion.  Neurasthenics  and  hypochondriacs 
sometimes  consult  their  physician  in  regard  to  a  splashing  sound 
which  they  produce  themselves  in  the  gastric  region  by  contracting  and 
retracting  their  abdominal  walls.  This  sound  may  be  a  true  splashing, 
but  it  is  important  only  when  it  occurs  under  the  conditions  mentioned 
above.  It  may  be  produced  when  the  stomach  is  quite  normal  and 
nearly  empty  by  an  alternate  separation  and  rubbing  together  of  the 
stomach  or  the  intestinal  walls. 

EXAMINATION  OF   THE  GASTRIC    FUNCTIONS  WITHOUT  THE 
USE  OF  THE  STOMACH  TUBE. 

The  functions  of  the  stomach  are  these  :  (1)  digestive,  (2)  recep- 
tive, (3)  antiseptic.  In  the  first  place  it  alters  albuminoids  and  carbo- 
hydrates and  partly  absorbs  them.  In  the  second  place  it  acts  as  a 
well-equipped  reservoir,  supplying  the  food  for  the  intestines,  which 
completely  digest  and  assimilate  it;  with  such  help  we  are  able  to  limit 
the  ingestion  of  food  to  definite  mealtimes.  In  the  third  place  it  acts  as 
a  sort  of  germicide,  protecting  the  intestines  from  the  injurious  action 
of  the  noxious  micro-organisms  contained  in  the  food. 

EXAMINATION    OF   THE    VOMITUS. 

Considerable  information  about  the  chemistry  of  digestion  may  be 
acquired  from  carefully  examining  the  vomitus.  Even  a  macroscopic 
examination  will  enable  us  to  draw  valuable  conclusions,  especially  in 
regard  to  the  digestion  of  meat,  if  the  vomiting  occurs  during  the  time 
when  the  digestion  ought  to  be  pretty  well  advanced  physiologically. 
If  we  find  bits  of  unchanged  meat  or  albumin  in  the  material  vom- 
ited two  to  three  hours  after  eating,  we  are  justified  in  assuming  some 
disturbance  of  albuminoid  digestion.     The  changes  of  other  kinds  of 


358    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

food  in  the  stomach  are  less  characteristic.  Bread,  however,  should  be 
altered  within  three  hours  after  ingestion  to  a  uniform  mass  of  puree- 
like consistence,  which  settles  to  the  bottom  when  the  vomitus  is  allowed 
to  stand.  So  that  if  the  vomitus  contains  crumbs  of  unaltered  bread, 
perhaps  covered  with  mucus,  we  are  usually  justified  in  assuming  dis- 
turbed albuminoid  digestion,  depending  usually  upon  a  deficient  secre- 
tion of  hydrochloric  acid.  We  may  also  employ  a  dilute  iodin  solu- 
tion to  determine  the  degree  of  amyloid  digestion,  as  will  be  described 
later  in  connection  with  the  Test  Breakfast  (p.  371  et  seq.).  But  we 
must  remember  that  after  the  completion  of  normal  gastric  digestion  we 
still  find  in  the  stomach  contents  microscopically  numerous,  apparently 
intact,  meat  shreds  and  starch  granules.  Hence,  very  little  depend- 
ence can  be  jilaced  upon  the  microscopic  examination  of  the  vomitus. 
The  vomitus  should  therefore  be  subjected  to  the  same  chemical  tests  as 
will  be  described  later  for  the  expressed  test  breakfast.  The  results 
will,  however,  not  be  very  valuable,  because  gastric  digestion  varies 
markedly  with  the  character  of  the  food  ingested  and  the  length  of 
time  since  ingestion.  Free  hydrochloric  acid  should  nevertheless  be 
found  in  the  gastric  j  dice  within  one  to  two  hours  after  eating  an  ordi- 
nary meal ;  and  the  filtrate  from  the  vomitus  should  digest  fibrin  or 
coagulated  albumin. 

Furthermore,  the  examination  of  the  vomitus  may  give  some  con- 
clusions about  the  gastric  motility.  If  an  individual  vomits  bits  of 
food  more  than  seven  hours  after  a  meal,  some  impairment  of  motility 
must  exist,  for  after  that  interval  even  a  hearty  meal  should  have  com- 
pletely left  the  stomach.  If  this  late  vomiting  is  very  noticeable,  or  if 
perhaps  a  larger  amount  is  vomited  than  was  ingested  at  the  last  meal, 
it  indicates  a  very  pronounced  motor  insufficiency,  and  is  usually  asso- 
ciated with  extreme  gastric  dilatation.  If  the  vomitus  contains  particles 
of  food  known  to  have  been  ingested  at  some  previous  meal  or  a  day 
or  two  before  (seeds  of  fruit,  etc.),  such  a  diagnosis  is  clinched. 

If  we  can  show  that  the  excess  of  the  vomitus  over  what  was 
ingested  at  the  last  meal  consists  largely  of  a  thin  acid  liquid  contain- 
ing free  hydrochloric  acid,  we  are  entitled  to  assume  a  hypersecretion  of 
gastric  juice.  The  vomiting  of  an  acid  liquid  without  food  particles 
from  a  supposedly  empty  stomach  is  especially  characteristic  of  this  con- 
dition. In  the  latter  case  the  secretion  of  the  gastric  juice  apparently 
does  not  depend  upon  the  ingestion  of  food,  but  occurs  continually 
(^super secretion,  gastrorrhcea  acida).  We  must,  however,  remember  that 
in  some  of  these  cases,  and  perhaps  in  the  majority,  the  hypersecretion 
is  due  entirely  to  a  motor  insufficiency — i.  e.,  to  the  fact  that  secre- 
tion is  continually  excited  in  a  stomach  which  never  empties  itself  com- 
pletely. In  contrast  to  these  cases  of  hypersecretion  in  the  strict 
sense,  there  are  others  characterized  as  simple  hyperacidity,  in  which  the 
vomitus  is  not  abnormally  abundant,  but  is  abnormally  and  intensely 
acid  (due  to  free  hydrochloric  acid).  The  method  of  determining  this  is 
by  titrating  the  filtrate  for  its  acidity.  It  will  be  described  later.  A 
quantitative  comparison  with  the  normal  is,  however,  justifiable  only 


EXAMINATION  WITHOUT  EMPLOYING  THE  STOMACH  TUBE,  359 

when  the  vomiting  occurred  one  or  two  hours  after  the  meal,  and  when 
longer-retained  food  portions  are  not  mixed  with  the  vomitus.  If  a 
considerable  quantity  of  ingested  fluid  which  need  not  be  digested 
(water,  coifee,  etc.)  is  vomited  several  hours  after  consumption,  and  if 
the  acidity  of  the  fluid  does  not  indicate  hypersecretion,  it  has  been 
assumed  that  both  the  motility  of  the  stomach  and  its  power  of  absorp- 
tion are  aifected.  For  it  has  been  claimed  that  physiologically  the 
absorption  even  of  large  amounts  of  fluids  by  the  stomach  is  exceed- 
ingly rapid.  But  v.  Mering's  recent  investigations  seem  to  prove  that 
under  physiologic  conditions    the  stomach    absorbs  hardly  any  water, 


Fig.  141.— Microscopic  constituents  of  vomitus:  a,  Fragment  of  an  apple  (crushed) ;  h,  pave- 
ment epitlielium ;  c,  Sarcina  ventriculi  (smaller  type) ;  d,  Sarcina  ventriculi  (larger  type) ;  e,  bac- 
terial clump ;  /,  large  bacilli,  such  as  are  especially  suggestive  of  a  gastric  carcinoma ;  g,  needles 
of  fatty  acids ;  /*,  white  blood-corpuscles  ;  i,  vegetable  starch  ;  k,  corn  starch  ;  I,  potato  starch ;  m, 
white-bread  starch;  n,  rice  starch;  o,  yeast  cells;  p,  muscle  fibers;  q,  vegetable  tissue ;  r,  fat- 
drops  ;  s,  milk  or  cream  drops. 

so  that,  unless  we  deny  that  his  observations  upon  dogs  can  apply 
to  healthy  man,  we  must  attribute  the  retention  of  fluids  as  due  to  defi- 
cient motility  alone. 

An  examination  of  the  vomitus  gives  us  im])ortant  information  about 
the  antiseptio  qualities  of  the  gastric  juice.  Decomposition  in  the  gas- 
tric contents  depends  either  upon  a  diminution  in  the  amount  of 
hydrochloric  acid  contained  in  the  secretion  (for  the  acid  acts  as  an  anti- 
septic) or  upon  stagnation  of  the  gastric  contents — i.  e.,  upon  some 
interference  with  the  motility  of  the  stomach.  The  vomitus  is  then 
apt  to  be  foamy  and  to  smell  of  some  of  the  volatile  fatty  acids  (buty- 


360    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

ric  acid,  acetic  acid,  p.  377),  or  to  have  some  other  disagreeable  odor; 
and  microscopically  we  find  abmidant  micro-organisms,  especially  Sar- 
cina  ventriculi,  yeast  fungi,  cocci,  and  bacilli  (Fig.  141).  This  con- 
dition is  most  pronounced  in  a  dilatation  of  the  stomach  due  to  stenosis, 
especially  from  carcinoma  of  the  pylorus.  The  food  stagnates  in  the 
stomach  as  a  result  of  mechanical  obstruction,  oftentimes  for  several 
days.  We  frequently  find  in  carcinoma  of  the  stomach,  and  more 
rarely  in  gastric  dilatation  due  to  other  causes,  peculiar  thin  bacilli, 
sometimes  arranged  in  long  threads  (Fig.  141).  Cocci  and  bacilli  are 
usually  found  in  larger  quantities  in  gastric  juice  which  is  poor  in 
hydrochloric  acid ;  whereas  sarcinse  and  yeast  fungi  may  flourish  in 
gastric  juice  rich  in  hydrochloric  acid.  We  meet  with  two  types  of 
gastrorrhoea  acida  (supersecretion).  In  both  the  stomach  always  con- 
tains material  with  free  hydrochloric  acid,  and  this  is  apt  to  be  vomited 
from  time  to  time.  In  the  milder  type  this  material  is  free  from  micro- 
organisms. In  the  more  severe  type  the  large  amount  of  hydrochloric 
acid  present  is  no  longer  capable  of  keeping  the  stomach  contents  asep- 
tic, but  micro-organisms  grow  abundantly,  owing  to  the  high  degree  of 
motor  insufficiency.  In  this  case  chiefly  yeast  fungi  and  sarcinse  are 
found  in  the  vomitus,  and  may  be  present  in  abundance  even  with 
30  per  cent.  HCl. 

It  must  be  noted  that  bread  itself  contains  greater  or  less  numbers  of  bacteria 
and  yeast  cells.  Hence,  before  conclusions  are  justified,  tbe  bacteriologic  exami- 
nation of  the  gastric  contents  after  the  ingestion  of  bread  should  first  be  compared 
with  a  similar  examination  of  the  bread. 

If  the  vomitus  contains  abundant  tough,  slimy  masses,  it  indicates  a 
mucous  catarrh  of  the  stomach  or  a  diminution  in  the  hydrochloric 
acid,  for  under  normal  conditions  the  mucus  produced  by  the  mucous 
membrane  is  in  part  digested.  (Compare  later  Examination  of  the  Mu- 
cous Secretion  of  the  Stomach.)  An  admixture  of  blood  may  be  found  in 
the  vomitus  under  many  different  conditions.  A  slight  streak-like  ad- 
mixture of  blood  in  the  vomitus  is  of  no  diagnostic  importance  M'hat- 
soever,  for  the  violent  act  of  vomiting  may  produce  some  slight  mechan- 
ical lesion  of  the  stomach,  esophagus,  or  pharynx.  An  abundant 
admixture  of  fresh  arterial  blood  or  of  blood  stained  dark  and  coag- 
ulated by  the  acid  gastric  juice  is  especially  suggestive  of  ulcer  of  the 
stomach.  Brown  or  black  material  resembling  coffee  grounds,  if  gran- 
ular and  intimately  mixed  with  the  stomach  contents,  is  suggestive  of 
gastric  carcinoma ;  but  the  same  condition  frequently  results  from 
hemorrhagic  erosions  of  the  gastric  mucous  membrane,  especially  if 
associated  with  hyperacidity  or  hypersecretion.  We  can  prove  that  this 
appearance  is  due  to  the  altered  blood  by  microscopic  or  spectroscopic 
examination,  or  by  Teichmann's  test.^     (See  under  Urine,  p.  470.) 

Pus  may  be  found  in  the  vomitus  due  to  the  very  rare  condition,  sup- 
purative or  phlegmonous  gastritis.  Admixture  of  bile  produces  a  yellow 
or  greenish   discoloration  of  the  vomitus.     In  a  doubtful  case  we  can 

1  The  author  recommends  tlie  modification  of  the  turpentine-guiacum  test  described 
upon  pages  447  and  471  (Examination  of  the  Feces  for  Blood). 


EXAMINATION  WITHOUT  EMPLOYING   THE  STOMACH  TUBE.  361 

apply  Gmelin's  test  for  biliary  pigment.  See  Examination  of  the  Urine, 
p.  472  et  seq.).  Admixture  of  bile  may  occur  with  any  type  of  vom- 
iting, for  the  contents  of  the  duodenum  may  be  forced  into  the  stomach 
mechanically  by  the  act  of  vomiting.  It  is,  however,  observed  most 
frequently  in  vomiting  from  an  empty  stomach,  perhaps  because  there 
is  then  no  counter-pressure  from  gastric  contents  to  prevent  the  regur- 
gitation from  the  duodenum.  This  is  probably  the  reason  that  biliary 
vomiting  is  so  frequently  observed  in  peritonitis.  The  vomitus  of 
cerebral  meningitis  is  less  apt  to  be  mixed  with  bile,  because  these 
patients  still  take  considerable  nourishment,  and  the  vomiting  generally 
starts  with  a  partially  filled  stomach — i.  e.,  the  vomiting  in  this  disease 
is  both  peripheral  and  cerebral  in  origin.  Green  biliary  vomitus  is,  of 
course,  by  no  means  pathognomonic  of  peritonitis.  Biliary  vomiting, 
for  evident  reasons,  accompanies  stenosis  of  the  duodenum. 

Fecal  vomiting  is  a  characteristic  sign  of  complete  motor  insufficiency 
of  the  intestines  (in  peritonitis),  or  of  intestinal  obstruction  in  the  lower 
part  of  the  small  intestine  or  in  the  large  intestine.  The  odor  and 
brownish  color  of  the  vomitus  are  distinctive.  Microscopically,  it  is  found 
to  contain  large  numbers  of  bacteria.  Cholera  nostras  and  cholera  asiatica 
are  characterized  by  the  vomiting  of  abundant  alkaline  rice-water-like 
material  (exactly  like  the  cholera  stools).  It  usually  contains  bits  of 
white  mucus.  In  cholera  asiatica  the  comma  bacillus  (Koch)  (see 
Examination  of  the  Feces)  may  be  found  in  the  vomitus.  We  are  not 
yet  certain  about  the  organism  of  cholera  nostras.  The  Finkler-Prior 
comma  bacillus,  the  colon  bacillus,  various  forms  of  the  proteus  group 
and  streptococci  (see  Pathognomonic  Bacteria  of  the  Feces)  have  all 
been  found  in  the  feces,  and  also  in  the  vomitus  of  cholera  nostras. 
The  occurrence  of  streptococci  in  the  vomitus  has  assumed  some  import- 
ance recently  in  the  etiologic  diagnosis  of  other  gastro-intestinal  infections. 

The  color,  odor,  and  chemical  examination  of  the  vomitus  may  some- 
times aid  in  tracing  the  occurrence  of  stomach  disturbance  to  some  sort 
of  poisoning  (hydrocyanic  acid,  alcohol,  etc.).  In  uremia  the  vomitus 
often  possesses  the  odor  of  ammonia,  for  the  urea  eliminated  in  the 
stomach  contents  may  be  converted  into  carbonate  of  ammonia  while 
still  in  the  stomach. 

Intestinal  worms,  more  especially  ascarides,  are  sometimes  found  in 
the  vomitus.     (See  later.  Animal  Parasites  in  the  Stools.) 

It  is  sometimes  difficult  to  decide  whether  food  particles  which  the 
patient  vomits  soon  or  some  time  after  ingestion  come  from  the  stomach 
itself,  or  whether  they  are  only  regurgitated  from  the  esophagus  [divertic- 
ulum from  stenosis  of  the  esophagus).  The  presence  of  free  hydrochloric 
acid  will  generally  settle  the  doubt. 

EXAMINATION  OF  THE  POWER  OF  ABSORPTION  OF  THE  GASTRIC  MUCOUS 
MEMBRANE  BY  MEANS  OF  POTASSIC   lODID. 

Penzoldt  and  Faber '  have  published  a  direct  method  of  testing  the  absorbing 
power  of  the  gastric  mucous  membrane.     The  procedure  depends  upon  the  prin- 

^  Penzoldt  and  Faber,  Berlin,  klin.  Woch.,  1882;  Zweifel.  Deulsch.  Arch.  f.  klin.. 
Med.,  vol.  xxxix. 


362    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

ciple  tliat_  under  physiologic  conditions  potassic  iodid  is  very  rapidly  absorbed  by 
the  gastric  mucous  membrane  and  then  eliminated  immediately  'in  the  saliya. 
The  length  of  time  from  the  ingestion  of  the  potassic  iodid  until  the  saliva  exhibits 
a  distinct  iodin  reaction  may  be  considered  as  a  measure  of  the  rapidity  of 
absorption,  provided  that  slight  differences  in  the  time  of  elimination  be  neglected. 
The  potash  is  administered  in  a  gelatin  capsule  filled  carefully  enough  to  avoid 
any  particles  of  the  salt  sticking  to  the  outside,  which  would  be  absorbed  by  the 
mouth  or  esophagus. 

To  demonstrate  the  iodin,  the  patient  spits  upon  the  edge  of  a  white  plate, 
a  little  starch  powder  is  added  to  the  saliva,  and  then,  while  it  is  being  stirred 
carefully,  1  or  2  di'ops  of  nitric  acid  are  added.  The  nitric  acid  sets  iodin  free 
from  the  i^otassic  iodid  in  the  saliva  and  produces  the  weU-kno\\Ti  violet  color 
(starch  iodid).  Any  excess  of  acid  will  oxidize  the  iodin  to  iodic  acid,  which  does 
not  give  this  violet  color.  The  acid  should  therefore  be  added  drop  by  drop  and 
stirred.  The  reaction  is  less  sensitive  if  the  saliva  remains  any  length  of  time  in 
contact  with  the  starch,  because  the  saliva  changes  the  starch  to'eiythrodextrin  and 
achrodextrin.  If  these  substances  unite  with  the  iodin,  colorless  or  only  pinkish 
combinations  result ;  hence  the  admixture  should  be  made  promptly.  '  If  a  few 
drops  of  chloroform  are  added  to  the  saliva  before  adding  the  acid,  the  chloroform 
will  dissolve  the  free  iodin  and  produce  a  rose  color. 

Experience  shows  that  under  normal  conditions  the  first  trace  of  iodin  appears 
in  the  saHva  ten  or  more  minutes  after  the  administration  of  0. 1  gm.  potassic  iodid 
upon  an  empty  stomach.  If,  however,  the  stomach  is  full,  or  if  food  is  given 
simultaneously  with  the  drug,  the  absorption  and  test  will  be  delayed.  Hence 
the  experiment  should  always  be  performed  either  upon  an  empty  stomach  or  coin- 
cidently  with  a  test  breakfast.  Bauer,  in  the  Bern  Clinic,  found  from  a  series  of 
experiments  that  if  the  drug  was  taken  with  an  Ewald  test  breakfast  the  reaction 
appeared  in  the  saliva,  under  normal  conditions,  in  from  five  to  twenty  minutes. 
If  retention  is  suspected,  the  stomach  should,  of  course,  be  first  washed  out.  If 
the  reaction  is  delayed,  although  the  stomach  is  supposed  to  be  empty,  retention 
is  the  probable  cause,  because  exjierience  shows  that  there  is  rarely  much  retarda- 
tion of  the  reaction  in  an  absolutely  emj^ty  stomach,  even  under  pathologic  con- 
ditions. 

Of  course,  this  method  does  not  give  any  information  as  to  the  absorption  of 
food  substances,  for,  as  a  matter  of  fact,  potassic  iodid,  even  under  the  most 
unfavorable  pathologic  conditions,  is  absorbed  with  very  noticeable  ease. 

If  V.  Mering"  s  i  experiments  are  confirmed,  this  method  becomes  entirely  use- 
less. He  finds  in  dogs,  and  very  likely  the  same  is  true  in  men,  that  potassic 
iodid  is  not  absorbed  at  all  from  the  stomach,  not  even  within  two  or  three 
hours.  Hence  we  must  acknowledge  that  the  rapid  appearance  of  the  iodin  reac- 
tion in  the  saliva  depends  upon  the  absorption  of  the  iodid  in  the  intestines,  and  is 
in  reality  only  a  measure  of  the  gastric  motility-  (see  the  following)  : 

EXAMINATION    OF  THE   MOTILITY   OF   THE    STOMACH   WITHOUT 
THE   USE  OF  THE  STOMACH    TUBE. 

Palpation  (p.  354,  etseq.),  especially  eliciting  the  splashing  sound  of  the  stomach, 
gives  us  some  idea  of  the  gastric  motility  ;  examination  of  the  vomitus  (p.  357 
et  seq.)  reveals  still  more.  Ewald  and  Sievers  and  Huber  recommended  the  em- 
ployment of  salol  to  test  the  motility.  Salol  or  salicylate  of  j^henol  passes  through 
the  stomach  unchanged,  and  splits  up,  only  after  it  reaches  the  intestine,  into 
salicylic  acid  and  phenol,  under  the  influence  of  the  pancreatic  juice  and  the  intes- 
tinal bacteria.  Salicylic  acid,  soon  after  absorption,  is  eliminated  in  the  urine  as 
salicyluric  acid  (chlorid  of  iron  produces  a  violet  color  when  added  to  the 
urine  ;  see  Examination  of  the  Urine). 

Assuming  that  the  salol  is  always  broken  up  with  equal  rapidity,  this  reaction 
should  measure  the  rapidity  with  which  it  reaches  the  intestines  ;  in  other  words, 
the  gastric  motility.  Ewald  and  Sievers  administer  the  drug  with  the  test  break- 
^Klin.  Jahrb.,  vol.  via,  1899. 


EXAMINATION  WITHOUT  EMPLOYING   THE  STOMACH  TUBE.  363 

fast ;  then  the  patient  urinates  at  regular  intervals  during  the  next  few  hours,  and 
the  chlorid  of  iron  test  is  performed  upon  each  specimen.  Normally,  the  salicyl- 
uric reaction  occurs  within  seventy-five  minutes.  If  delayed  beyond  this  period, 
motor  insufficiency  may  be  diagnosed. 

This  method  of  testing  is  liable  to  a  number  of  errors.  The  most  important 
one  is  that  we  can  never  be  sure  whether  the  movements  of  the  stomach  produce  a 
uniform  mixture  of  the  salol  and  stomach  contents,  so  that  whether  the  salol  leaves 
the  stomach  with  the  first  portion  of  the  food  mass  or  later  on  must  largely  depend 
upon  chance.  Hence  the  salol  should  be  intimately  mixed  with  the  food,  or  else 
taken  in  small  portions  (as  an  emulsion  in  water)  during  the  meal.  The  rapidity 
of  splitting  up,  of  absorption,  and  of  elimination  is  not  always  a  definitely  fixed 
and  constant  quantity.  However,  in  sj^ite  of  these  sources  of  error,  the  method 
gives  quite  reliable  information  regarding  the  more  pronounced  disorders.  In 
marked  gastric  retention  the  salol  may  remain  for  hours  in  the  stomach,  i 

Huber  has  modified  this  method  by  determining  the  length  of  time  which 
elapses  before  all  the  salicyluric  acid  is  excreted.  The  reasoning  is  clear.  The 
moment  of  the  appearance  of  the  salicyluric  acid  reaction  depends  principally 
upon  the  rapidity  with  which  the  stomach  passes  the  first  amount  of  salol  into 
the  intestine ;  but  the  persistence  of  the  reaction  in  the  urine  (assuming  rapid 
splitting  up  and  rapid  elimination  of  the  salol  in  the  intestines)  is  largely  due  to 
the  fact  that  there  is  still  some  salol  not  yet  split  up  in  the  intestines.  This  is, 
of  course,  due  to  the  fact  that  the  stomach  has  not  yet  passed  on  all  the  salol. 
Therefore  the  duration  of  the  salicyluric  acid  reaction  may  be  a  better  measure  of 
stomach  motility  than  the  period  of  its  first  appearance.  Huber' s  investigations 
have  shown  that  in  healthy  individuals  who  have  taken  1  gm.  of  salol  at  a  meal, 
the  salicyluric  reaction  has  always  disappeared  inside  of  twenty-six  or  twenty- 
seven  hours.  Motor  insufficiency  may  therefore  be  assumed  if  this  time  is 
exceeded.  With  this  method  the  urine  need  not  be  tested  until  about  twenty- 
seven  hours  after  taking  the  salol.  Of  course,  the  urine  should  be  voided  a  little 
beforehand — e.  g.,  one-half  hour — so  that  no  residual  urine  remains.  If  the 
salicyluric  reaction  is  present  twenty-seven  hours  after  the  ingestion  of  the  salol, 
the  test  should  be  repeated  every  three  hours  till  it  disappears.  The  degree  of 
motor  insufiiciency  is  in  direct  proportion  to  the  duration  of  the  reaction. 

The  author  has  observed  more  reliable  results  from  combining  Ewald's  aud 
Huber' s  methods,  as  follows:  1  gm.  of  salol  is  taken  with  the  meal,  either  inti- 
mately mixed  or  in  very  small  quantities,  and  then  the  time  of  appearance  and  of 
disappearance  of  the  salicyluric  acid  in  the  urine  is  noted.  This  combined  test 
will  reveal  impairment  of  motility  in  all  sorts  of  stomach  disorders.  The  appear- 
ance of  the  reaction  may  be  delayed  for  several  hours,  and  not  infrequently  it  per- 
sists for  forty  hours  or  more.  lodipin  has  recently  been  recommended  instead  of 
salol.  lodin  is  set  free  and  absorbed  in  the  intestines  and  then  tested  for  in  the 
saliva  (see  p.  361). 

Personally,  the  author  is  convinced  that  none  of  these  methods  is  perfectly 
trustworthy  for  estimating  the  gastric  motility.  In  the  first  place,  we  are  not  sure 
that  the  substances  employed  are  intimately  mixed  with  the  gastric  contents,  nor 
are  we  certain  that  they  may  not  be  precipitated  by  the  gastric  juice  and  reach  the 
intestines  too  soon  or  too  late.  Again,  the  results  will  be  very  decidedly  influenced 
by  the  rapidity  of  the  splitting  up  and  of  the  absorption  in  the  intestines.  If 
V.  Mering's  idea  is  confirmed  (see  p.  362),  that  potassic  iodid  is  not  absorbed  at 
all  in  the  stomach,  then  Penzoldt  and  Faber's  method  for  testing  the  absorption 
in  the  stomach  can  be  utilized  as  a  test  of  its  motility  (p.  361  et  seq.). 

Further  investigations  upon  the  point  are  necessarj\ 

?  There  is,  however,  reason  to  believe  that  in  cases  of  gi-ave  disturbances  of  motility, 
when  the  salol  remains  for  houi-s  in  the  stomach,  some  of  the  drug  may  also  be 
absorbed  by  this  organ.  Part  of  it  is,  perhaps,  fii-st  split  up  by  micro-organisms,  which 
are  rarely  absent  in  a  stagnant  stomach,  or  by  fat-splitting  ferments.  Such  a  slow 
absorption,  however,  would  rarely,  if  ever,  lead  us  to  assume  that  the  motility  was 
normal. 


364    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS, 

TESTING  THE  DIGESTION  "WITH  POTASSIC  lODID  FIBRIN-RUBBER 

CAPSULE. 

Although  this  method  was  detailed  at  length  in  the  previous  edition  of  this 
book,  it  has  since  led  to  no  practically  useful  results,  and  so  it  need  only  be 
alluded  to. 


METHODS  OF  EXAMINING  THE   STOMACH  WITH  THE 
AID  OF  THE  STOMACH  TUBE, 

INSTRUMENTS. 

Kussraaul  was  the  first  to  employ  the  stomach  tube  for  the  treat- 
ment, and  V.  Leube  the  first  to  use  it  for  the  diagnosis,  of  gastric  affec- 
tions. With  its  help  we  cannot  only  obtain  the  contents  of  the  stomach 
at  any  period  of  digestion,  but  we  can  inflate  it  with  air  or  fill  it  with 
fluid  at  will.  The  best  tubes  are  made  of  rubber,  and  are  quite  soft 
and  pliable.  The  English  (Jack's  patent  ^)  are  as  good  as  any.  They 
are  provided  with  a  lateral  opening  and  a  rounded  closed  end.  They 
might  well  be  even  softer.  The  surface  of  the  tube  must  be  smooth, 
the  rubber  soft  but  not  too  collapsible,  the  lumen  large  in  relation  to 
the  entire  diameter,  and  the  opening  at  the  lower  end  as  large  as  pos- 
sible. The  smaller-sized  tubes  are  generally  easier  to  pass  and  less 
disagreeable  to  the  patient,  but  become  stopped  up  easily.  In  passing 
the  smaller  sizes  we  require  the  patient's  help  in  swallowing,  whereas 
the  larger  can  be  more  readily  pushed  down  the  esophagus.  No.  22 
(Jack's  patent),  with  a  diameter  of  about  12  mm.,  is,  the  author  believes, 
the  most  convenient  size.  With  the  aid  of  a  small  glass  tube  for  con- 
nection, and  a  rubber  tube  about  2  feet  long,  the  stomach  tube  is  con- 
nected to  a  large  funnel  (preferably  of  glass).  These  three  pieces 
together  constitute  a  siphon  apparatus,  by  means  of  which  we  can  easily 
empty  and  wash  out  the  stomach. 

If  the  stomach  contains  large  solid  food  particles  which  clog  up  the 
tube  again  and  again,  it  may  be  convenient  to  have  some  sort  of  a  pump 
which  can  be  attached  in  order  to  suck  out  these  pieces.  The  same 
pump  is  useful  for  distending  the  stomach  with  air  in  order  to  estimate 
its  size.  Katsch,  of  Munich,  makes  a  very  good  one  (Fig.  142).  The 
pump  in  Potain's  aspirating  set,  attached  to  a  large  glass  bottle  (Fig. 
143),  may  be  used. 

Any  syringe  may  be  employed  with  a  stomach  tube — e.  g.,  Davidson's 
syringe,  a  fountain  syringe. 

TECHNIC  OF   INTRODUCING  A  SOFT   STOMACH   TUBE.' 

The  patient  should  be  in  the  sitting  posture,  with  his  mouth  wide 
open,  and  the  rounded  end  of  the  tube  should  be  pushed  back  and  down 

^  [We  bave  found  the  Jack  tubes  very  good,  but  a  rather  softer  and  more  pliable  tube 
will  sometimes  cause  less  gagging,  especially  upon  the  first  inti'odnction.  _  We  refer  the 
reader  to  Hemmeter's  Diseases  of  the  Stomach,  2d  ed.,  pp.  114-118,  for  additional  details 
and  hints  upon  the  introduction  of  the  tube. — Ed.] 

^  See  Examination  of  the  Esophagus. 


EXAMINING   THE  STOMACH  WITH  AID   OF  STOMACH  TUBE.   365 

over  the  base  of  the  tongue.  If  there  are  no  obstructions  in  the  esopha- 
gus, we  need  not  lubricate  the  tube  with  anything  but  water.  If  the 
patient  can  be  persuaded  to  relax  and  breathe  quietly  and  deeply,  the 
tube  can  be  quickly  pushed  into  the  stomach.     The  patient  need  not 


Fig.  142.— Stomach  pump. 


attempt  to  swallow  if  we  use  the  rather  larger  tubes.  It  is  important 
for  the  examiner  to  reassure  him  in  every  possible  way,  and  to  explain 
beforehand  the  steps  of  the  process  and  its  disagreeable  features,  so  as 
to  avoid  frightening  the  patient  during  the  ordeal  itself.  As  soon  as 
the  tube  has  entered  the  esophagus  but  a  few  centimeters,  the  complete 


Potain's  pump. 


stomach  tube. 


Fig.  143.— Arrangement  of  Potain's  pump  used  as  a  stomach  pump  :  a,  A  wide-necked  bottle 
fitted  with  a  rubber  stopper,  through  which  are  passed  two  glass  tubes  bent  at  right  angles  ;  o, 
tube  leading  to  Potain's  pump ;  c,  tube  connecting  with  the  stomach  tube. 

passage  is  readily  effected.  The  distance  from  the  teeth  to  the  cardiac 
orifice  in  an  adult  is  usually  about  40  cm.  (15|  in.).  Continued  deep 
breathing,  even  after  the  tube  has  been  completely  inserted,  is  very 
helpful  to  the  patient. 

Some  patients  exhibit  so  much  dyspnea  that  an  inexperienced  examiner  may- 
think  the  tube  is  in  the  larynx  or  trachea,  although  the  difficulty  in  breathing  is 
due  only  to  the  psychic  influence,  perhaps  to  the  pressure  of  the  tube,  or  to  ob- 
struction from  involuntary  swallowing  movements  (see  above).  Sometimes  audible 
whistling  respiratory  sounds  produce  the  impression  that  the  patient  is  breathing 
through  the  tube  (esophageal  breathing).  (Compare  section  on  Examination  of 
the  Esophagus. )  As  a  matter  of  fact,  it  is  extremely  difficult  to  introduce  the  tube 
into  the  larynx,  especially  if  soft  tubes  are  used,  because  the  larynx  closes  the  in- 
stant any  foreign  body  touches  its  entrance,  and  because  the  epiglottis  is  dejjressed 
and  the  tube  pushed  into  the  esophagus  by  the  voluntary  or  reflex  swallowing  act 
at  the  moment  the  tip  of  the  tube  gets  into  the  pharynx. 

If  a  fit  of  coughing  occurs  as  the  tube  is  being  introduced,  it  is  well  to 
withdraw  it  and  try  again.  Any  marked  resistance,  marked  dyspnea,  or  much 
.gagging  upon  the  part  of  the  patient  usually  means  that  the  tube  is  caught  in  one 


366    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

of  the  fossae  pyriformes  at  the  side  of  the  larynx,  and  rolled  up  over  the  entrance 
of  the  larynx  like  a  spiral.  Then,  if  the  examiner  attempts  to  push  it  farther, 
the  tube  usually  snaps  back  suddenly  into  the  mouth.  To  avoid  this  difficulty  we 
should  endeavor  to  introduce  the  tube  exactly  in  the  median  Hne. 

In  some  very  difficult  cases  it  may  be  necessary  to  paint  the  pharynx  with  a 
4  per  cent,  solution  of  cocairi.     (See  section  on  Laryngoscopy  and  Tracheoscopy.) 

INDICATIONS    AND    CONTRA-INDICATIONS    TO   THE   INTRODUC- 
TION OF  THE  STOMACH  TUBE  FOR  DIAGNOSTIC  PURPOSES. 

Indications. — Every  slight  gastric  complaint  does  not  indicate  the 
employment  of  a  stomach  tube,  for  it  causes  the  patient  too  much  dis- 
comfort ;  but  its  use  is  indicated  where  an  absolute  diagnosis  seems 
impossible  at  the  onset,  or  where  the  treatment  employed  has  failed  and 
the  physician  appreciates  the  necessity  of  revising  the  diagnosis  by 
more  exact  methods. 

Contra-indications. — The  stomach  tube  is  contra-indicated  in  all 
grave  disorders  of  respiration  or  circulation,  in  cardiac  failure,  cardiac 
neurosis — e.  g.,  when  the  excitement  accompanying  the  passing  of  the 
tube  may  in  itself  lead  to  danger — in  aortic  aneurisms  (on  account  of 
the  danger  of  perforation),  in  patients  liable  to  cerebral  hemorrhage, 
and  in  those  who  have  recently  had  hemorrhage  from  the  lungs  or  the 
stomach. 

THE   VARIOUS   STEPS   IN   THE   EXAMINATION. 

The  best  time  to  introduce  the  tube  is  in  the  early  morning,  upon  a 
fasting  stomach,  the  patient  having  ingested  the  previous  evening  a 
rather  abundant  mixed  meal. 

We  first  cleanse  the  fasting  stomach,  extracting  any  residue  or  secre- 
tion which  it  may  contain.  After  the  tube  has  been  introduced  the 
patient  is  instructed  to  strain  or  cough  gently,  to  aid  in  expelling  any 
stomach  contents.  If  nothing  appears  we  employ  gentle  suction  with 
a  pump  or  bulb.  If  this  obtains  nothing  we  pour  in  a  little  lukewarm 
water  at  first,  and  later  a  pint  at  a  time,  and  then  empty  the  stomach 
again  by  depressing  the  funnel  below  the  level  of  the  stomach.  If 
employing  a  funnel,  the  examiner  must  see  that  it  is  kept  filled,  so 
that  the  tube  does  not  become  empty,  and  hence  stop  the  siphonage. 
In  case  any  particles  stop  up  the  tube,  it  may  be  possible  to  force  them 
back  into  the  stomach  by  elevating  the  funnel  again.  The  stomach  is 
washed  out  in  this  way  till  the  fluid  recovered  comes  clear.  If  any 
material  was  removed  before  beerinning  the  washins^,  it  should  be  saved 
for  examination  (see  p.  368).  If  this  was  not  possible,  then  whatever 
was  obtained  after  the  first  dilution. 

After  emptying  and  cleansing  the  fasting  stomach,  the  next  pro- 
cedure is  to  determine  its  size  and  position  by  inflating  it  with  air.^ 
This  can  be  accomplished  quite  conveniently  with  the  aid  of  a  David- 
son's syringe.  The  patient  should  be  in  the  dorsal  decubitus,  with  the 
lower  chest  and  abdomen  exposed  to  view.     We  must  inflate  cautiously 

^  This  will  be  superfluous  if  we  have  already  determined  the  measure  accurately  by 
palpation  and  by  percussion. 


EXAMINING   THE  STOMACH  WITH  AID   OF  STOMACH  TUBE.  367 

and  stop  whenever  any  pain  is  produced.  After  it  is  moderately  dis- 
tended, inspection  will  generally  disclose  the  position  and  shape  of  the 
organ ;  but  to  avoid  confusing  a  dilated  stomach  with  a  gastroptosis  we 
must  determine  the  lesser,  as  well  as  the  greater,  curvature.  (Loop- 
shaped  stomach  may  also  occur.) 

The  "  hour-glass  "  stomach  is  very  rare.  It  consists  of  two  cavities 
connected  by  a  constricted  passage,  and  under  certain  conditions  may 
be  recognized  by  inspection  of  the  distended  stomach.^ 

When  inspection  alone  fails  to  determine  the  shape  and  size  of  the 
stomach  (e.  g.,  on  account  of  abnormally  thick  walls),  palpation  and 
percussion  of  the  organ  after  it  has  been  inflated  with  gas  will  usually 
settle  the  shape  and,  at  least,  the  position  of  the  greater  curvature. 
Luschka  has  estimated  that  a  normal  stomach  contains  between  IJ  and 
2  liters  of  gas ;  but  these  figures  were  determined  upon  cadavers,  and 
are  subject  to  considerable  variations  according  to  the  class  of  the  indi- 
vidual and  the  type  of  his  nourishment.^  A  large  stomach  is  not  neces- 
sarily diseased.  An  increase  in  size  becomes  pathologic  only  when 
motor  insufficiency  exists  and  food  remains.  If  continued  insufflation 
produces  a  diffuse  distention  of  the  abdomen  instead  of  a  localized 
bulging  in  the  epigastrium,  we  are  justified  in  diagnosing  an  insufficiency 
of  the  pylorus  (Ebstein). 

When  distending  the  stomach  we  should  note  if  any  tumors  are 
present,  and  also  any  changes  in  the  position  of  the  tumors.  As  soon 
as  all  of  these  points  have  been  determined,  the  air  is  allowed  to  escape, 
so  as  not  to  cause  the  patient  any  unnecessary  discomfort.  This  is 
accomplished  by  pressing  or  kneading  over  the  upper  abdomen  with  the 
tube  in  situ.     The  tube  should  then  be  quickly  pulled  out. 

The  fact  that  a  patient's  distention  can  be  instantly  relieved  (p.  354)  is  one 
of  the  chief  advantages  of  employing  the  tube  instead  of  an  effervescing  powder. 
This  method  of  gastric  inflation  furnishes  such  accurate  results  in  regard  to  the 
size  and  position  of  the  stomach  that  it  seems  very  questionable  if  ' '  gastro- 
diaphany ' '  can  supplant  it  for  practical  purposes.  The  latter  process  consists  in  in- 
troducing a  tube,  with  a  small  electric  lamp  at  the  tip,  into  the  stomach,  and  thus 
reflecting  light  through  the  stomach.  Rontgen  rays  seem  quite  as  unnecessary 
and  impractical  for  the  purpose.  Tumors  which  cannot  be  appreciated  by  palpa- 
tion will  probably  escape  both  these  methods. 

Inflation  may  be  supplemented  by  palpation  of  the  soft  tube  along  the  greater 
curvature  of  a  relaxed  stomach.  Its  tip  can  often  be  felt  especially  plainly,  and 
the  results  of  inflation  thereby  confirmed.  Such  palpation  should  be  practised 
very  cautiously. 

» 
TESTING  THE  GASTRIC  FUNCTIONS  BY  MEANS  OF  A  TEST  BREAKFAST. 

The  principle  involved  follows  :  The  patient  takes  a  definitely  deter- 
mined meal  upon  a  fasting  stomach — /.  e.,  after  the  stomach  has  been 
emptied  artificially  or  the  first  thing  in  the  morning.  We  then  draw 
conclusions  as  to  the  functions  of  the  stomach  from  the  amount  and 
from  the  chemical  character  of  the  contents  removed  by  the  tube  after 
the  lapse  of  a  certain  time. 

^  Virchorv's  Archiv,  1895,  vol.  cxl.,  No.  3,  p.  459. 

"^  [The  German  figures  are  generally  larger  than  the  American. — Ed.] 


368    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

Various  test  breakfasts  have  been  advocated.  For  some  purposes 
one  kind  is  better ;  for  others,  another  kind.  If,  for  instance,  vre  wish 
to  test  the  behavior  of  a  certain  food  in  the  stomach,  then  that  food 
should  be  selected  for  a  test  breakfast.  Again,  if  we  wish  to  determine 
the  behavior  of  the  stomach  under  an  ordinary  mixed  meal,  we  select 
such  a  meal  for  our  test — e.  g.,  Eiegel's  test  meal  consists  of  a  plate  of 
mutton  broth,  a  beefsteak  (150  to  200  gm.),  potato  puree  (50  gm.),  and 
a  roll.  Ewald-Boas'  test  breakfast  is  the  most  serviceable  for  general 
use.  It  is  convenient  and  uniform.  It  consists  of  1  roll  (about  35 
gm.),  or  the  same  amount  of  white  bread,  and  2  cups  (400  c.c.)  of  w^ater 
or  weak  tea  without  milk  or  sugar.  The  patient  should  chew  the  bread 
very  thoroughly.  More  useful  and  accurate  information  will  be  obtained 
from  the  " Sahli-Seiler's  Universal  Test  Meal"  (see  p.  397  d  seq.). 
The  test  meal  is  allowed  to  remain  in  the  stomach  a  definite  length  of 
time  until  acted  upon  by  the  gastric  secretion,  and  then  withdrawn 
through  the  tube.  Eiegel's  meal  is  ordinarily  withdrawn  at  the  end  of 
four  hours;  the  Ewald-Boas  and  the  "Universal"  at  the  end  of  an 
hour.  If  no  contents  can  be  obtained  after  the  usual  interval,  another 
meal  should  be  ingested,  and  expressed  after  a  shorter  interval  (better 
upon  the  succeeding  day). 

Ewald  and  Boas'  method  of  expression  is  the  most  convenient  way 
of  obtaining  the  stomach  contents.  The  patient  is  instructed  to  cough 
and  strain  down.  The  food  is  usually  expelled  better  if  the  patient  is 
in  the  right  or  left  lateral,  rather  than  m  the  sitting,  posture.  If  the 
tube  becomes  clogged  we  can  generally  free  it  by  forcing  a  little  air 
through,  which  is  more  convenient  than  diluting  the  contents  by  adding 
more  water.  When  but  little  is  expelled  it  is  advisable  to  employ  press- 
ure, so  as  to  be  sure  that  the  stomach  is  empty,  and  thus  to  correctly 
estimate  the  amount  of  the  meal  contained  in  the  stomach.  (See  p.  401 
in  regard  to  the  procedure  of  the  "residue  estimation."  This  is  only 
available  when  the  universal  meal  is  employed,  (See  p.  370  et  seq.  and 
p.  397  et  seq.  for  the  examination  of  the  expressed  meal.) 

EXAMINATION  OF  THE  CONTENTS    OF    A    FASTING  STOMACH. 

The  materials  removed  from  a  fasting  stomach  are  to  be  examined  in 
the  same  way  as  the  vomitus  so  far  as  their  microscopic  and  macroscopic 
peculiarities  are  concerned.  For  the  chemical  examination  the  same 
rules  apply  as  for  testing  the  expressed  breakfast.  (See  p.  370  et  seq.). 
If  the  fasting  stomach  contains  remnants  of  the  previous  day's 
food,  there  must  be  a  considerable  degree  of  motor  insufficiency,  because 
a  normal  stomach  would  be  empty  within  seven  to  eight  hours,  after 
even  quite  an  abundant  meal,  and  in  any  event  should  be  empty  in  the 
morning. 

Cranberry  or  Currant  Test.— If  we  have  not  the  opportunity  to  test  the 
fasting  stomach  for  determining  motor  insufficiency,  nearly  the  same  result  can  be 
accomplished,  according  to  E^\'ald  and  Strauss,  by  giving  the  patient,  at  his  even- 
ing meal,  a  tablespoonfhl  of  cranberry  or  currant  preserve.  We  can  decide  upon 
a  certain  degree  of  motor  insufficiency  of  the  stomach  if  the  expressed  meal  the 


EXAMINING   THE  STOMACH  WITH  AID   OF  STOMACH  TUBE.   369 

next  day  contains  any  of  tlie  fruit  or  seeds.  The  advantage  of  the  test  is  that  it 
does  not  make  any  difference  whether  or  not  the  patient  has  commenced  upon  his 
ordinary  nourishment. 

If  we  can  obtain  from  the  fasting  stomach  a  considerable  quantity 
of  fluid  containing  free  hydrochloric  acid  without  any  food  remnants, 
hypersecretion  may  be  diagnosed,  because,  if  empty,  the  stomach  should 
not  secrete  hydrochloric  acid.  The  irritation  of  the  tube  or  of 
the  saliva  swallowed  may  suffice  to  excite  a  mild  secretion.  Hence 
a  small  amount  of  such  fluid  is  not  sufficiently  characteristic.  The 
amount  of  acid  fluid  which  can  be  withdrawn  from  a  fasting  stomach 
and  still  remain  within  the  normal  limits  varies  considerably,  according 
to  the  individual  authority.  Ordinarily  not  more  than  10  c.c.  are 
found.  Cases  have  been  reported,  however,  where  20  to  50  c.c.  have 
been  recovered  without  any  noticeable  disorder.  Boas  considers  100  c.c. 
or  over  pathologic  for  a  fasting  stomach.  Evidently  there  are  no  very 
sharp  limits  between  a  physiologic  and  a  pathologic  amount  of  secretion. 
To  differentiate  between  primary  hypersecretion  and  hypersecretion  sec- 
ondary to  stagnation,  compare  p.  390,  Note  2.  Normal  gastric  juice 
from  a  fasting  stomach  is  thin,  not  at  all  slimy,  with  a  specific  gravity 
of  only  1004  to  1005.  It  thus  differs  from  gastric  juice  which  con- 
tains the  products  of  digestion,  such  as  is  obtained  after  a  test  breakfast 
or  when  the  food  is  retained  (compare  p.  371). 

If  much  lactic  acid  is  present  we  know  that  it  is  due  to  bacteriologic 
fermentation  and,  hence,  indicates  a  diminished  production  of  hydro- 
chloric acid,  for  normally  the  hydrochloric  secretion  of  gastric  juice 
prevents  lactic  acid  fermentation. 

Not  infrequently  a  little  yellowish  or  greenish  bile-containing  fluid, 
often  alkaline,  is  expressed  from  the  fasting  stomach.  It  consists  of 
duodenal  juice  which  entered  the  stomach  from  the  gagging  and  vomit- 
ing while  passing  the  tube.  But  if  repeated  examinations  show  that 
such  fluid  is  always  present,  even  if  there  have  been  no  vomiting  efforts, 
or,  again,  if  it  is  constantly  vomited  in  some  chronic  disease,  there  must 
be  some  stenosis  of  the  duodenum  below  the  ductus  choledochus  (Boas). 
This  statement  has  recently  been  corroborated  by  various  authors.^ 
Gmelin's  test  will,  of  course,  prove  that  the  color  is  really  due  to  bile 
(see  p.  472  et  seq.).  The  reaction  of  the  stomach  contents  in  such  cases 
may  be  alkaline  if  the  stomach  no  longer  secretes  enough  acid  to  pro- 
duce a  neutral  or  acid  reaction.  If,  on  the  other  hand,  the  stomach 
secretes  an  abundance  of  hydrochloric  acid  and  the  fluid  is  stagnant  for 
a  considerable  period,  then  the  reaction  may  remain  acid.  In  case  the 
reaction  is  neutral  or  alkaline,  we  can  prove  that  the  fluid  comes  from 
the  duodenum,  because  it  will  digest  in  an  alkaline  solution.  For  this 
purpose  the  fluid  is  placed  with  a  few  fibrin  flakes  colored  with  Magdala- 
red  in  an  inculiator,  the  reaction  having  been  rendered  (if  necessary) 
distinctly  alkaline  by  the  addition  of  1  per  cent,  soda  solution.  The 
fibrin  flakes  will  be  digested  by  the  trypsin  contained  in  the  fluid,  and  the 
fluid  will  be  colored  red.      If  the  fluid  is  of  acid  reaction,  it  is  usually 

^  Compare  Deutsch.  med.  Woch.,  1896,  No.  23,  "  Herz,  Uber  Duodenalstenosen." 
24 


370    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS, 

impossible  to  demonstrate  the  presence  of  trypsin,  because  in  acid  solu- 
tions trypsin  is  rapidly  destroyed  by  the  pepsin  of  the  gastric  juice. 

For  further  methods  of  demonstrating  the  action  of  trypsin  and  for  recognizing 
intestinal  juices  in  general,  see  later,  in  section  upon  Boas'  Method  of  Obtaining 
the  Intestinal  Juice  (p.  421  et  seq.). 

Gastric  carcinomata  which  cannot  be  palpated  may  sometimes  be  diagnosed 
by  washing  out  the  empty  stomach  and  finding  macroscopic  and  microscopic  con- 
stituents of  the  growth  in  the  wash  water.  The  best  method  is  to  wash  out  the 
stomach  thoroughly  the  evening  before,  and  then  to  repeat  the  lavage  the  next 
morning  without  allowing  the  patient  to  take  anything  overnight.  Sometimes 
a  little  undiluted  fluid  can  be  expressed  through  the  tube  for  microscopic  exami- 
nation before  the  morning  lavage.  Characteristic  bits  or  cells  can  thus  often  be 
obtained  for  examination,  especially  if  the  carcinoma  is  considerably  ulcerated. 
The  fluid  should,  of  course,  be  centrifiigated,  and  only  the  sediment  examined 
microscopically.  (Compare  Urine  Analysis,  p.  553  et  seq.).  The  following  is  a 
very  illustrative  case  :  Clinically  it  presented  the  features  of  pernicious  anemia, 
and  intra  vitam  the  diagnosis  of  carcinoma  of  the  stomach  could  not  be  made 
with  any  certainty.  No  tumor  could  be  felt.  Free  hydrochloric  acid  was 
absent,  to  be  sure,  but  the  stomach  was  of  normal  size  and  emptied  itself  even 
abnormally  rapidly.  As  is  commonly  known,  anacidity  with  hypermotility  of 
the  stomach  occurs  in  a  very  large  number  of  so-called  pernicious  anemias. 
Autopsy  showed  a  very  large  carcinoma  of  the  lesser  curvature.  It  could  not 
have  been  palpated,  because  it  was  entirely  hidden  under  the  liver.  It  had  not 
produced  any  stenosis  of  the  pylorus.  The  method  above  recommended  might 
easily  have  permitted  a  differential  diagnosis  from  pernicious  anemia,  because 
the  tumor  was  soft,  friable,  and  ulcerated. 

EXAMINATION  OF  THE  GASTRIC  FUNCTIONS  BY  MEANS  OF  THE 
ORDINARY  (EWALD-BOAS)  TEST   BPJEAKFAST, 

The  expressed  breakfast  is,  first  of  all,  filtered.  In  what  follows 
the  filtrate  is  called  the  "gastric  juice." 


APPEARANCE    AND    AMOUNT    OF    THE    EXPRESSED     MATERIAL;     SPECIFIC 
GRAVITY  OF  THE  GASTRIC  JUICE ;  JUDGMENT  OF  THE  GASTRIC  MOTILITY. 

The  conclusions  to  be  drawn  from  the  appearance  of  the  test  break- 
fast in  relation  to  the  digesting  function  of  the  stomach  are  the  same  a& 
were  mentioned  upon  p.  357  e^  seq.  with  reference  to  the  appearance  of 
vomited  gastric  juice  (c/*.  especially  the  peculiarity  of  the  particles  of 
bread). 

The  amount  of  the  expelled  material  is  of  special  diagnostic  impor- 
tance. The  Ewald-Boas  test  meal  does  not  usually  furnish  physiologically 
more  than  30  to  70  c.c.  of  filtrate.  But  too  much  importance  should  not 
be  given  to  these  figures,  because  many  variations  occur  and  much  larger 
amounts  are  within  physiologic  limits.  A  filtrate  to  the  amount  of  200 
to  300  c.c.  makes  motor  insufficiency  or  hypersecretion  probable.  If 
there  is  a  large  volume  of  fluid  and  it  is  strongly  acid  from  free  hydro- 
chloric acid,  hypersecretion  is  very  probable.  Hypersecretion  is,  how- 
ever, sometimes  secondary  to  motor  insufficiency,  and  is  due  to  the  con- 
tinual stimulation  of  residual  contents.  If  the  expressed  contents 
contain   a   large   proportion    of  solid  material,  motor  insufficiency  is 


EXAMINING   THE  STOMACH  WITH  AID   OF  STOMACH  TUBE.  371 

suggested.  This  diagnosis  is  confirmed  if  the  fasting  stomach  contains 
particles  of  food.  If  the  organ,  eight  hours  after  an  ordinary  meal, 
contains  any  remains  of  the  meal,  we  have  corroborative  evidence  of 
motor  insufficiency.  To  determine  the  existence  of  true  hypersecretion 
(independent  of  motor  insufficiency),  we  should  administer  a  roll  with 
but  very  little  of  any  fluid.  Then  if  we  can  express  a  goodly  amount 
of  acid  fluid,  hypersecretion  is  definitely  determined.  Hypermotility 
may  very  properly  be  assumed  if  the  volume  of  expressed  material  is 
decidedly  diminished,  but  only  when  we  have  become  convinced  after 
lavage  that  the  stomach  is  thoroughly  emptied. 

The  specific  gravity  of  the  filtrate  varies  normally  between  1012 
and  1020.  In  hypersecretion  and  in  sluggishness  of  the  digestive 
mechanism  it  is  diminished  either  by  dilution  or  by  deficient  formation 
of  soluble  digestive  products.  Pure  gastric  juice  without  digestive 
products  has  (see  p.  369)  a  specific  gravity  of  only  1004  to  1005. 

EXAMINATION    OF    STARCH   DIGESTION. 

As  is  well  known,  the  salivary  enzyme  changes  starch  first  into 
soluble  starch  (amylum  to  amidulin  or  amylodextrin).  lodin  still 
colors  the  latter  violet.  The  next  change  is  to  erythrodextrin ;  but  this 
gives  a  reddish  to  a  mahogany -brown  color  with  iodin.  Finally,  achro- 
odextrin  and  maltose  are  formed  (not,  as  was  formerly  believed,  dextrose). 
These  last  two  products  no  longer  produce  characteristic  colors. 

In  testing  the  gastric  contents  for  the  character  of  starch  digestion, 
the  point  to  determine  is  whether,  besides  starch,  which  always  exists 
in  considerable  quantity,  even  in  the  upper  portion  of  the  intestines, 
there  are  any  of  the  first  products  of  starch  digestion.  With  a  solu- 
tion of  iodin  this  can  be  easily  accomplished.  Achroodextrin  produces 
no  color,  but  it  has  a  greater  affinity  for  iodin  than  has  starch  itself. 
Consequently,  when  slight  traces  of  iodin  are  added  to  a  uniform  mixt- 
ure of  starch  and  achroodextrin,  the  iodin  combines  with  the  achro- 
odextrin before  it  affects  the  starch.  Therefore,  if  we  add  traces  of 
iodin  to  a  mixture  of  starch  and  achroodextrin,  no  color  will  result 
until  an  excess  of  iodin  brings  out  the  violet.  A  drop  of  a  very 
dilute  (wine  yellow)  Lugol's  iodin  solution  ^  upon  a  glass  rod  is  added 
to  the  residue  on  the  filter  paper,  or  even  to  the  filtrate  (because  the 
latter  always  contains  soluble  starch).  If  achroodextrin  is  present,  no 
color  will  appear  until  an  excess  of  iodin  is  added.  If,  on  the  other 
hand,  no  starch  digestion  has  occurred,  the  slightest  trace  of  iodin  will 
produce  a  violet  color. 

If  a  large  volume  of  gastric  contents  is  at  our  disposal,  the  test  may 
be  performed  as  follows  :  Lugol's  solution  (0.1  gm.  iodin,  0.2  gm. 
potassium  iodid,  200  c.c.  water)  is  added  drop  by  drop  to  the  filtrate. 
The  amount  added  before  a  violet  color  appears  will  furnish  an  approxi- 
mately accurate  quantitative  measure  of  the  degree  of  starch  digestion. 
The  latter,  of  course,  depends  not  only  upon  the  rapidity  of  enzyme 

^  A  few  drops  of  tincture  of  iodin  added  to  a  1  per  cent,  solution  of  potassic 
iodid. 


372    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

action,   but  also  upon  the  degree  of  the  absorption   of  the  product 
formed. 

Starch  digestion  is  a  function  of  the  salivary  enzyme.  Its  action  is 
apparent  partly  in  the  mouth  and  partly  in  the  stomach  for  a  short  time 
after  the  meal.  Hence,  starch  digestion  would  naturally  seem  of  little 
importance  in  the  diagnosis  of  stomach  diseases.  But  this  is  not  really 
so,  because  an  increased  acidity  will  interrupt  starch  digestion  very 
quickly.  On  the  contrary,  with  hypoacidity  starch  digestion  progresses 
very  favorably  and  completely.  Hence,  the  degree  of  starch  digestion 
serves  as  a  rough  test  of  the  hydrochloric  acid  secretion.  Boas  claims 
that  a  gastric  fluid  containing  0.15  per  cent,  hydrochloric  acid  will 
arrest  starch  digestion.  Nevertheless,  even  with  normal  gastric  diges- 
tion achroodextrin  is  present  in  the  Ewald  breakfast  one  hour  after  its 
ingestion.  It  was,  of  course,  produced  before  enough  acid  had  been 
secreted  to  reach  the  above  degree  of  concentration.  Achroodextrin  is 
often  absent  in  hyperacidity.  Lactic  acid  does  not  impede  starch  diges- 
tion until  it  is  more  concentrated  than  hydrochloric  acid  ;  so  that  starches 
are  frequently  well  digested  in  the  gastric  contents  from  a  passively 
congested  stomach  (Stauungsmagen)  in  case  it  contains  lactic,  instead 
of  free  hydrochloric,  acid. 

QUALITATIVE    EXAMINATION  OF    THE    FILTERED    GASTRIC    JUICE    FOR 

ACIDS. 

The  reaction  of  the  filtered  gastric  juice  is  first  of  all  tested  with 
litmus  paper.  If  the  reaction  is  acid  (as  is  almost  universally  the 
case),  we  get  no  information  about  the  presence  of  hydrochloric  acid, 
and  especially  of  free  acid,  in  the  gastric  juice,  since  other  salts,  par- 
ticularly the  acid  phosphates,  also  turn  blue  litmus  red. 

To  determine  whether  the  acid  reaction  is  due  to  free  acid  or  only  to 
acid  salt  we  employ  Congo-red,  in  the  form  of  commercial  Congo-red 
paper.  If  the  gastric  juice  turns  a  strip  of  this  paper  blue,  some  free 
acid  must  be  present ;  either  free  hydrochloric  or  some  organic  acid.^ 

To  decide  whether  the  acid  is  organic  or  free  hydrochloric  we  employ 
various  qualitative  tests.  In  the  following  we  describe  only  those  tests 
which  in  our  experience  have  proved  to  be  the  best. 

Tests  for  Free  Hydrochloric  Acid. — The  tests  for  free 
hydrochloric  acid  which  are  of  clinical  value  all  depend  upon  color 
reactions. 

Methyl=violet  Reaction. — A  pale-violet  solution  is  made  by  adding 
considerable  water  to  one  drop  of  a  moderately  concentrated  aqueous  or 
alcoholic  stock  solution  of  methyl-violet  in  a  test  tube.  This  solution 
is  divided  into  equal  parts.  To  one  a  little  of  the  filtered  gastric  juice 
is  added  ;  to  the  second,  an  equal  quantity  of  water.  If  free  hydro- 
chloric acid  is  present,  the  methyl-violet  in  the  first  changes  to  a  beauti- 
ful blue.     The  second  half  is  used  for  a  control.     Even  a  very  slight 

^  If  the  paper  is  colored  intensely  blue,  an  expert  would  nearly  always  decide  that 
it  was  due  to  free  HCl,  because  organic  acids — in  the  concentrations  in  which  they  are 
found  in  the  gastric  juice — always  produce  lighter  shades. 


EXAMINING   THE  STOMACH  WITH  AID   OF  STOMACH  TUBE.   373 

amount  of  free  hydrochloric  acid  in  the  gastric  juice  will  produce  this 
change  from  violet  to  blue. 

Tropaeolin  00  Reaction. — Tropseolin  OO  is  a  yellow  pigment.  Even 
a  minute  trace  of  free  hydrochloric  will  turn  a  solution  of  this  substance 
red  or  reddish  brown.  It  is  better  not  to  employ  too  concentrated  a 
solution.  The  best  is  a  pale-orange  solution,  prepared  freshly  by 
diluting  with  water  a  concentrated  alcoholic  stock  solution.  If  the  test 
is  made  in  the  same  way  as  with  methyl-violet  (see  above),  the  reaction 
is  not  as  sensitive.  Boas  increases  the  delicacy  of  the  reaction  by 
the  following  modification  :  Two  or  three  drops  of  the  concentrated 
alcoholic  tropseolin  OO  solution  are  dropped  into  a  porcelain  dish,  and 
then  distributed  in  an  irregular  smear  to  the  edges  by  tilting  the  dish. 
The  same  quantity  of  gastric  juice  is  added  and  mixed  with  the  tropaeolin. 
The  dish  is  then  gently  warmed  over  a  small  flame  or  over  a  water  bath, 
and  if  free  hydrochloric  acid  is  present,  beautiful  violet  to  blue  stripes 
form. 

Phloroglucin-vanillin  Reaction  (Giinzburg's  Reagent).  —  The 
reagent  consists  of  phloroglucin  2  gm.,  vanillin  1  gm.,  alcohol  30Qgm. 
One  or  two  drops  of  this  solution  are  placed  in  a  porcelain  dish  and 
mixed  with  the  same  amount  of  gastric  juice.  The  dish  is  then  gently 
warmed  over  a  small  flame.  If  free  hydrochloric  acid  is  present,  the 
drying  margins  of  the  mixture  will  develop  a  beautiful  carmin-red  color. 
If  absent,  the  solution  dries  up,  leaving  a  brown  or  yellow  color.  The 
reaction  becomes  a  little  more  sensitive  in  doubtful  cases  if  we  employ 
rather  more  gastric  juice  than  reagent. 

Value  of  These  Tests  for  Hydrochloric  Acid. — An  objection  to 
two  of  these  tests,  methyl-violet  and  tropaeolin,  is  that  free  organic 
(especially  lactic)  acid  will  produce  the  same  color.  But,  as  a  matter  of 
fact,  organic  acids  are  never  present  in  sufficient  concentration  in  the 
stomach  to  produce  these  reactions.  Giinzburg's  reaction,  however, 
admits  of  only  one  interpretation — the  presence  of  free  hydrochloric 
acid.  It  not  only  admits  of  but  one  meaning,  but  also  is  the  most  sensi- 
tive of  all  the  tests. 

Another  objection  to  these  tests  cannot  be  disposed  of  so  easily. 
They  may  be  negative  and  still  free  hydrochloric  acid  be  present,  but 
"  masked  "  by  other  substances — e.  ^.,  proteids  or  peptones.  We  can 
easily  prove  this  experimentally  by  adding  a  little  neutral  commercial 
peptone  (this  consists  chiefly  of  proteoses)  or  common  salt  to  a  solution 
of  methyl-violet  which  has  been  turned  blue  by  a  trace  of  hydrochloric 
acid.  The  violet  color  immediately  returns,  as  if  there  were  no  free 
hydrochloric  acid.  The  same  objection  applies  to  tropseolin  and  to 
phloroglucin-vanillin  ;  in  fact,  to  all  the  tests  for  free  hydrochloric  acid 
which  are  known.  But  this  is  no  reason  against  employing  these  color 
reactions  clinically.  The  reason  the  reaction  no  longer  occurs  is  because 
in  such  a  mixture  of  free  hydrochloric  acid  and  proteids  and  peptones 
the  hydrochloric  acid  is  no  longer  free  enough  to  act  upon  the  coloring 
matter  (Riegel,  Boas).  The  proteids,  as  is  well  known,  form  combinations 
with  acids,  just  like  the  typical   acid  albumin.      These  combinations 


374    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

still  react  acid  to  litmus  and  phenolphthalein,  but  the  affinity  of  the 
acid  is  just  as  loosely  held  as  in  the  so-called  acid  salts.  Hence  these 
color  tests  react  negatively  when  considerable  quantities  of  proteids  or 
peptones  are  present  because  a  positive  reaction  appears  only  in  the  pres- 
ence of  perfectly  free  acids.  From  a  clinical  point  of  view,  this  fact 
should  really  be  considered  advantageous,  because  it  is  of  no  diagnostic 
importance  to  learn  that  the  gastric  mucous  membrane  has  preserved 
ta^ces  of  its  acid-secreting  power.  AVhat  we  want  to  determine  is 
whether,  after  saturating  the  proteids  introduced  with  the  test  breakfast, 
there  still  remains  enough  perfectly  free  acid  to  continue  the  digestion. 
Experience  has  proved  that  one  hour  after  the  ingestion  of  an  Ewald's 
test  breakfast  there  should  still  be  free  HCl  in  the  mixture.  The  more 
recent  methods,  which  try  to  demonstrate  roughly  the  hydrochloric  acid 
which  is  combined  with  proteid,  as  well  as  the  free  acid,  are  of  no  diag- 
nostic value  except  for  quantitative  purposes.  The  great  difference 
between  a  gastric  juice  which  reacts  to  the  color  tests  for  free  hydro- 
chloric acid  and  one  which  does  not  would  no  longer  be  striking  and 
useful  if  we  should  select  tests  to  demonstrate  quantitatively  the  amount 
of  hydrochloric  acid  combined  with  the  proteid.  Experiments  with 
artificial  gastric  juice  prove  the  same  thing ;  if  the  juice  contains  free 
hydrochloric  acid,  it  is  eifective  in  digestion,  otherwise  not.  This  would 
seem  to  show  that  for  the  artificial  digestion  of  proteids  only  that  portion 
of  the  hydrochloric  acid  is  of  use  which  is  not  already  combined  with 
the  proteids  contained  in  the  stomach  contents,  and  this  portion  still 
reacts  to  color  reagents.  Such  an  excess  of  acid  should  be  present 
normallv,  and  it  must  be  of  diagnostic  importance  to  determine  whether 
this  is  the  case  or  not.  Therefore  the  so-called  "  masking  "  of  the  color 
reaction  by  proteids  is  not  a  disadvantage,  but,  on  the  contrary,  a  very 
marked  diagnostic  advantage.  The  "  masking  "  of  the  reaction  by  salts 
(the  cause  of  which  is  not  known)  has  no  practical  importance  in  gastric 
diagnosis,  because  with  the  usual  test  meal  the  gastric  juice  never  con- 
tains salts  in  sufficient  concentration  to  hinder  the  reaction. 

Ewald  quotes  the  following  figures  to  show  the  degree  of  sensitive- 
ness of  the  three  reagents  : 

Reaction  positive  when  there  is  present : 

Hydrochloric  Lactic  acid.        Butyric 
acid.                                            acid. 

Per  cent.  Per  cent.  Per  cent. 

Methvl-violet 0.24  4            

Tropjeolin  00      0.30  2.4-3  5-  6 

Phloroglucin-vanillin       0.05  5-10 

Tests  for  I/actic  Acid.  —  Ufelmann's  reagent  is  commonly 
employed  to  test  the  gastric  juice  for  free  lactic  acid.  It  consists  of  a 
mixture  of  20  c.c.  of  a  1  per  cent,  carbolic  acid  solution,  with  1  drop 
of  dilute  ferric  chlorid.  This  solution  is  diluted  until  the  color  becomes 
a  transparent  amethyst  blue.  The  reagent  should  be  freshly  prepared 
before  each  test,  since  the  violet  color  disappears  after  a  short  time. 
This  is  a  very  delicate  reagent  :  even  traces  of  lactic  acid    change  it 


EXAMINING   THE  STOMACH  WITH  AID   OF  STOMACH  TUBE.  375 


to  a  beautiful  canary  yellow  or  greenish  yellow.  Mere  decoloration 
without  the  formation  of  any  pronounced  yellow  shade  does  not  suggest 
lactic  acid,  because  proteids,  salts,  and  hydrochloric  acid  might  produce 
such  a  result.  Uffelmann's  reaction  may  also  be  performed  by  adding 
to  the  fluid  to  be  tested  1  to  2  drops  of  a  very  weak  (5  per  cent.)  solu- 
tion of  ferric  chlorid  (without  carbolic  acid).  If  the  fluid  contains 
lactic  acid,  it  will  become  distinctly  yellow  to  green.  In  a  doubtful 
case  the  same  amount  of  ferric  chlorid  should  be  added  to  water  for 
comparison.  Uifelmaun's  reaction  is  not  quite  reliable,  because  certain 
sugars,  peptones,  alcohol,  tartaric  acid,  citric  acid,  oxalic  acid,  and 
various  other  substances  produce  a  similar  color.  Another  objection  is, 
that  the  reaction  may  be  prevented  by  the  presence  of  phosphates  and  a 
considerable  excess  of  hydrochloric  acid.  The  yellowish  tint  of  the 
stomach  contents,  and  sometimes  the  turbidity  due  to  the  addition  of 
the  ferric  chlorid,  may  also  affect  the  reaction.  Greater  accuracy  will 
result  if  we  isolate  the  lactic  acid  by  extracting  the  gastric  juice  with 
€ther,  removing  the  ether  by  evaporation,  and  then  perform  the  test 
upon  the  ether  residue  dissolved  in  water.  Uffelmann's  test  has  been 
very  appropriately  modified  by  H.  Strauss.^  By  this  method  all  sources 
of  error  are  avoided  and  a  quantitative  result  obtained. 

Strauss'  Method  of  Determining  Lactic  Acid. — He  extracts  the  gastric 
contents  with  ether,  but  does  not  evaporate  the  ether.  He  shakes  the  ethereal  ex- 
tract with  a  dilute  solution  of  ferric  chlorid,  according  to  Fleischer's  method.  If 
the  watery  layer  shows  a  greenish  coloration  the  reaction  is 
positive.  By  employing  definite  quantities  of  reagent  and 
solution  the  intensity  of  the  coloration  can  be  made  to  furnish 
an  approximate  estimate  of  the  amount  of  lactic  acid.  The 
procedure  is  as  follows  :  5  c.c.  of  gastric  juice  are  put  into  a 
separatory  funnel  (Fig.  144)  having  two  division  marks,  one 
corresjjonding  to  a  volume  of  5  c.c,  the  other  to  that  of  25 
c.c;  ether  is  now  added  to  the  25  c.c.  mark.  The  solutions 
are  then  shaken  vigorously.  After  the  mixture  has  settled 
into  layers,  the  gastric  juice  at  the  bottom  is  drawn  off  by 
means  of  the  stopcock.  Distilled  water  is  then  added  until 
the  liquid  rises  again  to  the  25  c.c  mark.  Then  2  drops  of 
a  dilute  solution  of  ferric  chlorid  (containing  1  part  ferric 
chlorid  to  9  parts  of  distilled  water)  are  added  and  the  mixt- 
ure again  vigorously  shaken.  If  more  than  1  per  cent,  of 
lactic  acid  is  present,  the  layer  of  water  below  is  colored  an 
intense  greenish  yellow.  Smaller  amounts  do  not  produce 
any  distinct  color  change.  Strauss'  method  eliminates  all 
the  sources  of  error  of  the  ordinary  Uffelmann's  reaction 
(above  mentioned).  None  of  the  substances  which  produce 
a  similar  reaction  (peptones  and  carbohydrates),  nor  sub- 
stances which  mask  the  reaction  (hydrochloric  acid  and  phos- 
phates) will  be  taken  up  by  the  ether  in  any  appreciable 
quantities.  The  ether  employed  should  be  free  from  alcohol. 
This  method  suffices  for  all  practical  purposes.  It  should  be 
remembered  that  Strauss'  test  may  be  negative  if  the  lactic 
acid  present  is  completely  combined  with  the  proteids  of  the  gastric  juice.  The 
acid  albuminate  of  lactic  acid  does  not  then  give  up  lactic  acid  to  the  ether.  In 
such  a  case,  which  can  occur  only  when  the  gastric  juice  does  not  react  for  free 

1  Berlin,  klin.  Woch.,  1895,  No.  37. 


Fig.  144.— Separatory 
funnel. 


376    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

acids,  it  is  advisable  to  repeat  the  shaking  after  hydrochloric  acid  has  been  added 
to  the  gastric  juice  up  to  a  beginning  of  the  Congo-red  reaction. 

Boas'  Method  for  Detecting  Lactic  Acid. — Boas' ^  method  depends  upon 
the  fact  that  oxidizing  agents  change  lactic  acid  into  aldehyd,  and  that  the  alde- 
hyd  can  be  easily  distilled  off  and  transformed  into  iodoform  by  adding  some  alka- 
line iodin  solution,  very  much  as  acetone  in  Lieben's  reaction  is  transformed  into 
iodoform.  (See  Urine  Analysis,  p.  495.)  The  iodoform  is  easily  recognized  by 
its  characteristic  crystalline  form  (compare  ibid.)  and  by  its  peculiar  odor.  By 
oxidation  carbohydrates  are  also  changed  to  aldehyd  ;  hence  the  test  should  be  per- 
formed with  an  ethereal  extract  of  the  gastric  contents,  which  will  not  contain  any 
carbohydrate.  The  technic  of  Boas'  method  is  as  follows  :  10  to  20  c.c.  of  the 
filtrate  from  the  stomach  contents  are  evaporated  in  a  small  dish  over  a  water  bath 
to  a  syrupy  consistence.  If  free  acid  is  absent  (Congo  test)  this  can  be  done 
directly  ;  but  if  present  the  lactic  acid  should  first  be  combined  and  its  volatiliza- 
tion prevented  by  the  addition  of  a  saturated  solution  of  barium  carbonate.  A 
few  drops  of  phosphoric  acid  are  then  added  to  the  syrupy  fluid  to  set  the  lactic 
acid  free  again,  and  it  is  boiled  just  once  to  remove  the  carbon  dioxid  ;  then  it  is 
allowed  to  cool,  and  finally  extracted  with  100  c.c.  of  ether  free  from  alcohol.^ 
After  digesting  for  a  half-hour  the  clear  layer  of  ether  is  poured  off*,  the  ether 
evaporated,  the  residue  extracted  with  45  c.c.  of  water,  carefully  shaken  and  fil- 
tered, and  5  c.  c.  of  sulphuric  acid  and  a  little  powdered  manganese  dioxid  are  added 
to  the  filtrate  and  distilled  into  the  receiving  vessel,  which  contains  5  to  10  c.c.  of 
an  alkaline  solution  of  iodin.  ^  If  aldehyd  passes  through  into  the  receiving  vessel  a 
cloudiness  is  produced.  This  consists  of  iodoform  ciystals,  and  the  characteristic 
odor  of  iodoform  is  noticed. 

Martins'  experiments  (see  p.  388  et  seq.),  contrary  to  the  old  idea, 
prove  that  the  formation  of  lactic  acid  is  not  a  part  of  normal  gastric 
digestion,  but  is  rather  due  to  bacterial  fermentations,  which  are  nor- 
mally prevented  by  the  presence  of  the  hydrochloric  acid  of  the  gastric 
juice.  The  occurrence  of  lactic  acid  in  the  expressed  meals,  as  demon- 
strated by  Strauss'  method,  must  therefore  be  considered  a  pathologic 
phenomenon.  This  points  either  to  a  stagnation  of  the  gastric  contents 
or  to  the  absence  or  diminution  in  the  amount  of  the  free  hydrochloric 
acid,  or  to  both  of  these  factors,  for  only  when  they  occur  together  is 
opportunity  furnished  for  abundant  lactic  acid  fermentation.  Hence  a 
large  quantity  of  lactic  acid  is  found  with  moto?'  insufficiency  of  the 
stomach,  more  particularly  from  a  stenosis  of  the  pylorus,  when  associ- 
ated with  diminished  hydrochloric  acid  production.  As  experience 
shows,  this  is  generally  due  to  carcinoma  of  the  pylorus ;  hence 
recently  a  certain  amount  of  significance  has  justly  been  attached  to 
the  demonstration  of  lactic  acid  in  the  stomach  contents  as  suggesting 
the  diagnosis  of  carcinoma  of  the  stomach.  But  the  opinion  originally 
advanced  by  Boas,  that  the  presence  of  lactic  acid  in  the  gastric  juice 
was  pathognomonic  of  this  lesion,  has  not  been  confirmed.  Benign  sten- 
osis and  gastric  insuffieiencies,  Avhen  combined  with  deficient  secretion  of 
hydrochloric  acid,  have  repeatedly  furnished  a  positive  test  to  lactic 
acid. 

'  Deutseh.  med.  WocL,  1893,  No.  39. 

^  Because  alcohol  when  oxidized  becomes  aldehyd. 

^  Prepared  by  mixing  equal  parts  of  a  solution  of  56  gm.  of  dry  potassium  hydroxid 

in  1000  gm.  of   distilled  water  and  of  a  —  iodin  solution.     (Compare  text-books  on 
chemistry. ) 


EXAMINING  THE  STOMACH  WITH  AID   OF  STOMACH  TUBE.   377 

One  objection  to  all  the  lactic  acid  tests  which  demonstrate  lactic 
acid  fermentation  in  the  stomach  is,  that  ordinary  food,  and  in  particular 
Ewald's  test  breakfast,  always  contains  preformed  lactic  acid.  Boas, 
for  this  reason,  substituted  a  thin  oatmeal  porridge  for  the  ordinary  test 
meal,  there  being  no  lactic  acid  in  oatmeal.  However,  this  precaution 
seems  really  unnecessary,  considering  the  slight  amount  of  preformed 
lactic  acid  which  is  contained  in  the  ordinary  test  breakfast,  if  diagnostic 
importance  should  be  attached  only  to  a  very  pronounced  lactic  acid 
reaction.  The  advantage  of  Strauss'  method  is,  that  while  it  estimates 
fairly  accurately  the  amount  of  lactic  acid,  it  is  not  sufficiently  sensitive 
to  give  a  positive  reaction  from  the  lactic  acid  in  an  ordinary  roll  made 
with  water  (not  milk),  without  lactic  acid  fermentation  in  the  stomach. 
This  is  a  marked  advantage  over  Boas'  test,  which,  on  account  of  its 
sensitiveness,  is  only  of  practical  value  when  employed  as  a  quantitative 
method  (see  p.  386). 

Detection  of  Volatile  Fatty  Acids. — If  the  volatile  fatty 
acids — butyric,  acetic,  or  valerianic — are  present  to  any  extent,  they  are 
easily  recognized  by  their  characteristic  odor.  More  accurate  tests  are 
too  complicated  and  hardly  practical.  Traces  of  butyric  acid  occur 
normally  after  the  ingestion  of  foods  containing  butter.  Its  presence  is 
to  be  attributed  to  the  action  of  the  fat-splitting  ferment  of  the  gastric 
juice,  recently  more  exactly  studied  by  Volhard.  The  two  other  vola- 
tile fatty  acids,  like  lactic  acid,  arise  only  as  the  result  of  fermentation 
and  stagnation  of  the  gastric  contents,  although  traces  do,  of  course, 
occur  from  what  is  contained  in  the  various  foodstuffs. 

QUANTITATIVE   TESTS   FOR  ACIDS. 

The  quantitative  analysis  of  the  gastric  juice  is  peculiarly  difficult 
because  organic  acids,  and  especially  acid  salts,  may  be  present  as  well 
as  hydrochloric  acid,  and  because  we  must  also  differentiate  between  free 
hydrochloric  acid  and  that  which  is  combined  loosely  with  the  proteids, 
as  we  have  already  explained  in  connection  with  the  qualitative  hydro- 
chloric acid  tests.  To  make  clear  the  complexity  of  the  condition,  we 
may  arrange  in  the  following  table  the  acid-reacting  components  of  the 
gastric  juice — i.  e.,  those  turning  blue  litmus  paper  red — in  one  group, 
and  the  chlorin-containing  constituents,  which  we  must  consider  in  test- 
ing for  hydrochloric  acid,  in  another  : 

1.  Acid-reacting  constituents  of  the  gastric  juice. 

(a)  Free,  and  combined  with  proteids,  hydrochloric  acid. 

(b)  Organic  acids. 

(c)  Acid  salts  (acid  phosphate). 

2.  Chlorin-containing  constituents  of  the  gastric  juice. 

(d)  Free  hydrochloric  acid  (producing  color  reactions). 

(e)  Hydrochloric  acid  which  is  combined — i.  e.,  with  proteids — 
producing  no  color  reaction,  but  reacting  to  litmus  and  jihcnolphthalein 
acid.      (This  is  usually  called  combined  hydrochloric  acid). 

(/)  Chlorids,  neither  reacting  acid  nor  producing  any  color  reaction. 
Titration  of  the  Total  Acidity  of  the  Gastric  Juice. — In 


378    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

order  to  determine  the  total  acidity,  we  first  of  all  titrate  the  gastric 
juice  with  a  ^  sodium  hydroxid  solution — i.  e.,  we  determine  the  num- 
ber of  cubic  centimeters  of  the  sodium  hydroxid  solution  which  is 
necessary  to  neutralize  a  definite  volume  of  gastric  contents.  The  tech- 
nic  is  as  follows  :  As  is  well  known,  a  normal  sodium  hydroxid  solution 
is  one  which  contains  in  each  liter  as  many  grams  of  the  substance  in 
question  as  its  equivalent  weight.  A  decinormal  (^)  solution  is  made 
from  this  by  diluting  10  times.  According  to  the  definition,  equal  vol- 
umes of  normal  solutions  neutralize  each  other ;  1  c.c.  of  a  ^  NaOH 
solution  neutralizes  exactly  0.1  c.c.  of  a  N — HCl,  etc.  In  preparing  a 
normal  sodium  hydroxid  solution,  it  is  best  to  start  with  a  normal  oxalic 
acid  solution  :  63  gm.  of  a  well-crystallized  and  chemically  pure  oxalic 
acid  are  dissolved  in  distilled  water  and  the  volume  made  up  to  exactly 
1  liter.  Now,  a  normal  sodium  hydroxid  solution  will  require,  in  order 
to  neutralize  a  given  volume  of  the  normal  oxalic  acid  solution,  exactly 
the  same  volume.  A  few  drops  of  alcoholic  phenolphthalein  solution 
are  added  as  an  indicator  to  10  c.c.  of  normal  oxalic  acid  solution.  Then 
to  this  the  approximately  normal  sodium  hydroxid  solution  ^  is  added 
from  a  buret  until  the  acid  is  neutralized — i.  e.,  until  the  mixture  takes 
on  a  permanent  reddish  color.  If  the  normal  NaOH  solution  is  cor- 
rect, it  will  require  exactly  10  c.c.  Generally  speaking,  less  is  needed. 
For  instance,  if  we  employed  9.5  c.c.  of  the  f^  NaOH  for  neutralization, 
we  must  add  0.5  c.c.  of  water  to  each  9.5  c.c.  of  the  solution.  Then 
10  c.c.  of  the  normal  NaOH  solution  will  correspond  to  exactly  10  c.c. 
of  the  normal  oxalic  acid  solution.  From  this  we  can  easily  estimate 
how  much  water  to  add  to  the  1000  c.c.  of  solution — i.  e.,  (~i  X  0.5). 
Normal  sodium  hydroxid  solution  is  too  strong  to  use  for  the  titration 
of  the  gastric  juice ;  hence  we  prepare  fo  by  diluting  the  normal  10 
times.  We  fill  a  graduated  buret,  provided  with  a  stopcock,  with  this 
I,  sodium  hydroxid  solution.  We  measure  10  c.c.  of  the  filtered  gastric 
juice  ^  into  a  porcelain  dish  (or  into  a  beaker  if  we  have  a  white  back- 
ground) and  add  a  few  drops  of  alcoholic  phenolphthalein  solution  as  an 
indicator. 

While  stirring  the  mixture  continually  we  add  enough  of  the  ^  NaOH 
solution  to  make  the  red  color  persistent.  The  amount  of  the  fo  solution 
employed  represents  the  acidity  of  the  gastric  juice.  It  may  be  expressed 
in  two  ways — either  with  reference  to  some  fixed  acid,  or  in  so-called 
aciditv  percentages  (Jaworski).  The  acidity  of  the  gastric  juice  is  per- 
haps most  frequently  expressed  in  terms  of  HCl.  For  this  purpose  w^e 
must  remember  that,  according  to  the  definition,  equal  volumes  of  nor- 
mal solutions  will  react — i.  e.,  neutralize  each  other.  Therefore  1  c.c. 
of  normal  sodium  hydroxid  solution  corresponds  (for  neutralization)  to 
exactly    1    c.c.    of    normal   hydrochloric   acid   solution.      Normal   HCl 

1  This  is  made  by  dissolving  about  42  gm.  of  pure  sodium  hydroxid  (in  sticks)  in  1 
liter  of  distilled  water.  ... 

='Martius  has  showed  that  we  reallv  should  employ  the  unhitered  gastric  juice  to 
prevent  errore  in  the  quantitative  acid  tests.  This  is  because  the  solid  material  contains 
a  larger  proportion  of  the  acid.  For  practical  purposes,  however,  titration  of  the  filtrate 
will  suffice. 


EXAMINING   THE  STOMACH  WITH  AID   OF  STOMACH  TUBE.   379 

contains  to  a  liter  1  equivalent — i.  e.,  as  the  equivalent  weight  of  HCl 
is  36.5,  1  c.c.  of  normal  HCl  acid  contains  0.0365  gm.  of  hydro- 
chloric acid.  This  amount  of  hydrochloric  acid  corresponds  to  1 
c.c.  of  normal  NaOH  solution ;  1  c.c.  of  ^„  NaOH  therefore  corre- 
sponds to  0.00365  c.c.  of  HCl.  From  this  the  acidity  as  expressed  in 
hydrochloric  acid  is  easily  figured  out.  If  5  c.c.  of  f^  sodium  hydroxid 
solution  are  required  to  neutralize  10  c.c.  of  gastric  juice,  the  acidity  of 
the  10  c.c,  in  terms  of  hydrochloric  acid,  would  equal  5X0.00365  = 
0.01825  gm.  of  hydrochloric  acid;  or,  expressed  in  percentage — i.e., 
calculated  for  100  c.c.  of  gastric  juice — 0.1825  hydrochloric  acid. 
This  method  of  calculating  the  percentage  of  free  hydrochloric  acid 
does  not  give  us  the  actual  amount  of  HCl  contained  in  the  gastric 
juice,  for  other  factors  aid  in  determining  the  acidity.  But  it  does  give 
us  an  estimate  of  the  maximum  of  hydrochloric  acid  which  the  gastric 
juice  in  question  may  contain.  To  calculate  the  so-called  degree  of 
acidity  we  simply  estimate  how  many  cubic  centimeters  of  ~  NaOH  are 
used  to  neutralize  100  c.c.  of  the  gastric  juice — i.  e.,  the  percentage  of 
its  own  volume  necessary  for  the  neutralization  of  the  gastric  juice  under 
examination.  To  express  the  acidity  in  per  cent.,  we  multiply  by  10 
the  number  of  cubic  centimeters  of  the  j^  NaOH  solution  necessary  to 
neutralize  10  c.c.  of  stomach  contents.  A  gastric  juice,  10  c.c.  of 
which  require  5  c.c.  of  f-^  NaOH  solution  for  neutralization,  has  there- 
fore an  acidity  of  50.  This  method  of  calculation  possesses  an  advan- 
tage in  corresponding  exactly  to  the  actual  conditions,  whereas  the 
reckoning  in  terms  of  HCl  incorrectly  assumes  that  the  acidity  may  be 
due  exclusively  to  hydrochloric  acid.  On  the  other  hand,  changing 
over  to  hydrochloric  acid  perhaps  gives  us  a  more  distinct  idea. 

Quantitative  Estimation  of  the  Hydrochloric  Acid  and 
Chlorids  in  the  Gastric  Juice. — The  estimation  of  the  total  acidity 
of  the  gastric  juice  is  a  very  simple  chemical  procedure ;  but  the  deter- 
mination of  the  amount  of  hydrochloric  acid  contained  in  the  gastric 
juice  appears  more  difficult,  because  we  have  to  consider  separately  the 
factors  d,  e,  and/  (p.  377).  A  chlorin  estimate  alone  is  of  no  value  in 
judging  of  the  amount  of  hydrochloric  acid,  for  it  would  give  only  the 
total  sum  of  d  -\-  e  -\-  f,  and  include  chlorids  of  the  food  as  well. 
What  we  wish  to  determine  is  the  sum  of  d  -\-  e  (i.  e.,  the  amount 
of  free  and  combined  hydrochloric  acid  secreted  by  the  stomach). 

Estimation  of  the  Total  TJnneutralized  (Secreted)  Hydrochloric  Acid 
of  the  Gastric  Juice  (d  +  e,  p.  377). — Sjoqvisfs  Method. — This  depends  upon 
the  fact  that  the  acids  which  are  absolutely  free,  as  well  as  those  which  are  but 
loosely  combined  with  proteids,  are  changed  to  their  corresponding  barium  salts 
if  mixed  with  barium  carbonate.  If  the  mixture  is  then  evaporated  to  diyness 
and  incinerated,  the  barium  salts  of  the  organic  acids  will  be  transformed  to 
barium  carbonate,  ]:)ut  the  hydrochloric  acid  will  remain  fixed  as  barium  chlorid. 
This  can  then  be  isolated  from  the  ash  l)y  extraction  with  water,  and  then  titrated 
with  a  solution  of  potassium  bichromate,  and  the  amount  of  hydrochloric  acid  be 
estimated  from  this. 

The  steps  of  Sjoqvisfs  method  are  as  follows:  10  c.c.  of  gastric  juice  are 
slowly  evaporated  to  dryness,  in  a  silver  or  platinum  dish,,  with  an  excess  of  barium 
carbonate  (free  from  chlorin).     The  residue  is  then  kept  at  a  red  heat  for  a  few 


380    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

moments.     After  cooling,  the  residue  is  first  digested  with  10  c.  c.  of  water,  and  then 
extracted  repeatedly  with  hot  water  until  the  filtered  extract  amounts  to  50  c.  c. 

In  order  to  titrate  for  barium  we  add  to  the  solution  one-fourth  to  one-third 
its  volume  of  alcohol,  and  3  to  4  c.c.  of  a  solution  of  10  gm.  of  acetic  acid  and 
10  gm.  of  sodium  acetate  in  100  c.c.  of  water.  These  additions  facilitate  the 
separation  of  the  barium  chromate  and  prevent  the  precipitation  of  calcium  chro- 
mate  from  any  calcium  salt  that  may  be  present.  An  8. 5  per  cent,  solution  of 
chemically  pure  potassium  bichromate  is  added  irom  a  buret  to  the  solution 
until  the  barium  is  completely  precipitated.  So-called  "  tetra  paper"  (tetra- 
methyl-paraphenyldiamin  paper)  will  serve  to  indicate  the  end  of  the  reaction.  Any 
excess  of  potassium  bichromate  will  produce  a  blue  color.  Every  cubic  centi- 
meter of  bichromate  solution  which  it  was  necessary  to  add  in  order  to  complete 
the  end-reaction  corresponds  to  4.05  mg.  of  hydrochloric  acid.  Sjoqvist  has 
recently  improved  his  method  by  changing  the  final  titration  with  bichromate, 
because  the  reaction  is  not  sharply  defined,  to  a  much  more  sharply  defined  iodin 
titration.  Iodin  is  quantitatively  liberated  by  adding  KI  and  HCl  to  the  bichro- 
mate, and  the  iodin  is  determined  in  the  well-known  way  by  titrating  with  sodium 
thiosulphate  and  starch.  For  the  technic  of  this  modification  we  must  refer  to 
the  original  communication  in  Vol.  V.  of  the  Scandinavian  Archives  of  Physi- 
ology, 1895. 

Leo's  Method. — Leo's  method  is  based  on  the  fact  that  both  free  and  combined 
hydrochloric  acid  are  neutralized  by  calcium  carbonate,  while  acid  phosphates  and 
other  combinations  reacting  in  the  titration  with  sodium  hydrate  show  the  same 
acidity  after  treating  with  calcium  carbonate  as  before. 

Leo  first  removes  the  fatty  acids  by  distillation,  and  the  lactic  acid  by  extrac- 
tion with  ether,  and  then  estimates  the  total  acidity  of  the  specimen  of  gastric 
juice.  In  another  portion  he  combines  with  calcium  carbonate  both  the  free 
hydrochloric  acid  and  that  combined  with  the  proteids,  and  then  titrates  again. 
The  amount  of  the  acidity  which  disappears  after  the  addition  of  calcium  car- 
bonate corresponds  to  the  hydrochloric  acid  present.  Calcium  chlorid  formed 
in  the  neutralization  of  the  hydrochloric  acid  necessitates  (on  account  of  the 
probable  presence  of  acid  phosphates)  especially  skilful  manipulation  when  per- 
forming the  test.  If  calcium  chlorid  is  absent,  the  titration  of  the  acid  phos- 
phates will  be  represented  by  the  following  formula  :  PO^H^K  +  NaOH  = 
PO^HKNa  +  HjO.  But  if  calcium  chlorid  is  present  in  the  solution  at  the  same 
time,  the  following  formula  will  represent  the  titration  :  2PO^H2K  +  4NaOH  + 
SCaClj  =  (POJ^Caj  +  2KC1  +  4NaCl  +  411  fi.  In  the  latter  case  we  need  double 
the  quantity  of  sodium  hydroxid  for  neutralization.  Leo  adds  an  excess  of  calcium 
chlorid  to  both  specimens  before  titration,  in  order  to  exclude  the  influence  of  the 
calcium  chlorid  formed  by  the  neutralization  with  calcium  carbonate,  when  com- 
paring the  two  titrations.  For  the  details  of  the  technic  consult  Leo's  own  com- 
munication, i 

Leo's  method  will  also  serve  the  purpose  of  estimating  at  the  same  time  the 
quantity  of  acid  phosphates. 

Liitke-Martius'  Method. — Liitke-Martius'  is  one  of  the  simplest  methods  for 
the  determination  of  the  total  amount  of  hydrochloric  acid  secreted  (free  HCl  -f 
that  combined  with  proteids). 

We  first  estimate  the  total  amount  of  chlorin  in  a  specimen  of  gastric  con- 
tents^ (see  below).  This  is  represented  by  a.  Another  specimen  of  the  gastric 
contents  is  incinerated,  the  chlorin  in  the  ash  estimated,  and  represented  by  b. 
The  latter  then  represents  the  chlorin  of  the  chlorids,  because  the  HCl  is  volatile. 
By  subtracting  b,  the  chlorin  of  the  chlorids,  from  a,  the  total  chlorin,  we  get 
a  —  b,  the  chlorin  of  the  hydrochloric  acid  secretion.'* 

^  IHagnostik  der  Erkrankungen  der  Verdauungsorgane,  Berlin,  1890. 

^  Martius  employs  the  plain  gastric  contents  exclusively,  instead  of  the  filtmte 
(compare  note  2,  p.  .378). 

*  See  following  pages.  For  a  correction  of  this  method  see  Reissner,  Zeit.  f.  klin. 
Med.,  vol.  xliv.,  p.  75. 


EXAMINING  THE  STOMACH  WITH  AID   OF  STOMACH  TUBE.   381 

Volhard's  method  also  estimates  the  total  amount  of  chlorin.  An  excess  of 
strongly  acid  silver  nitrate  solution  is  added  to  a  measured  quantity  of  the  gastric 
contents  so  that  all  the  chlorin  present  will  be  combined  with  the  silver.  We  can 
then  determine  whatever  excess  of  silver  remains  uncombined  in  the  filtrate  by 
titration  with  ammonium  sulphocyanid.  The  silver  will  be  precipitated  as  insol- 
uble silver  sulphocyanid.  Iron  alum  or  sulphate  will  serve  as  an  indicator  to  show 
when  the  precipitation  is  complete.  It  may  be  added  to  the  silver  solution  at  the 
beginning.  In  adding  the  ammonium  sulphocyanid.  the  red  color  of  the  sulpho- 
cyanid will  persist  only  after  all  of  the  silver  has  been  completely  precipitated  as 
silver  sulphocyanid.  The  details  of  the  technic  are  contained  in  the  following 
quotation  from  Liitke  : 

The  following  normal  solutions  are  essential  : 

1.  —  silver  solution  containing  17  gm,  of  silver  nitrate  in  a  liter  :  Ferrous 

sulphate  is  also  added  to  the  solution  as  an  indicator,  and  an  excess  of  nitric  acid. 

The  method  of  preparation  is  as  follows  :  17.5  gm.  of  silver  nitrate  are  dissolved 

in  about  900  c.c.  of  25  per  cent,  nitric  acid,  and  50  c.c.  of  liq.  ferri  sulphurici 

oxydati  are  added  to  the  solution  and  the  volume  made  up  to  1  liter.     The  solu- 

N 
tion  is  standarized  with  a  —  HCl  solution  in  the  usual  way. 

N 

2.  —  ammonium  sulphocyanid  solution :    7. 6  gm.   of  CNSNH4  in  a  liter. 

About  8  gm.  of  ammonium  sulphocyanid  are  dissolved  in  1  liter  of  water,  and  the 

N 
absolute  quantity  contained  in  this  solution  estimated  by  means  of  the  —  silver 

solution.     For  this  purpose   10  c.c.  of  the  (iron-containing)   silver  solution  are 

placed  in  a  beaker,  and  150  to  200  c.c.  of  water  added  ;  then  the  sulphocyanid 

solution  is  allowed  to  flow  in  from  a  buret  until  a  faint  reddish  color  appears  and 

persists — e.  g.,  if  9.7  c.c.   had  been  used  for  this  purpose,  then  970  c.c.  of  the 

sulphocyanid  solution  should  be  diluted  up  to  1000  c.c.     After  such  dilution  a 

N 
further  trial  is  made  to  determine  accurately  that  it  is  a  -—  solution. 

(a)  Estimation  of  the  Total  Chlorin. — Ten  c.c.  of  the  stomach  contents,  well 

mixed,  are  placed  in  a  100  c.c.  graduated  flask.     The  graduate  in  which  the  10  c.c. 

are  measured  must  previously  be  rinsed  out  twice  with  water.     Then  20  c.c.  of 

N    .  . 

—  silver  solution  are  added  ;  the  mixture  is  well  shaken  and  allowed  to  stand  ten 

minutes.     If  there  is  a  marked  color  to  the  stomach  contents,  we  may  decolorize 

by  adding  5  to  10  drops  of  a  potassium  permanganate  solution  (15  :  1).     This  is 

not  often  necessary.     The  permanganate  solution  should  not  be  added  until  all  the 

chlorin  is  already  combined  with  the  silver,  otherwise  the  permanganate  will  split 

up  the  hydrochloric  acid  and  form  free  chlorin,  which  volatilizes,  so  the  result  of 

the  analysis  would  be  questionable.     After  decolorization  has  taken  place  we  add 

up  to  100  c.c,  shake  well,  and  filter  through  a  dry  filter  paper  into  a  dry  glass. 

Fifty  cubic  centimeters  of  this  filtrate   placed  in  a  beaker  are  now  titrated 

N 
with  the    —    sulphocyanid   solution. 

The  total  amount  of  chlorin  is  calculated  as  follows  :  The  number  of  cubic 
centimeters  of  sulphocyanid  solution  required  is  multiplied  by  2,  and  the  product 
deducted  from  the  volume  of  the  silver  solution  used  (20  c.c. ). 

(6)  Determination  of  the  Chlorids. — Ten  c.c.  of  well-mixed  gastric  contents 
in  a  jilatinum  dish  are  evaporated  to  dryness  over  a  water  bath.  The  residue  is 
incinerated  over  the  direct  flame  so  long  as  the  ash  burns  with  a  bright  luminous 
flame.  Excessive  and  prolonged  heating  is  superfluous  and  to  be  avoided,  because 
the  chlorids  volatilize  at  red  heat.  After  the  burning  of  the  residue  the  moistened 
ash  is  pulverized  with  a  glass  rod  and  extracted  with  about  100  c.c.  of  warm  water, 
and  the  fluid  then  thrown  upon  a  filter.     Experience  has  shown  that  this  amount 


382    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

of  water  is  sufficient  for  a  complete  extraction  of  the  ash.  If  it  is  doubtful,  how- 
ever, whether  all  the  chlorin  has  been  washed  out,  a  few  drops  of  the  silver  solu- 
tion may  be  added  to  the  last  few  drops  of  the  filtrate.  Any  cloudiness  would 
indicate  the  presence  of  chlorin  and  necessitate  farther  extraction.     The  entire 

N 
filtrate  is  then  placed  in  a  beaker  with  10  c.c.  of  —  silver  solution,  and  titrated 

N 
with  the  —  sulphocyanid  solution.      The  am.ount  of  chlorin  held  in  combination 

is  calculated  by  subtracting  the  number  of  cubic  centimeters  of  the  sulphocyanid 

solution  from  the  amount  of  silver  used  (10  c.c). 

(c)  Determination  of  the  Hydrochloric  Acid. — The  amount  of  hydrochloric  acid 

contained  in  10  c.c.  of  gastric   contents  is   calculated  from  the  two  values  found 

(total  chlorin  (a)  and  chlorin  of  the  chlorids  (b))  by  subtraction.   From  the  amount 

N 
of  total  chlorin,  expressed  in  cubic  centimeters  of  ~  solution,  the  amount  of  chlorin 

of  the  chlorids,  expressed  in  the  same  way,  is  deducted.  By  multiplying  the  result 
by  0.0365,  the  absolute  amount  of  hydrochloric  acid  contained  in  100  c.c.  of 
stomach  contents,  or  the  percentage  of  the  hydrochloric  acid,  is  obtained. 

N 
The  author' s  own  experience  shows  that  the  amount  of  —  silver  solution  em- 
ployed in  both  determinations  (a=20  c.c,  6=10  c.c.)  has  been  found  quite  suffi- 
cient to  combine  with  all  the  chlorin.     If  it  should  happen  that  a  gastric  content 

be  observed  with  a  greater  content  of  chlorin,  then  more  of  the  —  silver  nitrate 

solution  must  be  added. 

O.  Reissner  ^  has  called  attention  to  the  fact  that  the  hydrochloric  acid  values 
obtained  by  means  of  the  Liitke-Martius  method  are  erroneous  in  one  respect, 
since  the  gastric  juice  contains  ammonium  chlorid,  the  ammonia  of  which,  as 
showTi  by  Sticker,  is  obtained  chiefly  from  the  saliva,  although  under  pathologic 
conditions  it  may  also  arise  within  the  stomach,  from  the  putrefaction  of  albumin. 
When  the  residue  of  the  gastric  contents  is  incinerated  in  the  Ltitke-Martius 
method,  to  remove  the  hydrochloric  acid  and  to  obtain  the  value  b  (see  p.  381), 
the  ammonium  chlorid  is  volatilized  as  well.  The  value  b  for  the  chlorin  of  the 
chlorids  is  consequently  too  low,  and  the  value  a  —  6  for  the  secreted  acid  will  be  cor- 
respondingly too  high.  This  explains  the  fact  that  the  Liitke-Martius  method 
sometimes  gives  a  value  for  the  secreted  hydrochloric  acid  which  is  greater  than 
the  total  acidity,  a  condition  of  affairs  which  is  manifestly  impossible,  since  the 
total  acidity  includes  not  only  the  hydi'ochloric  acid,  but  the  acid  phosphates  as 
well.  Reissner  has  also  shown  how  to  avoid  this  source  of  error.  He  eliminates 
the  ammonium  chlorid  before  determining  the  value  of  a  ;  the  subtraction  a  —  b 
will  then  give  a  correct  result.  Instead  of  determining  a  directly  by  titrating  the 
gastric  contents  with  the  silver  and  sulphocyanid  solutions,  Reissner  advises  neu- 
tralization of  a  measured  quantity  of  the  gastric  contents,  its  incineration  in  a 
platinum  dish,  the  solution  of  the  ash  in  hot  water,  and  the  titration  of  the  fil- 
trate in  the  customary  manner.  By  this  modification  the  ammonium  chlorid 
is  volatilized  and  eliminated  from  the  chlorin  value  a.  In  the  neutralization 
Reissner  believes  it  is  best  not  to  go  beyond  the  neutral  reaction  upon  litmus,  since, 
when  phenolphthalein  is  employed  as  an  indicator,  the  end-reaction  is  postponed, 
and  there  is  danger  that  the  chlorin  of  the  ammonium  chlorid  will  be  partly  fixed 
by  the  sodium  as  sodium  chlorid. 

Hehner-Maly' s  Method. — Hehner-Maly' s  method  (recommended  by  Leube  for 
clinical  work)  is  based  on  the  fact  that  where  a  mixture  of  organic  and  inorganic 
acids  is  neutralized  and  reduced  to  an  ash,  the  organic  salts  are  changed  to  alka- 
line carbonates  by  the  process  of  combustion,  but  the  inorganic  salts  remain  neu- 
tral. If  this  alkalinity — i.  e.,  an  equivalent  acidity — is  deducted  from  the  total 
acidity,  the  remainder  is  the  acidity  due  to  mineral  acid. 

'^Zeit.f.  klin.  Med.,  vol.  xlviii.,  parts  1  and  2,  p.  106. 


EXAMINING   THE  STOMACH  WITH  AID   OF  STOMACH  TUBE.   383 

For  the  gastric  juice  the  process  is  as  follows  :  10  c.c.  of  gastric  juice  are  titra- 

N 
ted  in  the  usual  way  with     -  NaOH,    and  with  phenolphthalein  as  an  indicator. 

The  neutralized  solution  is  evaporated  to  dryness  in  a  platinum  dish  and  then 

incinerated,  the  ash  dissolved  in  distilled  water,  and  the  alkaline  solution  titrated 

N 
with    --  acid  (oxalic  acid  or  hydrochloric  acid,  with  phenolphthalein  again  added 

N 

as  an  indicator)  till  the  decoloration  is  complete.     The  -   acid  used  in  the  titration 

corresponds  to  the  acidity  caused  by  organic  acids.     To  determine  the  amount  of 

hydrochloric  acid,   this  value  is   simply  to  be  deducted  from  the  total   acidity. 

This  method   is  very  simple  and  well  adapted  for  clinical  purposes.     The  only 

disadvantage  is  that  the  acid  phosphates  are  estimated  as  HCl,  for  they  act  as 

mineral  acids  when  reduced  to  ashes.     Very  accurate  results  can  be  obtained  by 

estimating  the  acid  phosphates  according  to  Leo's  method  (j3.380),  and  deducting 

the  acidity  belonging   to   them  from  the  HCl   as    obtained   by   Hehner-Maly's 

method.     Of  course,  the   hydrochloric    acid   would  be    determined   at  the  same 

time  by  Leo's  method,  so   that   Hehner-Maly's   method  would  be  needed  only 

for  the  determination  of  the  organic  acids. 

This  method,  however,  gives  incorrect  results  in  respect  to  organic  acids  in 

case  these  include  the  higher  fatty  acids,  which  are  insoluble  in  water,  and  conse- 

N 
quently  not  completely  neutralized  by  the  addition  of  —  NaOH.     Should  it  be 

desired  to  estimate  these  higher  fatty  acids,  the  gastric  contents,  neutralized  by 

N 
means   of  the  —  NaOH,  must  be  well  shaken  with  a  generous  quantity  of  ether, 

and  any  acidity  arising  from  these  fatty  acids  neutralized  by  the  addition  of  an 

N 
alcoholic  —  NaOH.  This  neutralized  ethereal  solution  is  then  added  to  the  neu- 
tralized watery  solution  of  the  gastric  contents,  and  the  mixture  evaporated.  By 
proceeding  in  this  manner  we  are  certain  that  the  hydrochloric  acid,  as  well  as  all 
of  the  organic  acids,  has  been  neutralized  in  the  residue.  The  alkalinity  of  the 
ash  is  the  measure  of  the  previously  present  organic  acids.  By  means  of  this 
modification  the  Hehner-Maly  method  is  also  of  value  in  estimating  the  higher 
fatty  acids. 

If  it  is  desired  to  estimate  the  higher  fattj^  acids  by  means  of  this  procedure, 
the  unfiltered  gastric  contents  must  be  employed,  since  these  acids  (with  the  excep- 
tion of  butyric  acid),  on  account  of  their  insolubility,  are  simply  susjjended  in  the 
gastric  contents,  and  would  consequently  remain  upon  the  filter. 

Determination  of  the  Free  Hydrochloric  Acid  (Even  Free  from 
Proteids)  which  Gives  the  Color    Reactions   Previously   Mentioned 

— i.e.,  of  the  Excess  of  Acid  (p.  377). — Miutz's  method  of  titration 
is  the  best — that  of  adding  a  ,7,  NaOH  solution  to  the  gastric  juice  from 
a  buret  until  we  fail  to  get  the  usual  color  reaction  for  free  hydrochloric 
acid  (see  p.  372  et  seq.).  Phloroglucin-vanillin  is  the  most  highly 
recommended  of  the  reagents  by  Mintz.  It  requires  but  a  few  drops 
of  the  gastric  contents,  it  is  not  influenced  by  any  organic  acid,  and  the 
final  reaction  is  sharply  defined.  A  still  more  convenient  method  than 
that  described  upon  p.  373  is  to  add  25  to  30  drops  of  phloroglucin- 
vanillin  to  the  10  c.  c.  of  gastric  contents  before  titrating,  for  then,  by 
heating  the  end  of  a  glass  rod  moistened  in  the  contents,  we  can  observe 
the  reaction  directly.  Of  course,  the  glass  rod  should  be  cooled  and 
washed  carefully  each  time. 


384    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

Another  reaction,  the  addition  of  methyl-violet  to  normal  gastric  con- 
tents, and  then  ^^  NaOH  solution  until  the  blue  color  produced  changes 
again  to  violet,  has  not  given  the  author  any  satisfactory  results,  because 
it  is  so  difficult  to  recognize  the  final  reaction.  But  the  end-reaction 
may  be  very  well  recognized  with  Congo  paper,  adding  the  ^  NaOH 
solution  until  the  Congo  paper  is  no  longer  colored  blue.  Rugil  recom- 
mends this  method.  The  Tiipfel  method  is  still  more  convenient,  car- 
rying the  fluid  in  a  platinum  loop  to  the  Congo  paper.  We  must,  how- 
ever, remember  that  the  titration  with  the  phloroglucin  reaction  will 
not  necessarily  give  the  same  results  as  with  Congo-red,  on  account  of 
the  degrees  of  delicacy  of  the  indicators,  and  also  on  account  of  the 
sensitiveness  of  Congo-red  to  organic  acids. 

Determination  of  the  Hydrochloric  Acid  Deficit  in  a  Gastric 
Contents  which  Does  Not  Give  a  Reaction  for  Free  Hydrochloric 
Acid. — By  hydrochloric  acid  deficit  we  mean  the  amount  of  HCl  which 
must  be  added  to  a  definite  volume  of  the  stomach  contents  in  order 
to  bring  out  the  color  reactions  for  free  hydrochloric  acid.  This  figure 
varies,  of  course,  on  the  one  hand,  with  the  amount  of  proteids  and 
peptones  present,  and  perhaps  with  the  aliialine  components  of  the  secre- 
tion, all  of  which  combine  with  the  acid ;  and,  on  the  other  hand,  with 
the  amount  of  hydrochloric  acid  already  attached  to  the  proteids.  We 
might  therefore  call  it  a  deficit  in  HCl  saturation.  To  determine  this 
deficit  we  add  a  i^  HCl  solution  from  a  buret  to  10  c.c.  of  stomach  con- 
tents until  the  reaction  for  free  hydrochloric  acid  is  obtained  in  the 
mixture ;  this  reaction  is  indicated  most  accurately  by  phloroglucin- 
vanillin  or  Congro-red. 

[The  Topfer  method  for  the  estimation  of  the  total  acidity  of  the 
gastric  contents,  consisting  of  free  and  combined  acid,  has  found  wide 
use  in  the  chemical  laboratories  in  the  country.  The  results  obtained 
by  it  are  sufficiently  accurate  for  the  purposes  of  diagnosis,  for  which 
they  are  employed. 

The  basis  of  the  method  is  as  follows  : 

The  total  acidity  is  estimated  by  means  of  phenolphthalein  ;  the  indi- 
cator reacts  acid  to  free  and  combined  acid  and  acid  salts,  and  can, 
therefore,  be  used  for  this  purpose. 

The  combined  acidity  is  determined  by  subtracting  the  acidity  as 
found  by  alizarin  8  from  the  total  acidity.  This  value  corresponds  to 
the  acid  combined  with  proteids,  since  alizarin  S  reacts  acid  to  all  acid 
compounds  except  the  acid  proteid  combinations. 

The  free  acidity  is  found  by  titration,  using  dimethylamidoazobenzol. 
This  indicator  is  only  sensitive  toward  free  acids. 

The  following  solutions  are  necessary  for  the  performance  of  the 
method  : 

1.  A  0.5  per  cent,  alcoholic  solution  of  dimethylamidoazobenzol. 

2.  A  1  per  cent,  aqueous  solution  of  alizarin  S. 

3.  A  1  per  cent,  alcoholic  solution  of  phenolphthalein. 

4.  A  I  NaOH  solution. 

The  details  of  the  method  follow  : 


EXAMINING   THE  STOMACH  WITH  AID   OF  STOMACH  TUBE.   385 

The  total  acidity  is  found  by  titrating  5  or  10  c.c.  of  the  gastric 
contents  with  the  j^  NaOH  solution  after  the  addition  of  3  drops  of 
phenolphthalein.  The  titration  is  continued  until  the  pink  color,  which 
becomes  permanent  near  the  end  of  the  reaction,  can  no  longer  be  deep- 
ened by  the  further  addition  of  a  drop  of  the  ^  NaOH  solution.  The 
number  of  cubic  centimeters  required  for  the  end-reaction  corresponds 
to  the  total  acidity. 

The  combined  acidity  is  determined  by  adding  3  drops  of  the  aliz- 
arin solution  to  5  to  10  c.c.  of  the  gastric  contents  and  titrating  witii  the 
NaOH  solution.  The  color  of  the  solution,  when  the  end-reaction  is 
reached,  is  a  pure  violet.  The  red  color  which  appears  after  the  yellow 
of  the  indicator  has  disappeared  must  be  completely  removed,  and  the 
€olor  must  be  a  decided  violet. 

The  difference  between  the  number  of  cubic  centimeters  found  in  this 
titration  and  that  of  the  total  acidity  equals  the  combined  acidity  of  the 
gastric  contents. 

The  free  acid  is  estimated  by  taking  5  to  10  c.c.  of  the  gastric  con- 
tents, adding  4  drops  of  dimethylamidoazobenzol,  and  titrating  with 
the  j^  NaOH.  The  titration  is  continued  until  the  pink  has  disappeared 
and  the  color  has  become  greenish  yellow.  This  number  of  cubic 
centimeters  is  equivalent  to  the  free  acidity. 

The  value  of  these  various  acid  factors  can  bo  expressed  in  many 
ways.  If  it  is  required  that  they  be  in  terms  of  HCl,  then  it  is  simply 
necessary  to  multiply  the  number  of  cubic  centimeters  found  in  the  titra- 
tion by  0.00365.  The  product  will  equal  the  number  of  grams  of 
HCl  in  the  volume  of  gastric  contents  employed  for  the  titration.  If 
percentage  is  required,  the  above  product  must,  of  course,  be  further 
multiplied  by  the  fraction  ^^,  where  x  =  the  cubic  centimeters  employed 
in  the  titration. 

As  Prof.  Sahli  has  suggested,  it  is  more  usual  to  express  these  values 
in  terms  of  the  number  of  cubic  centimeters  of  the  j^  NaOH  which  are 
required  to  complete  the  respective  end-reactions  for  100  c.c.  of  gastric 
contents.  If  10  c.c.  of  the  stomach  contents  are  used,  the  number  of 
cubic  centimeters  used  up  in  titration  is  multiplied  by  10,  etc. 

In  cases  where  only  small  volumes  of  gastric  contents  stand  at 
the  disposal  of  the  investigator,  Einhorn's  modification  may  be  found 
to  be  very  useful.  It  consists  in  the  performance  of  the  dimethyl- 
amidoazobenzol and  phenolphthalein  reaction  upon  the  same  portion  of 
contents. 

Ten  cubic  centimeters  are  measured  ofF,  and  to  these  are  added  3 
drops  of  phenolphthalein  and  4  drops  of  the  dimethylamidoazobenzol. 
Since  the  former  is  colorless  in  acid  solution,  the  color  of  the  mixture 
is  entirely  dependent  upon  the  latter  indicator,  and  the  titration  may  be 
carried  on  with  the  f„  NaOH  in  the  same  manner  as  in  the  determination 
of  free  acid — i.  e.,  to  the  appearance  of  the  greenisli-yellow  color.  The 
reading  is  then  made  upon  the  buret,  and  the  ^^  NaOH  soUition  further 
added  until  the  pink  color  appears  and  allows  of  no  furtlier  deepen- 
ing   upon  the  addition  of  another   drop  of  the  alkali.     This  second 

26 


386    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

reading  will  correspond  to  the  total  acidity,  and  the  first  reading  to  the 
free  acidity,  when  both  readings  are  made  from  the  original  position 
of  the  fluid  in  the  buret, — H.  C.  J.] 

Determination  of  the  Clilorids  of  the  Gastric  Contents. — O.  Reiss- 
ner  ^  has  recently  pointed  out  that  the  estimation  of  the  combined  chlorin 
or  of  the  neutral  chlorids  has  a  certain  diagnostic  significance  in  the 
recognition  of  gastric  carcinoma.  He  has  found  a  greater  increase  in 
the  chlorids  in  this  disease  than  in  other  affections  of  the  stomach,  a 
fact  which  is  the  more  striking  since  the  secretion  of  hydrochloric  acid 
is  usually  greatly  diminished  in  gastric  cancer  (see  p.  390).  Eeissner 
believes  this  to  be  due  to  the  neutralization  of  the  hydrochloric  acid, 
provided  such  be  secreted  at  all,  by  the  alkaline  juice  of  the  carcinoma, 
and  to  the  chlorids  contained  in  this  cancerous  secretion.  If  it  is 
desired  to  estimate  the  chlorids  in  this  connection,  the  directions  will  be 
found  in  the  description  of  the  method  of  Liitke-Martius  (p.  380).  In 
carrying  out  this  procedure  the  modification  of  Reissner  must  be 
employed  (see  p.  382).  By  this  method  Reissner  found  that  in  other 
gastric  diseases  100  c.c.  of  gastric  contents  corresponded  to  a  chlorid 
value  of  24  to  40  c.c.  of  ^  silver  solution  ;  while  in  carcinoma  the 
chlorids  in  the  same  quantity  of  gastric  contents  required  50  to  70  c.c. 
of  f^  silver  solution.  It  has  not  been  determined  whether  gastric  ulcer 
resembles  carcinoma  in  this  respect. 

Quantitative  Determination  of  the  Total  Organic  Acids 
of  the  Gastric  Contents. — The  amount  of  total  organic  acids  may 
be  calculated  after  an  Ewald  test  breakfast  by  subtracting  the  hydro- 
chloric acidity,  as  found  by  Liitke-Martius'  method,  from  the  total 
acidity,  allowing,  of  course,  that  the  acid  salts  do  not  play  much  of  a 
part  in  the  acidity.  Martins  considers  that  normally  organic  acids  are 
absent  during  the  digestion  of  the  test  breakfast  in  the  stomach  (see  p. 
382  et  seg.)  ;  hence,  this  remainder  should  equal  nil. 

The  organic  acids  may  also  be  estimated  by  Hehner-Maly's  method 
(p.  382).     This  gives  the  acidity  due  to  the  organic  acids  directly. 

Quantitative  Bstimation  of  I^actic  Acid. — Strauss'  modifi- 
cation of  Uffelmann's  method  (p.  374)  is  practical  and  sufficiently 
accurate  for  the  quantitative  estimation  of  the  lactic  acid  in  the  gastric 
contents.  Boas^  employs  the  iodoform  reaction  (p.  376  d  seg.)  when 
a  more  accurate  estimation  is  required.  The  amount  of  iodin  required 
to  change  the  aldehyd  formed  from  the  lactic  acid  to  iodoform  is  deter- 
mined by  titration. 

If  there  is  required  a  more  accurate  quantitative  estimation  of  these 
acids  than  can  be  obtained  by  the  Strauss  modification  of  UfiPelmann's 
test,  the  Hehner-Maly  method  for  the  organic  acids  may  be  employed 
(p.  382) ;  for  other  organic  acids  have  the  same  diagnostic  significance 
as  lactic  acid,  and  are  quantitatively,  at  least,  subordinate. 

Practical  Utili^sation  and  Choice  of  the  Quantitative 
Methods  for  the  Determination  of  Acids. — At  first  sight 
the  most  accurate  methods    would    seem    absolutely  essential  for  cor- 

1  Zeits./.  klin.  Med.,  vol.  xliv.  ^  Deutsch.  med.  Woch.,  1893,  No.  34. 


EXAMINING  THE  STOMACH  WITH  AID   OF  STOMACH  TUBE.   387 

rect  gastric  diagnosis.  We  should,  then,  naturally  select  Ltitke- 
Martius'  or  Sjoqvist's  method  to  determine  the  total  HCl  secreted, 
Leo's  method  for  the  acid  phosphates,  Mintz's  for  the  excess  of 
acid — i.  e.,  the  acid  deficit  according  to  Mintz — and,  finally.  Boas' 
for  the  determination  of  the  lactic  acid.  But,  as  a  matter  of  fact, 
none  of  these  methods  is  absolutely  accurate ;  and  so  many  would 
make  gastric  examination  too  complicated  and  tedious  for  practical  use. 
Even  the  washing  out  of  the  stomach  after  all  the  test  breakfast 
capable  of  expression  has  been  removed,  and  the  including  of  this  wash 
water  in  the  tests,  will  not  furnish  absolutely  accurate  values  for  the 
secretory  powers  of  the  stomach.  For  the  rinsing  of  the  stomach,  as 
well  as  the  efforts  in  expressing  the  meal,  will  produce  new  and  incon- 
stant stimulants  to  secretion.  Besides,  before  the  test  breakfast  is 
removed  an  unknown  portion  of  the  acid  has  been  already  passed  on 
into  the  duodenum. 

Fortunately,  in  practice  it  is  much  more  simple.  The  acidity  due 
to  acid  phosphates  is  of  no  practical  importance  for  titration  if  we 
employ  Ewald's  test  breakfast  (compare  p.  388).  The  investigations 
of  Moritz  ^  and  Martins  show  that  the  acidity  is  almost  entirely  made 
up  of  the  organic  and  hydrochloric  acids. 

The  hydrochloric  acids  are  composed  of  hydrochloric  acid  combined 
with  the  proteids,  and  of  the  free  acid — reacting  to  Congo-red  and 
phloroglucin-vanillin.  A  few  examples  will  show  that  (if  these  facts 
are  considered)  even  a  simple  acidity  titration  of  the  gastric  contents 
furnishes  considerable  information  about  the  gastric  chemistry,  pro- 
.  vided  the  qualitative  tests  have  been  already  performed. 

Let  us  assume  a  case  where  the  tests  for  free  hydrochloric  acid  are 
negative.  The  acidity  is  found  to  be  quite  high — e.  g.,  reduced  to 
terms  of  HCl,  0.25  per  cent.  We  may  then  be  pretty  certain  that  most 
of  this  high  acidity  is  due  to  free  organic  acids,  and  that  the  hydro- 
chloric acid  secretion  is  slight.  If  the  lactic  acid  test  is  very  marked, 
if  the  odor  of  butyric  or  acetic  is  strong,  and  if  the  stomach  contents 
contain  an  abundance  of  bacteria,  this  assumption  is  practically  proved. 
Conversely,  if  the  hydrochloric  acid  reaction  is  very  pronounced,  the 
lactic  acid  reaction  very  faint  or  absent,  and  the  acidity  very  high,  in 
all  probability  there  is  an  abnormal  or  excessive  secretion  of  free  HCl. 
If  the  acidity  is  relatively  low  and  the  hydrochloric  acid  reaction  posi- 
tive, the  probability  is  still  greater  that  the  acidity  depends  largely  upon 
free  hydrochloric  acid.  The  titration  for  the  total  acidity  is  valuable, 
quite  independent  of  the  tests  for  free  hydrochloric  acid,  for  it  indientes 
the  maximum  limit  of  HCl  which  is  possible.  For  example  :  If  the 
acidity  is  found  to  be  0.08  per  cent,  (calculated  as  HCl)  we  are  sure 
that  the  amount  of  free  hydrochloric  acid  is  not  more  than  0.08  per  cent,, 
anyway  ;  which  means  that  it  is  considerably  diminished. 

The  excess  or  deficit  of  acid  (see  p.  383  et  seq.)  is  easily  estimated 
and  gives  us  an  important  insight  into  the  gastric  chemistry.  Some 
authors,  as  is  well  known,  consider  that  in  the  determination  of  hydro- 
'  Deutsch.  Arch./,  klin.  Med.,  1889,  vol.  xliv.,  p.  279. 


388    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

chloric  acid  the  free  hydrochloric  acid  is  the  important  part  to 
be  estimated,  because  in  artificial  digestion  that  is  the  only  part  which 
is  effective.  But  other  authors,  on  the  contrary,  consider  that  the  free 
HCl  can  be  neglected,  as  being,  so  to  speak,  useless,  wliile  the  hydro- 
chloric acid  which  is  combined  with  the  proteids  is  the  important  part, 
because  it  is  accomplishing  digestion  in  the  stomach.  Both  are  prob- 
ably correct  in  a  measure.  The  combined  acid  is  doing  the  work,  but 
the  presence  of  a  moderate  excess  is  a  favorable  sign.  It  shows  that 
there  is  enough  to  saturate  the  proteids  and  still  leave  more  ready  for 
anything  else  to  be  digested.  The  excess  also  aids  in  the  antiseptic 
function  of  the  stomach.  But  at  the  same  time  the  hydrochloric  acid 
deficit  cannot  be  considered  to  measure  an  actual  deficiency  for  the 
organism. 

A  comparison  of  the  total  acidity,  as  indicating  the  degree  of  acid 
secretion,  with  the  excess  of  acid  or  acid  deficit  will  aid  in  determining  the 
condition  of  the  other  gastric  functions,  especially  the  motility  and  the 
power  of  absorption.  For  example  :  If  the  total  acidity  is  high,  and 
we  suppose  that  this  is  mainly  due  to  hydrochloric  acid  secreted,  and  if 
further  examination  reveals  no  excess  or  only  a  slight  excess  of  hydro- 
chloric acid,  or  perhaps  even  an  acid  deficit,  the  high  acidity  can  be 
due  only  to  a  deficient  motility  and  absorption,  so  that  much  of  the 
proteids  remained  in  the  stomach.  A  low  total  acidity  with  an  excess 
of  hydrochloric  acid  proves,  on  the  contrary,  that  the  motility  and  the 
absorbing  power  of  the  stomach  are  excellent. 

If  a  qualitative  examination  of  the  gastric  juice  shows  that  lactic 
acid  is  present,  it  may  be  quantitatively  determined  by  Strauss'  method 
(p.  375),  the  result  deducted  from  the  total  acidity,  and  the  remainder 
of  the  acidity  calculated  as  above.  Generally  speaking,  when  much 
lactic  acid  is  present  we  find  low  HCl  values  and  only  combined  HCl- 
i.  e.,  diminished  secretion  and  diminished  motility. 

PHYSIOLOGIC   RELATIONSHIP   OF  THE  ACIDS  OF  THE  GASTRIC  JUICE. 

Under  physiologic  conditions,  one  hour  after  Ewald's  test  breakfast 
we  find  that  the  total  acidity  of  the  gastric  juice  varies  between  0.15 
and  0.2  per  cent,  (calculated  in  terms  of  HCl).  The  hydrochloric  acid 
tests  with  methyl-violet,  tropaeolin,  and  phloroglucin-vanillin  all  react 
positively ;  the  lactic  acid  test  is  negative.  In  healthy  individuals, 
Martius  has  shown  that  these  values  for  the  total  acidity  during  the 
whole  of  the  digestion  correspond  fairly  accurately  to  the  amount  of 
hydrochloric  acid  secreted  (estimated  by  Liitke-Martius'  method). 
This  proves  that  the  organic  acids  are  absent,  and,  at  the  same  time, 
that  the  acid  phosphates  influence  the  total  acidity  but  very  little.  The 
occurrence  of  organic  acids  in  the  stomach  during  the  digestion  of  an 
Ewald  test  breakfast  is  pathologic  if  we  disregard  the  very  slight 
amount  of  lactic  acid  which  the  test  breakfast  itself  contains.  As  a 
matter  of  fact,  the  antifermentation  action  of  the  hydrochloric  acid 
inhibits  the  formation  of  these  organic  acids.     Miller  claims  that  lactic 


EXAMINISG  THE  STOMACH   WITH  AID   OF  STOMACH  TUBE.  389 

acid  fermentation  will  cease  if  the  amount  of  hydrochloric  acid  con- 
tained in  the  mixture  amounts  to  0.16  per  cent.,  and  Cohn  puts  it  even 
as  low  as  0.07  per  cent.  Schiile^  has  contributed  valuable  facts  in 
regard  to  the  normal  course  of  the  acidity  of  the  gastric  juice  and 
its  individual  components  with  different  diets.  He  pictures  the  follow- 
ing curves  (Fig.  145)  to  show  the  relations  of  the  acidities  after  the 
ingestion  of  an  Ewald  test  breakfast. 


0^9 
0,25 
0,22 
0,18 

0,1 

0,07 

0,03 

0 


^ 

- 

V 

/ 

/ 

-^ 

\^ 

V 

/. 

/ 

N 

k\ 

/ 

'A 

[^ 

tj 

// 

— ._. 

.-^•■^ 

Na 

/// 

/ 

ta 

^ 

V 

Total  acidity. 


Free  HCl. 


Combined  acids. 


# 


Last  lavage.  Stomach  empty. 


Last  expression  (with  chemical 
investigation). 

15  30  ^45  60  75  90  95  MinuteS. 

Fig.  145.— Course  of  the  acidity  of  the  gastric  juice  after  a  test  breakfast  of  300  gm.  of  tea  and 
50  gm.  of  milk-bread  (after  A.  SchtileJ. 

We  quote  his  observations  upon  healthy  persons  in  the  following : 
"  1.  The  values  of  the  free  as  well  as  of  the  combined  HCl  and  of  the  total 
acidity  often  differ  considerably  in  the  same  individual,  and  in  different  people, 
too,  without  any  demonstrable  cause.  2.  The  maximum  of  free  HCl  varies  be- 
tween 0.05  to  0.07  and  0.2  percent.;  the  combined  acids,  between  0.012  and 
0. 11  per  cent.  The  maximum  of  the  total  acidity  lies,  in  round  figures,  between 
30  (0.11  per  cent.  HCl)  and  70  (0.26  per  cent.  HCl)  at  the  height  of  digestion. 
3.  The  height  of  digestion  occurs  sixty  minutes  after  an  Ewald  test  breakfast, 
varying  in  incUvidual  ca.ses  from  forty-five  to  seventy-five  minutes.  4.  The  upper 
limits  of  these  figures  must  be  regarded  as  pathologic  for  many  individuals  with 
sensitive  gastric  mucous  membranes." 

Diagnostic  Notes  upon  Acid  Contents  of  the  Gastric  Juice. 

So  long  a.s  we  do  not  attempt  to  draw  conclusions  in  regard  to  the  volume  of 
the  secretion  from  the  percentage  of  acidity  (see  p.  397),  experience  teaches  as 
follows: 

(a)  Normal  hydrochloric  acid  secretion  is  present : 

(1)  Very  often  in  gastric  ulcers,  and  in  the  pyloric  stenosis  due  to  a  healed 

gastric  ulcer. 

(2)  In  some  of  the  gastric  neuroses. 

(3)  In  simple  atony  of  the  stomach. 

(J)  The  hydrochloric  acid  secretion  is  found  to  be  increased  •} 
(1)  In  the  majority  of  the  cases  of  gastric  ulcers. 

^  Zeits.f.  klin.  Med.,  1895,  vol.  xxviii. 

'  If  the  free  hydrochloric  acid  after  an  Ewald's  test  breakfast  exceeds  0.2  per  cent, 
or  if  the  total  acidity  amounts  to  more  than  about  70  (0.26  per  cent.  HCl),  we  may  speak 
of  it  as  an  increased  secretion.  Pathologically,  total  acidity  as  high  as  0.8  per  cent,  has 
been  observed,  due  chiefly  to  HCl,  but  values  over  0.35  per  cent,  are  rare. 


390    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

(2)  In  passive  congestion  of  the   stomach.   (Schreiber)  with   maintained 

secretion  of  acid. 

(3)  In  diseases  of  continual  hypersecretion^  where  the  secretion  continues 

to  be  excessive  after  the  removal  of  the  meal. 
The  most  important  diflFerential  diagnostic  sign  between  true  continued  hyper- 
secretion (gastrorrhoea  acida)  and  Schreiber's  so-called  "stagnant  stomach" 
(where  prolonged  secretion  of  the  gastric  juice  occurs,  due  to  motor  insufficiency 
with  or  without  stenosis  of  the  jDylorus)  is  the  condition  of  the  fasting  stomach  in 
the  morning,  after  it  has  been  completely  emptied  the  evening  before.  If  it,  then, 
the  next  morning  contains  fluid  rich  in  hydi'ochloric  acid,  the  condition  is  one  of 
true  hypersecretion. 

(4)  In  simple  hyperacidity  and  hypersecretion  where  (in  contrast  to  (3))  the 

increased  hydrochloric  acid  production  occurs  only  during  digestion.  ^ 

(5)  In  temporary  hypersecretion  (gastroxynsis).  This  occurs  in  nervous 
individuals,  as  a  result  of  severe  mental  exertion,  associated  with  migraine,  acid 
vomiting,  and  all  sorts  of  nervous  disturbances. 

(6)  In  the  early  stages  of  chronic  gastric  catarrh. 

(7)  In  some  types  of  mental  disorders. 

(c)  Diminished  secretion  of  hydrochloric  acid  occurs : 

(1)  In  anemic  conditions,  especially  in  the  severe  forms. 

(2)  In  most  cases  of  chronic  gastric  catarrh. 

(3)  In  some  disorders  of  the  stomach  developing  in  the  course  of  general 

neuroses  (neurasthenia^). 

(4)  In  some  types  of  mental  disorders. 

(5)  In  continued  icterus. 

(6)  In  some  chronic  cachexias — e.  g.,  tuberculosis  of  the  lung  (not  con- 

stant). 

(7)  Sometimes  in  diseases  with  congestion  (heart  disease,  emphysema). 

(8)  At  times  in  chronic  nephritis. 

(9)  After  prolonged  use  of  alkalies  and  saline  purgatives. 

(10)  In  chlorin  hunger. 

{d)  Free  hydrochloric  acid^  is  absent  in  those  conditions  which  are  mentioned 
under  (c)  when  the  disorder  is  very  pronounced,  and,  besides  this,  more  or  less 
typically: 

(1)  In  severe  febrile,  especially  infectious,  diseases. 

(2)  In  carcinoma  of  the  stomach. 

(3)  In  atrophic  gastric  catarrh. 

(4)  In  pernicious  anemia. 

In  reality  numerous  deviations  are  observed  in  all  of  the  conditions  which  are 
grouped  in  the  above  scheme. 

We  are  justified  in  attaching  great  weight  to  the  absence  of  free  hydrochloric 
acid — i.  e.,  to  a  negative  result  in  the  color  tests — for  the  diagnosis  of  gastric  car- 
cinoma, especially  if  this  HCl  absence  can  be  noted  regularly  before  any  tumor  can 
be  felt.  Nevertheless  the  presence  of  free  HCl  does  not  necessarily  exclude  the 
diagnosis  of  a  carcinoma.  One  case  was  especially  instructive  to  the  author  in 
this  respect.  For  months  he  found  a  normal  amount  of  hydrochloric  acid  after  a 
test  breakfast,  although  the  patient  presented  a  carcinomatous  stenosis  of  the 
pylorus  with  marked  nocturnal  retention  of  food.      In  the   retained  material  he 

^  See  p.  368  for  the  amount  of  secretion  occurring  in  the  fasting  stomach  of  healthy 
individuals. 

^  There  is  really  no  sharp  boundary  line  between  these  two  conditions.  If  merely 
the  percentage  of  acid  contained  is  too  high,  we  call  it  hyperacidity ;  but  if,_  besides  this, 
the  volume  of  the  gastric  juice  is  also  increased,  we  call  it  also  hypei-secretion.  Hyper- 
acidity and  hypersecretion  may  occur  independently,  or  they  may  result  from  a  motor 
insufficiency  (stagnation). 

*  The  more  exact  quantitative  methods  for  testing  the  total  and  the  combined  hydro- 
chloric acid — e.  <;.,  Liitke-Martius'— would  still  generally  show  that  a  slight  amount  of 
hydrochloric  acid  was  secreted.  Yet  the  secretion  may  even  be  completely  suppressed 
and  the  gastric  juice  then  give  a  neutral  or  weakly  alkahne  reaction. 


EXAMINING   THE  STOMACH  WITH  AID   OF  STOMACH  TUBE.  391 

found  a  very  greatly  increased  amount  of  hydrochloric  acid  (up  to  0.4 percent.). 
Moreover,  other  disturbances  cited  in  groups  c  and  d  are  frequently  accompanied  by 
a  complete  absence  of  the  color  reaction  for  free  HCl,  so  that  an  absence  of  free 
HCl  can  hardly  be  claimed  as  distinctive  of  gastric  carcinoma. 

(e)  A  considerable  amount  of  organic  acids,  especially  of  lactic  acid,  occurs 
only  when  hydrochloric  acid  is  absent  and  when,  at  the  same  time,  motor  insuffi- 
ciency exists,  especially  when  the  latter  depends  upon  some  stenosis  of  the  pylorus. 
This  is  the  reason  that  a  considerable  amount  of  lactic  acid  in  the  gastric  contents 
strongly  suggests  a  carcinoma. 

Testing  of  the    Digestive  Power  of  the    Gastric  Juice;    Examination    for    Pepsin, 

The  digestive  power  of  the  filtered  stomach  contents  from  the 
expressed  test  breakfast  depends,  on  the  one  hand,  upon  the  amount  of 
pepsin  contained,  and,  on  the  other  hand,  upon  the  amount  of  free  acid 
contained,  especially  free  hydrochloric  acid.  Artificial  digestion  is  the 
only  means  at  our  command  to  test  the  amount  of  pepsin.  This 
furnishes  also  indirect  evidence  of  the  amount  of  acid  contained  in  the 
gastric  juice. 

For  artificial  digestion  we  usually  employ  fibrin  stained  with  carmin 
(Griitzner),  or  disks  of  coagulated  egg  albumin. 

The  fibrin  is  best  prepared  by  beating  freshly  drawn  ox  blood.  The  stringy 
■coagula  are  washed  in  running  water  until  decolorized,  and  then  cut  into  small 
pieces  of  uniform  size,  which  are  then  placed  in  alcohol  for  several  days.  They 
&re  then  transferred  for  one  to  two  days  into  a  neutral  concentrated  solution  of 
■carmin  and  kept  cool  until  they  are  thoroughly  stained,  washed  in  water  until  the 
wash  water  is  no  longer  colored,  well  squeezed,  and  then  preserved  in  carmin  con- 
taining glycerin.  Before  being  used  they  should  be  washed  in  water  until  they  do 
not  give  off  any  colored  glycerin. 

The  egg-albumin  disks  are  prepared  by  boiling  an  egg  hard,^  and  then  with  a 
■cork  borer  punching  out  the  white  cylinders  of  about  5  mm.  diameter. 

For  the  digestive  test  a  few  bits  of  fibrin  or  some  egg-albumin  disks 
are  put  into  a  test  tube  with  a  measured  quantity  of  the  gastric  con- 
tents and  the  tube  then  set  in  an  incubator.  The  digestion  of  the 
fibrin  releases  the  carmin  and  becomes  evident  from  the  red  color  of  the 
fluid.  The  digestion  of  the  egg  albumin  always  progresses  much  more 
slowly.  It  shows  itself  first  in  the  rounding  of  the  edges  of  the  disk, 
followed  gradually  by  complete  solution. 

The  following  methods  are  to  be  recommended  for  a  more  accurate 
quantitative  examination  : 

Hammersclilag's  ^  Method  for  Estimating  Pepsin. — Ten  c.c.  of  an  approxi- 
mately 1  per  cent,  filtered  solution  of  egg  albumin^  in  0.4  per  cent.  HCl  are 
poured  into  two  tubes.  To  one  5  c.c.  of  gastric  contents  are  added,  and  to  the 
other  5  c.c.  of  distilled  water.  They  are  both  set  in  the  incubator.  An  hour 
later  the  albumin  in  both  tubes  is  estimated  volumetrically  according  to  Esbach's 
method  (p.  505  et  seq.).     The  difference  between  the  precipitate  of  albumin  in  the 

^  The  egg  should  be  boiled  only  long  enough  to  coagulate  completely  the  egg  albu- 
min, otherwise  it  becomes  too  difficult  to  digest.  The  necessary  boiling-period  must  be 
found  experimentally.  These  cylinders  are  sectioned  with  a  razor  into  small  disks  of 
1  mm.  thickness,  preserved  in  glycerin,  and  also  washed  off  before  using. 

^  Internal,  klin.  Unndsehau,  vol.  viii..  No.  39,  1895. 

^  Fresh  egg  albumin  contains  about  13  per  cent,  of  dry  proteid,  and  should  therefore 
bediluted  about  13  times  in  order  to  make  approximately  a  1  per  cent,  solution  of  egg 
albumin. 


392    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

two  tubes  is  equal  to  the  amount  of  albumin  which  has  been  digested,  and  forms, 
therefore,  a  measure  of  the  peptic  activity  of  the  gastric  juice.  The  square  root 
of  the  amount  of  pepsin  is  proportional  to  the  quantity  of  albumin  dissolved,  ac- 
cording to  Schiitz,'  Borrissow,^  and  Linossier.^  The  objections  to  this  method  are 
that  the  Esbach  test  is  not  very  accurate  and  that  the  albumoses  are  also  partly  pre- 
cipitated. The  error  in  regard  to  the  precipitation  of  the  albumoses  is  negligible, 
since  they  come  down  so  finely  divided  and  settle  with  so  much  difficulty  that 
practically  they  do  not  influence  the  amount  of  the  sediment  to  any  appreciable 
extent.  The  method  is  sufficiently  accurate  for  practical  utility  in  judging  of  the 
quantity  of  pepsin  in  the  stomach  contents.  It  would  be  better,  however,  to 
employ  a  diluted  gastric  juice,  for  the  reasons  given  in  the  description  of  Mett's 
method. 

Mett's  *  Method  of  Pepsin  Determination. — Glass  capillary  tubes,  from  1 
to  2  mm.  in  diameter  and  20  to  30  cm.  in  length,  are  filled  by  suction  with  the 
fluid  portion  of  fresh  egg  albumin.  In  order  to  avoid  accidental  variations  in  the 
egg  albumin,  the  whites  of  several  eggs  should  be  mixed,  and  the  fluid  portion  of 
the  mixture  employed.  These  filled  capillary  tubes  are  closed  with  bread  crumbs- 
and  placed  horizontally  in  a  boiling  water  bath,  in  order  to  coagulate  the  albumin 
quickly.  At  the  end  of  five  minutes  they  are  withdrawn,  wiped  off",  and  their 
ends  plunged  into  melted  paraffin,  in  order  to  prevent  drying.  A  number  of  these 
capillary  tubes  may  be  prepared  and  kept  in  stock  ;  but  before  they  are  employed 
it  should  be  noted  that  the  cylinders  of  albumin  are  still  in  contact  with  the  walls 
of  the  tube  and  have  not  dried  out  and  contracted,  in  which  case  they  are  unfit 
for  use.  At  first  the  capillary  tubes  contain  countless  bubbles,  which,  however, 
gradually  disappear,  and  in  two  days  they  are  ready  for  use.  They  are  then  cut 
into  lengths  of  about  2  cm.  with  glass  scissors,  and  2  of  them  are  placed  in  a. 
little  dish  with  5  c.c.  of  the  acidulated  gastric  contents,  the  pepsin  value  of 
which  is  to  be  determined.  The  manner  in  which  the  digesting  mixture  is  to  be 
prepared  from  the  gastric  contents  will  be  subsequently  stated.  Digestion  is  now 
allowed  to  proceed  in  the  incubator  ;  it  is  manifested  by  the  fact  that  the  albumin 
gradually  disappears  from  the  ends  of  the  tubes,  the  disappearance  gradually, 
becoming  more  rapid. 

According  to  Nirenstein  and  Schiflf,^  the  length  of  the  cylinder  of  albumin 
digested  by  any  gastric  juice  is  proportional  to  the  duration  of  digestion  and  inde- 
pendent of  the  diameter  of  the  capillary  tube,  provided  that  the  length  of  the 
digested  cylinder  does  not  exceed  7  mm.  within  the  time  of  observation.  If  the 
digested  cylinder  exceeds  7  mm.,  however,  the  length  is  not  proportional  to 
the  time,  since  the  digestion  beyond  this  point  seems  to  proceed  more  slowly  as- 
a  result  of  the  difficulty  of  the  diffusion  of  the  digested  products  into  the  surround- 
ing fluid.  To  obtain  a  correct  quantitative  estimate  of  the  amount  of  pepsin 
in  the  gastric  contents  we  must  consequently  keep  within  this  limit,  which  may 
be  done  by  preparing  the  digesting  mixture  in  the  manner  to  be  presently  given, 
and  measuring  the  mass  of  albumin  dissolved  at  the  end  of  twenty-four  hours. 
This  may  be  roughly  estimated  macroscopically,  and  more  exactly  by  a  low-power 
microscope  provided  with  an  objective  micrometer.  If  two  capillary  tubes  are 
employed,  their  four  ends  furnish  four  digestion-lengths,  from  which  an  average 
may  be  obtained. 

For  solutions  of  pure  pepsin,  Schiitz  has  discovered  the  law  that  the  relative 
quantities  of  pepsin  in  digesting  mixtures  containing  the  same  quantity  of  hydro- 
chloric acid  are  proportional  to  the  squares  of  the  quantities  of  albumin  digested 
in  the  same  time.  Borissow  has  confirmed  this,  particularly  in  reference  to  this 
method  of  Mett,  so  that  in  this  connection  Schiitz' s  law  is,  that  the  square  of  the 
length  of  the  digested  cylinder  of  albumin  is  proportional  to  the  pepsin  concen- 
tration of  the  solution.     From  the  studies  of  Nirenstein  and  Schiff,  however,  this- 

^  Zeit.  f.  physiol.  Cheniie.,  1885. 

^  Quoted  by  Samoiloff,  Arch,  des  .sci.  biol,  St.  Petersburg,  vol.  ii.,  No.  5. 

^  Jour,  (le  phys.  et  de  path,  gen.,  vol.  i.,  No.  2,  1899. 

*  J.  A.  D.,  Petersburg,  1889,  from  Pawlow's  Laboi-atory. 

^  Arch.  f.  Verdauungskrankh.,  vol.  viii.,  part  6,  1903. 


EXAMINING   THE  STOMACH  WITH  AID   OF  STOMACH  TUBE.   393 

is  true  only  for  the  less  concentrated  pepsin  solutions.  If  the  quantity  of  pepsin 
in  the  digesting  fluid  is  so  large  that  more  than  3. 6  mm.  of  albumin  are  digested  in 
twenty-four  hours,  the  law  of  Schiitz  does  not  obtain  reliable  values  for  the  quan- 
tity of  pepsin  in  any  gastric  juice  by  Mett's  method  ;  then  it  must  be  diluted  so 
that  the  digestion  length  will  not  exceed  3. 6  mm.  in  twenty-four  hours.  We  have 
already  given  two  reasons  which  make  it  necessary  to  dilute  the  gastric  juice  in 
determining  the  amount  of  the  contained  pepsin.  A  third  and  far  more  import- 
ant reason  for  such  dilution,  to  which  the  author  referred  in  the  last  edition  of 
this  book,  and  which  has  recently  been  more  critically  fliscussed  by  Nirenstein 
and  Schiflf,  is  that  the  gastric  juice,  as  obtained  from  the  patient  by  filtering 
the  gastric  contents  after  a  test  breakfast,  always  contains  an  uncertain  quantity 
of  substances  which  inhibit  pepsin  digestion.  These  inhibiting  substances  are  the 
products  of  the  peptic  digestion  itself ;  Nirenstein  and  Schiflf  state  that  they  are 
particularly  the  dissolved  carbohydrates,  and  also  sodium  chlorid.  Gastric  juices 
with  diminished  amounts  of  hydrochloric  acid,  on  account  of  the  large  quantities 
of  carbohydrates  which  they  contain,  are  the  richest  in  such  inhibiting  substances. 
The  important  role  played  by  these  inhibiting  substances  is  shown  by  the  fact 
that,  if  Mett's  method  is  carried  out  with  different  slight  dilutions  of  the  same 
gastric  juice,  the  relative  pepsin  values,  as  obtained  by  applying  Schiitz' s  law  to 
the  digestion  lengths,  never  agree  with  the  relative  amounts  of  pepsin  as  calcu- 
lated from  the  dilution.  As  a  matter  of  fact,  it  will  be  found  that  if  the  gastric 
juice  be  diluted  to  two  or  three  times  its  volume,  a  higher  digestive  value  will 
frequently  be  obtained  than  if  the  undiluted  juice  be  employed.  This  is  evidently 
due  to  the  fact  that  in  such  a  dilution  the  diminished  amount  of  pepsin  is  more 
than  compensated  for  by  the  weakening  of  the  activity  of  these  inhibiting  sub- 
stances. The  presence  of  these  substances  consequently  gives  rise  to  conditions 
beyond  computation,  which  make  it  impossible  to  arrive  at  accurate  conclusions 
if  the  pepsin  value  is  calculated  from  the  pure  gastric  juice. 

It  is  apparent  that  the  way  to  avoid  this  difficulty  is  to  eliminate  this  inhib- 
itory action  by  diluting  the  gastric  juice.  In  the  last  edition  of  this  book,  having 
this  end  in  view,  the  author  recommended  a  tenfold  dilution  of  the  total  gastric 
juice  in  diluted  hydrochloric  acid.  Nirenstein  and  Schiff,  however,  have  shown 
that  it  is  better  to  carry  the  dilution  still  farther.     They  recommend  a  sixteen- 

N 
fold  dilution  with  —  hydrochloric  acid  (  =  0.18  per  cent.   HCl),  and  state  that 
^u 

Schiitz's  law  obtains  with  this  and  all  further  dilutions.     The  latter  requisite  is 

absolutely  necessary  if  we  wish  to  have  a  relative  expression  for  the  quantity  of 

pepsin  as  estimated  from  the  digestion  length.     This  marked  dilution  also  decreases 

the  amount  of  pepsin  in  the  mixture,  so  that  the  digestion  length  is  kept  within 

the  limits  of  Schiitz's  law  (3.6  mm.   in  twenty-four  hours).     The  author  must 

nevertheless  observe  that  this  is  not  always  the  case  with  a  very  active  gastric 

juice,  so  that  if  the  digestion  length  exceeds  3. 6  mm.  with  a  sixteenfold  dilution, 

it  becomes  necessary  to  repeat  the  pepsin  test  with  a  dilution  of  1  :  32. 

According  to  Nirenstein  and  Schiff,  the  method  of  Mett  will  consequently  be 

carried  out  in  the  following  manner  if  exact  quantitative  results  are  to  be  obtained  : 

N 
1  c.c.  of  the  filtered  gastric  contents  is  diluted  with  16  c.c.  of  —  HCl  (=  0. 18  per 

cent.  HCl).  Two  Mett's  tubes  are  then  laid  in  this  mixture,  which  is  placed  in 
the  incubator.  At  the  end  of  twenty-four  hours  the  digestion  lengths  are 
read  [and  the  mean  digestion  length  obtained].  The  square  of  this  digestion 
length  is  the  measure  for  the  relative  amount  of  pepsin  in  the  sixteenfold  diluted 
gastric  juice,  and  this  number,  multiplied  by  16,  gives  the  relative  amount  of 
pepsin  in  the  undiluted  gastric  juice.  In  those  cases  in  which  the  length  of  the 
digested  cylinder  of  albumin  exceeds  3.6  mm.  in  length,  in  spite  of  the  sixteen- 
fold dilution,  the  estimation  must  be  repeated  with  a  dilution  of  1  :  32.  By 
squaring  the  digestion  length  as  before,  and  multiplying  this  quantity  by  32,  the 
relative  amount  of  pepsin  in  the  undiluted  gastric  juice  will  be  obtained.  It  is 
clear  that  in  this  method  of  estimation  the  unit  of  the  relative  amount  of  pepsin  will 


394    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

be  that  quantity  of  pepsin  by  which  1  mm.  of  albumin  in  a  Mett's  tube  will  be  di- 
gested in  twenty-four  hours  with  an  acidity  of  0. 18  per  cent,  free  hydrochloric  acid. 
In  this  estimation  we  do  not  consider  the  absolute  quantity  of  the  pepsin,  but 
simply  the  degree  of  its  concentration,  for  the  result  of  Mett's  method  is  the  same 
whether  large  or  small  quantities  of  the  digesting  mixture  be  employed  ;  at  least 
for  quanties  above  the  16  c.c.  above  recommended.  By  employing  this  method 
Nirenstein  and  Schiff  have  found  striking  differences  between  individual  gastric 
secretions,  which  vary  between  0  and  256  pepsin  units.  The  pepsin  concentra- 
tion is  consequently  entirely  independent  of  the  amount  of  acid  in  the  gastric 
juice,  as  we  might  expect  from  the  fact  that  physiologists  have  demonstrated  a 
different  localization  for  the  formation  of  pepsin  and  hydrochloric  acid  in  the 
gastric  glands. 

It  is  usually  assumed  that  the  pepsin  secretion  is  of  less  diagnostic  sig- 
nificance than  that  of  hydrochloric  acid,  because  it  is  less  often  disturbed. 
In  view  of  the  Mett's  method  as  just  described,  however,  this  belief 
must  be  more  critically  tested,  since  it  may  be  due  to  the  fact  that  the 
earlier  methods  of  pepsin  estimation  were  faulty. 

Pepsin  and  pepsinogen  may  be  entirely  absent,  but  then  usually  only 
in  grave  stomach  disorders,  especially  in  atrophic  gastric  catarrh,  in 
carcinoma  of  the  stomach,  and  in  certain  types  of  pernicious  anemia. 
It  is  a  very  unfavorable  prognostic  sign,  so  far  as  the  possibility  of 
restoring  the  gastric  function  is  concerned. 

Examination  of  the  Gastric  Juice  for  Rennin   and  Rennin  Zymogen. 

Normal  gastric  juice  contains,  besides  hydrochloric  acid  and  pepsin,  rennin  fer- 
ment and  rennin  zymogen  as  additional  secretory  products  of  the  mucous  mem- 
brane. As  we  well  know,  rennin  possesses  the  property  of  coagulating  milk,  inde- 
pendently of  the  help  of  acid.^  Rennin  zymogen,  inactive  in  itself,  is  converted 
into  rennin  by  acids.  Rennin  is  rapidly  destroyed  by  alkalies,  but  the  zymogen  is 
much  more  resistant  to  them. 

To  demonstrate  rennin,  3  to  5  drops  of  gastric  juice  are  added  to  5  to  10  c.c. 
of  fresh  uncooked  neutral  or  amphoteric  milk,  and  the  mixture  is  placed  in  an 
incubator.  If  the  rennin  is  present  in  normal  amounts,  curdling  should  take 
place  in  from  ten  to  fifteen  minutes  (Leo).  In  this  process  the  slight  amount  of 
acid  added  in  the  gastric  juice  will  cause  no  precipitation.  If  the  curdling  takes 
place  very  slowly,  it  is  questionable  whether  it  is  due  to  the  action  of  the  rennin 
or  to  the  formation  of  lactic  acid,  and  so,  to  be  exact,  the  reaction  of  the  mixture 
is  taken  before  and  after  curdling  has  taken  place.  Rennin  action  is  sure  to  have 
occurred  only  when  curdling  occurs  without  any  change  in  the  reaction. 

In  the  absence  of  rennin  ferment.  Boas  claims  that  rennin  zymogen  may  be 
demonstrated  by  rendering  10  c.c.  of  the  gastric  juice  feebly  alkaline  by  the  addi- 
tion of  lime  water,  mixing  it  with  an  equal  volume  of  unboiled  milk,  and  placing 
the  mixture  in  an  incubator  ;  if  zymogen  be  present,  a  dense  coagulum  will  form 
within  eleven  to  fifteen  minutes.  The  utility  of  this  method  of  demonstrating 
rennin  zymogen  must  be  questioned,  since  Fuld  has  shown  that  zymogen  is  not 
converted  into  ferment  by  calcium  salts.  It  is  probable  that  in  Boas'  method 
there  is  simply  an  acceleration  of  a  weak  rennin  action  by  the  action  of  calcium 
salts. 

Boas  claims  that  an  approximately  quantitative  estimate  of  the  rennin  action 
can  be  made  by  determining  to  what  degree  the  gastric  juice  can  be  diluted  with- 

1  This  process,  in  which  insoluble  casein  is  formed  from  the  caseinogen  of  the  milk 
by  the  simultaneous  action  of  rennin  ferment  and  calcium  salts,  must  not  be  confounded 
with  the  precipitation  of  unchanged  caseinogen  by  acids  (the  curdling  of  milk  by  lactic 
acid  fermentation). 


EXAMINING   THE  STOMACH  WITH  AID   OF  STOMACH  TUBE.  395 

out  arresting  its  function.  The  gastric  juice  or  contents  is  first  almost  completely- 
neutralized  and  then  diluted.  A  certain  amount  is  added  to  an  equal  volume  of 
milk.  If  coagulation  can  still  be  demonstrated,  another  similar  specimen  is  pre- 
pared with  still  further  diluted  gastric  juice.  Normally  the  dilution  may  exceed 
1  :  100  ;  but  if  the  secretion  is  decidedly  insufficient,  the  limit  of  dilution  will  be 
reached  at  1:  5  or  1:  10.  The  action  of  rennin  and  that  of  pepsin  are  of  about 
equal  importance  in  the  study  of  the  gastric  contents.  Pepsin  and  rennin  forma- 
tion usually  run  a  parallel  course,  although,  according  to  Hammarsten,  rennin  is 
different  from  pepsin.  The  test  for  the  rennin,  however,  has  the  advantage  of  sim- 
plicity, and  it  can  be  performed  more  quickly  than  that  for  pepsin.  A  decided 
diminution  or  absence  of  rennin  secretion,  like  that  of  the  pepsin  secretion,  is  as- 
sociated only  with  very  grave  affections  of  the  gastric  mucous  membrane.  Boas 
considers  that  the  limit  to  which  the  gastric  juice  can  be  diluted  without  inhibit- 
ing the  rennin  action  is  of  important  diagnostic  and  prognostic  significance.  A 
complete  absence  of  both  rennin  and  its  zymogen  and  of  pepsin  is  found  in  car- 
cinoma of  the  stomach,  in  atrophic  gastric  catarrh,  and  in  certain  cases  of  perni- 
cious anemia. 

Examination  of  the  Mucoos  Secretion  of  the  Stomach. 

The  gastric  juice  always  contains  mucus  (mucin),  in  the  form  of  more  or  less 
tough  transparent  or  cloudy  fiakes.  If  the  conditions  are  normal,  these  mucous 
flakes  are  always  very  small.  They  are  easily  stirred  up  in  the  rinse  water.  Swal- 
lowed mucus  from  the  pharynx,  esophagus,  or  bronchi  is  generally  distinctive.  It 
usually  occurs  in  isolated  larger  lumps  and  contains  more  pus  corpuscles  than  the 
mucus  from  the  stomach.  If  it  is  foamy  or  pigmented  (lung  pigment),  and  if  it 
contains  no  food  particles,  which  are  so  often  intimately  mixed  with  stomach 
mucus,  the  distinction  is  usually  easy.  The  microscope  will  often  solve  the  origin 
of  the  mucous  constituents,  for  fi-equently  in  the  interior  of  the  mucous  flakes  a 
characteristic  type  of  epithelium  may  be  found — e.  g. ,  pigmented  lung  epithelium. 
True  stomach  mucus,  if  the  digestion  is  good,  contains  only  the  nuclei  of  large 
round  or  oblong  epithelium  cells  and  of  leukocytes,  because  the  cell  plasma  has 
been  destroyed  by  the  digestion.  If  the  digestion  is  impaired  we  can  often  see 
the  cells  of  the  stomach  epithelium  in  toto.  An  increase  in  the  amount  of  mucus 
with  an  abundance  of  the  polymorphous  nuclei  of  leukocytes  is  characteristic  of 
gastric  catarrh.  We  must  be  very  cautious  before  assuming  the  presence  of  an 
increased  mucous  production,  for  an  abundant  admixture  of  mucus  in  the  stomach 
contents  quite  as  frequently  depends  upon  a  diminished  solution  of  the  mucus 
in  consequence  of  a  diminished  production  of  HCl.  Besides,  we  must  remember 
that  the  mucus  swells  considerably  if  free  hydrochloric  acid  is  absent,  and  so  the 
amount  may  seem  increased.  For  this  reason  very  noticeable  amounts  of  mucus 
are  found  with  carcinoma  of  the  stomach.  We  may  finally  mention  that  a  quan- 
titative estimation  of  mucus,  which  is  so  frequently  advocated,  is  usually  impos- 
sible by  chemical  means.  The  mucus  cannot  be  precipitated  in  the  filtrate  of  a 
test  breakfast,  because  the  mucin  which  is  dissolved  in  a  gastric  juice  that  contains 
hydrochloric  acid,  or  that  which  is  even  partly  digested,  can  no  longer  be  precipi- 
tated by  acetic  acid.i 

The  view  that  mucus  is  not  digestible  has  been  changed  by  modern  inves- 
tigations. 

Examination  of  Gastric  Contents   for  the   Products  of  Proteid  Digestion. 

Although  it  would  seem  valuable  and  practical  to  obtain  some  insight 
into  the  digestive  functions  of  the  stomach  from  an  analysis  of  the 
chemical  changes  that  the  various  foods  undergo  during  digestion,  yet 
experience  has  proved  this  is  not  feasible.     The  processes  are  too  com- 

^  Compare  A.  Schmidt,  "Tiber  die  Schleimabsonderung  im  Magen,"  Deutseh.  Arch, 
f.  klin.  Med.,  1896,  vol.  Ivii.,  parts  1  and  2,  p.  65. 


396    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

plicated,  for  the  changes  from  proteids  to  albumoses  and  peptones  depend 
not  only  upon  chemical  reactions,  but  also  to  a  high  degree  upon  the 
power  of  absorption  and  of  motility  of  the  stomach.  Because  a  test 
meal  is  rich  in  albumoses,  for  instance,  we  cannot  conclude  that  the 
digestion  is  especially  good,  but  rather  the  contrary,  because  the  albu- 
moses formed  are  normally  either  quickly  absorbed  or  passed  on  into 
the  intestine.  An  abundance  of  proteid,  therefore,  or  an  increase  in 
the  amount  of  peptone  contained  in  the  stomach  contents,  would  indi- 
cate (generally  speaking)  disturbed  gastric  digestion.  But  any  such 
deductions  could  be  based  only  upon  an  accurate  quantitative  deter- 
mination of  the  proteids  of  the  stomach  contents,  and  as  yet  we  possess 
no  available  clinical  methods  for  such  a  deterniination.^ 

EXAMINATION    OF  THE    STOMACH    CONTENTS   FOR  GAS    FERMENTATION. 

The  fermentative  processes  which  take  place  in  the  stomach  when 
the  digestion  is  affected,  especially  if  there  is  also  a  motor  insufficiency, 
have  been  studied  recently,  partly  by  bacteriologic  examination  and 
partly  by  a  chemical  analysis  of  the  gases  which  develop  in  the  ferment- 
ing gastric  contents — i.  e.,  in  the  expressed  test  breakfast.  These  ex- 
aminations as  yet  have  been  productive  of  no  practical  results.  The 
existence  of  fermentation  can  be  demonstrated  by  placing  some  of  the 
gastric  contents  in  a  fermentation  tube  (like  the  one  used  for  estimating 
sugar  in  the  urine)  and  letting  it  stand  in  an  incubator  (Fig.  170). 
If  gas  is  forming  it  will  accumulate  above  the  fluid.  If  we  wish  to 
examine  it  more  closely,  we  can  collect  the  gas  formed  from  a  considerable 
amount  of  the  stomach  contents  in  a  larger  vessel  by  conducting  it 
through  a  tube  and  a  pneumatic  trough  into  an  inverted  glass  filled 
with  mercury.  The  gases  which  are  found  most  frequently  in  the  gas- 
tric contents  are  carbon  dioxid  and  marsh  gas,  CH4.  The  former  is 
easily  recognized  by  its  characteristic  of  clouding  baryta  water,  and  the 
marsh  gas,  by  the  peculiar  flame  with  which  it  burns. 

DIAGNOSTIC  IMPORTANCE  OF  THE  USE  OF  RIEGEL'S  TEST  MEAL. 

Concerning  the  value  of  Eiegel's  test  meal,  it  is  to  be  noted  that, 
since  from  a  motor  as  well  as  a  chemical  standpoint  it  makes  greater 
demands  upon  the  stomach  than  the  Ewald  test  breakfast,  it  at  the  same 
time  acts  as  a  greater  stimulus  to  digestion,  and  consequently  exhibits 
to  better  advantage  existent  anomalies.  It  can  easily  come  about  that 
a  stomach  whose  motility  appears  perfectly  normal,  as  indicated  by  the 
test  breakfast,  may,  when  tested  with  Riegel's  meal,  show  itself  decidedly 
insufficient  in  motility  by  not  having  completely  emptied  itself  for  hours 
afterward.  By  the  use  of  this  test  meal,  there  are  obtained  two  dia- 
metrically opposed  results  to  those  given  by  means  of  the  test  breakfast. 
For  example  :  a  chemical  insufficiency  of  the  stomach  (hyperacidity, 
lack  of  enzyme)  may  be  made  to  appear  more  plainly  by  the  use  of  the 
test  meal  than  by  the  breakfast ;  on  the  other  hand,  a  hyperacidity  or 
hypersecretion  that  has  escaped  notice  in  the  test  breakfast  may  become 

1  This  subject  is  treated  in  Neumei^ter's  Text-book  of  Physiologic  Chemistry. 


EXAMINING   THE  STOMACH  WITH  AID   OF  STOMACH  TUBE.  397 

manifest  by  the  strong  stimulation  of  secretion  by  the  Riegel  meal. 
From  these  facts  it  is  evident  that  in  stomach  affections  where  the  use 
of  the  test  breakfast  does  not  lead  to  a  clear  interpretation,  the  exam- 
ination is  to  be  repeated  by  means  of  Riegel's  test  meal. 

Concerning  the  most  advantageous  time  for  the  siphonage  of  the 
Riegel  meal,  compare  p.  368.  There  unfortunately  still  exist  too  few 
results  for  us  to  be  able  to  calculate  normal  figures  for  the  acid  and 
enzyme  contents  of  the  stomach  contents,  as  well  as  for  the  volume  of  the 
fluid  removed  by  siphonage,  at  various  times  after  administration.  As  a 
rule,  it  will  be  found  that  after  four  hours  the  percentage  acidity  of  the 
Riegel  test  meal  will  correspond  to  that  of  the  Ewald-Boas  test  break- 
fast after  one  hour,  and  that  after  seven  hours  a  normal  stomach  will 
have  easily  emptied  itself  of  the  Riegel  meal. 

PROOF  OF  THE  ABSORPTIVE  ACTIVITY  OF  THE  STOMACH   BY   MEANS    OF 
V.  MERING'S  TEST  BREAKFAST. 

The  method,  in  principle,  is  as  follows  :  There  is  introduced  into  the  stomach  a 
mixture  of  a  sugar  solution  and  a  fat-emulsion  of  known  composition.  After  a 
definite  period  this  mixture  is  siphoned  off,  and  the  quantitative  relation  between 
the  fat  and  the  sugar  is  determined. 

This  ratio  will  be  changed  during  the  sojourn  of  the  mixture  in  the  stomach 
only  in  so  far  as  sugar  becomes  absorbed,  since  it  can  be  altered  neither  by  secre- 
tion nor  by  the  passage  of  the  contents  into  the  intestine.  This  allows  of  the 
drawing  of  a  conclusion  as  to  the  amount  of  absorbed  sugar  from  the  altered 
ratio  of  the  quantities  of  sugar  and  fat. 

The  practical  application  of  the  method  is  as  follows: 

There  are  prepared  300  c.c.  of  a  watery  solution  containing  about  90  gm.  of 
dextrose  and  5  to  6  gm.  of  the  yolk  of  egg.  Of  this  mixture,  250  c.c.  are  intro- 
duced into  the  empty  stomach.  After  two  and  a  half  hours  the  solution  obtained 
by  expression  is  examined  quantitatively  for  dextrose  and  fat  (ether  extract),  and 
from  the  altered  proportion  of  these  two  components  the  sugar  absorption  is  cal- 
culated. V.  Mering  was  able  to  show  that,  although  water  was  not  absorbed  from 
the  stomach,  considerable  quantities  of  sugar  were. 

Volhard'  raised  the  objection  that  the  method  did  not  give  correct  results, 
since  the  emulsion  was  destroyed  by  the  splitting  of  the  fat  in  the  stomach. 

It  is  likely  that  the  soup  prepared  from  browned  flour,  as  suggested  by  the 
author,  would  be  better  adapted  for  this  experiment  than  is  the  emulsion  (see 
p.  411). 

EXAMINATION  OF  THE  FUNCTIONS   OF  THE  STOMACH  BY  MEANS  OF  THE 
BUTYROMETRIC  METHOD  OF  SAHLI  AND  SEILER. 

It  can  hardly  escape  the  thoughtful  reader  how  great  must  be  the 
uncertainty  attached  to  conclusions  as  to  the  functions  of  the  stomach 
which  are  drawn  from  examinations  of  test  meals,  even  those  in  which  the 
most  exact  chemical  methods  are  employed.  The  main  difficulty  lies  in 
the  fact  that  the,  results  of  the  quantitative  examination  of  the  stomach 
contents  are  influenced  by  many  different  factors  which  do  not  allow 
ol  separate  calculation.  For  example,  the  amount  of  the  expressed 
meal  is  not  entirely  dependent  upon  the  motility  of  the  stomach,  but  is 
altered  also  by  the  quantity  of  the  secretion.  Again,  the  acidity  or  the 
percentage  content  does  not  represent  directly  the  amount  of  the  secre- 

'  Miinch.  med.  Woch.,  1900,  parts  5  and  6. 


398    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

tion,  but  is  influenced  to  a  great  degree  by  the  motor  activity.  For 
the  acidity  which  is  present  indicates  a  very  different  secretory  activity 
according  to  whether  the  expressed  meal  contains  besides  the  secreted 
gastric  juice  a  greater  or  less  part  of  the  ingested  test  meal,  or  accord- 
ing to  whether  a  greater  or  less  part  of  the  secretion  has  passed, 
before  expression,  through  the  pylorus.  If  the  greater  part  of  the  test 
meal  has  passed  quickly  into  the  intestine  during  the  hour  before  the 
expression,  then  even  a  small  secretion  may  apparently  be  normal  or 
even  hypernormal ;  and  the  reverse  is  also  conceivable — namely,  that 
even  a  normal  secretion  may  present  subnormal  acidity,  and  perhaps  even 
indicate  a  lack  of  free  hydrochloric  acid,  in  case  the  food  which  was 
introduced  has  passed  only  in  small  amounts  into  the  intestine  during 
the  time  of  the  observation.  For  the  percentage  content  of  free  hydro- 
chloric acid  is  influenced  not  only  by  the  motility  of  the  stomach,  but 
also  by  the  solution  and  absorption  of  the  proteids  in  that  organ.  It 
is,  for  example,  clear  that  if  the  proteids  are  quickly  absorbed,  the  ex- 
cess of  acid  will  appear  much  more  quickly  than  if  at  the  time  of  the 
examination  all  the  proteids  of  the  food  have  been  saturated  by  the  acid. 

It  must  be  emphasized  that,  if  we  determine  the  presence  of  a 
chemical  abnormality  in  the  gastric  contents  according  to  the  older 
methods,  it  is  not  possible  to  say  whether  the  disturbance  is  dependent 
upon  the  secretion  or  upon  the  motility  or  upon  absorption,  or  upon  all 
these  three  factors  together.  If,  then,  we  consider  this,  it  must  be 
admitted  that  the  experiments  of  Pawlow,  who  succeeded  in  collecting 
pure  gastric  juice  free  from  the  admixture  of  water  and  food,  were  the 
first  to  give  us  exact  data  concerning  the  laws  of  the  secretion  by  the 
stomach. 

From  the  preceding  description  of  the  usual  methods  of  examina- 
tion it  is  evident  that  the  apparent  accuracy  of  the  results  of  these 
methods  as  applied  to  the  stomach  is  really  a  delusion,  and  that  a  part 
of  the  trouble  which  has  been  expended  upon  them  must  be  considered 
as  actually  lost,  since  it  has  not  been  possible  to  differentiate  in  the 
results  the  separate  factors  mentioned  above.  We  have  to  do  with  an 
equation  containing  several  unknown  quantities  which  cannot  be  solved 
so  long  as  other  equations  are  not  at  our  disposal.  Proceeding  along 
similar  lines,  Pfaundler,  in  his  very  interesting  work,  has  brought  forth 
several  equations  for  the  chemical  process  of  digestion,  and  so  has 
found  a  method  of  getting  more  exact  information  regarding  the  secre- 
tion and  motility  of  the  stomach.  The  essentials  of  Pfaundler's  method 
consist  in  removing,  during  the  period  of  the  digestion  of  the  test  meal, 
portions  of  the  stomach  contents  at  different  times,  either  on  the  same 
day  or  with  a  repetition  of  the  test  meal  on  different  days.  The  analytic 
data  obtained  from  the  examination  of  these  various  portions  have  been 
used  by  Pfaundler  to  prepare  equations  from  which  he  has  been  able  to 
calculate,  in  absolute  figures,  the  motor  activity  and  the  amount  of  the 
secretion  of  the  stomach.  But  this  method  is  entirely  too  complicated 
for  practical  purposes,  and  for  the  patient  is  much  too  troublesome ; 
besides  this,  it  is  not  entirely  free  from  physiologic  objections. 


EXAMINING   THE  STOMACH  WITH  AID   OF  STOMACH  TUBE.   399 

Principle  of  the  New^  Method. 

In  order  to  obviate,  in  part  at  least,  the  indefiniteness  of  our  exam- 
ination of  the  stomach,  the  writer  reasoned  as  follows  :  If  it  is  possible 
to  add  to  the  test  meal  a  substauce  which  is  not  easily  absorbed  and 
yet  allows  of  ready  quantitative  determination,  then  after  introduction 
and  subsequent  expression,  from  the  amount  of  this  substance  present 
in  siphonage,  it  can  be  calculated  how  much  of  the  test  meal  has  passed 
into  the  intestine,  how  much  is  still  remaining  in  the  stomach,  and  con- 
sequently what  fraction  of  the  expressed  content  can  be  ascribed  to  the 
secretion  of  gastric  juice.  One  obtains,  therefore,  a  measure  not  merely 
of  the  motor  activity  of  the  stomach,  but  also  of  the  secretion  as  well. 
For  the  success  of  such  a  method  it  is  evident  that :  first,  the  test  meal 
must  be  homogeneous  throughout,  and  that  in  order  to  serve  as  an 
indicator  of  the  motility  the  unabsorbed  substance  must  remain  thor- 
oughly mixed  in  the  stomach  contents — e.  g.,  present  no  inclination  to 
separate  or  sediment ;  and,  second,  that  absorption  of  water  must  not 
take  place  from  the  stomach.  According  to  the  experiments  of 
V.  Mering,  this  latter  fact  may  be  considered  as  definitely  settled. 
Concerning  the  choice  of  indicators  for  the  motility  of  the  stomach, 
the  writer  thought  first  to  add  an  insoluble  colored  powder  or  lycopodium 
to  the  test  meal,  and  to  determine  this  quantitatively  by  colorimetric 
means  or  by  counting  the  lycopodium  granules.  It  was  soon  shown, 
however,  that  neither  the  insoluble  colored  particles  nor  the  lycopodium 
was  sufficiently  well  mixed  throughout  the  test  meal  to  serve  as  a  meas- 
ure for  the  amount  of  the  test  meal  remaining  in  the  stomach.  The 
powders  attached  themselves  so  intimately  to  the  solid  particles  of  the 
test  meal  that  the  experiment  was  abandoned.  Moreover,  there  was 
still  another  point  to  be  considered.  The  substances  mixed  with  the 
test  meal  must  not  give  it  the  character  of  a  non-physiologic  food,  even 
if  this  character  consist  merely  in  an  abnormality  of  appearance  or 
taste.  On  this  account  the  writer  was  convinced  that  the  only  substance 
which  appeared  feasible  for  the  purpose  in  question  was  fat. 

The  use  of  fat  in  test  meals  essentially  for  the  sole  purpose  of  the 
determination  of  motility  had  previously  been  proposed  by  Matthieu.^ 
This  author  added  to  a  test  meal  consisting  of  60  gm.  of  bread,  20  to 
70  gm.  of  oil,  in  the  form  of  an  emulsion  with  gum,  and  250  gm.  of 
tea.  He  then  obtained  by  means  of  the  determination  of  fat,  data 
concerning  the  motility  and  secretion  of  the  stomach,  although  the  latter 
was  merely  incidental  and  was  not  carried  out  to  any  definite  conclusion. 
The  writer  does  not  know  whether  this  method  of  Matthieu  has  been 
found  to  be  practicable.  In  any  case,  this  test  meal  did  not  appear  to 
the  writer  to  be  available  for  the  point  in  question,  because  it  did  not 
fulfil  the  postulate  of  homogeneity,  in  that  the  pieces  of  bread  exhibit  a 
decided  inclination  to  sediment,  and  thereby  mechanically  remove  the 
greater  part  of  the  fat.  In  consequence  of  this  the  fat,  other  food  con- 
stituents, and  the  secreted  juice  do  not  allow  of  quantitative  determina- 
'  Arch.  f.  Verdauungskrankk.,  vol.  i.,  1896. 


400    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

tion.  Besides  this,  such  a  mixture  of  an  emulsion  of  oil  with  the 
ordinary  test  meal  cannot  be  considered  as  a  usual  diet,  nor  on  account 
of  its  unpleasant  taste  is  it  a  test  meal  of  physiologic  composition. 
The  experiments  of  Pawlow  show  sufficiently  how  very  easily  the 
physical  characteristics  of  the  test  meal  influence  the  functions  of  the 
stomach. 

Again,  v.  Mering,  in  his  method  of  proving  the  power  of  absorp- 
tion of  the  stomach,  employed  fat  in  the  form  of  an  emulsion  of  the 
yolk  of  egg.  T.  Volhard,  nevertheless,  has  shown  that  such  emulsions 
of  the  yolk  of  egg  are  not  permanent  within  the  stomach  ;  as  a  result 
of  the  influence  of  the  hydrochloric  acid  the  eg^  yolk  separates,  and 
the  postulate  of  homogeneity  is  consequently  not  fulfilled. 

The  attempt  was  next  made  to  use  milk,  since  this  presents  a  mix- 
ture of  proteid,  carbohydrate,  and  finely  divided  fat,  which  is  easily 
obtainable  and  nearly  ideally  constituted  for  the  purposes  of  nutrition. 
The  experiments  with  milk  resulted  unfavorably,  in  that  the  coagula- 
tion of  this  substance  which  took  place  in  the  stomach  disarranged  its 
homogeneous  composition.  It  was  easy  to  show  that  in  the  coagulation 
the  fat  was  carried  down  almost  completely  by  the  precipitation,  and 
that  the  coagulum  and  whey  in  the  expressed  test  meal  of  milk  con- 
tained very  different  amounts  of  acid.  We  were  not  able  by  various 
artificial  means  to  compel  the  milk  to  coagulate  in  fine  flocks,  and  thus 
to  avoid  any  considerable  appearances  of  sedimentation  in  the  stomach. 
The  employment  of  milk  was  consequently  also  excluded.^  Finally  a 
soup  made  of  flour  browned  in  fat  proved  to  be  adequate  for  our  pur- 
pose, and  yet  completely  suitable  for  ordinary  nutrition.  At  the  writer's 
suggestion,  his  assistant.  Dr.  Seiler,  tested  the  feasibility  of  the  employ- 
ment of  this  test  meal  for  the  purpose  in  hand,  and  made  a  number  of 
examinations,  which  have  been  published  in  his  dissertation. 

Preliminaries  of  the  Method. 

Preparation  of  the  Flour  Soup. — This  can  be  very  readily 
prepared  by  the  physician  immediately  before  the  examination,  and 
requires  only  a  few  minutes'  time.  The  method  is  as  follows  :  25  gm. 
of  flour  and  15  gm.  of  butter  are  fried  in  an  iron  pan  until  well 
browned ;  and  about  350  c.c.  of  water  are  then  added  gradually  with 
constant  stirring.  The  mixture  is  then  boiled  for  five  minutes,  and  the 
loss  in  volume  replaced  by  fresh  water.  Salt  (sodium  chlorid)  is  now 
added  to  give  the  soup  a  pleasant  flavor.  No  lumps  must  remain  in 
the  mixture.^  This  soup  presents  a  well-mixed  emulsion  of  fat  which, 
probably  because  it  is  mechanically  well  mixed  with  the  flour,  remains 
intact,  in  spite  of  the  action  of  the  acid  in  the  stomach,  and  shows  no 

^  A  further  reason  for  abstaining  from  the  use  of  milk  was  the  fact  that,  in  opposi- 
tion to  the  resuks  of  Schiile  (Zeits.f.  kiln.  Med.,  vol.  xxviii.),_  the  author  was  never  able 
to  detect  free  hydrochloric  acid  in  an  expressed  test  meal  of  milk  of  200  to  300  c.c.  This 
difference  is  attributable  to  the  better  quality  (fat  and  proteid  content)  of  the  cows'  milk 
used  in  his  laboratory. 

'■*  Quite  a  number  of  the  adverse  criticisms  of  this  method  are  due  to  the  fact  that 
this  soup  has  not  been  prepared  with  sufficient  care  in  reference  to  its  homogeneity. 


EXAMINING   THE  STOMACH   WITH  AID   OF  STOMACH  TUBE.   401 

inclination  within  the  time  of  the  examination  to  form  a  sediment  or  for 
the  fat  to  separate.^  In  fact,  at  the  end  of  the  digestion  such  a  flour 
soup  is  expressed  in  about  tha  same  physical  condition  as  it  was  intro- 
duced.     It  is  merely  more  or  less  diluted. 

The  patient  takes  with  a  spoon  300  c.c.  of  this  soup,  while  the 
remaining  50  c.c.  are  retained  for  control  determination  of  the  content 
of  fat.  The  stomach  must  have  been  thoroughly  washed  before  admin- 
istration, and  after  one  hour  the  contents  are  expressed. 

The  next  step  to  be  taken  is  first  to  determine  the  absolute  amount 
of  fat  remaining  in  the  stomach  after  the  test  digestion,  and,  secondly, 
to  compare  this  amount  with  that  introduced.  As  it  is  not  possible  to 
be  sure  that  the  entire  stomach  contents  are  expressed,  this  determination 
can  be  exact  only  when  the  amount  of  the  stomach  contents  which 
escaped  expression  is  obtained.  For  this  purpose  the  determination  of 
the  residue  ^  according  to  the  method  of  Matthieu  is  resorted  to. 

The  principle  of  this  method  consists  in  the  dilution  of  the  residue 
in  the  stomach  by  means  of  a  definite  volume  of  water,  which  is  intro- 
duced by  means  of  a  tube,  and  in  the  expression  of  the  diluted  stomach 
contents  after  the  water  has  been  thoroughly  mixed  in  the  stomach  by 
means  of  light  kneading.  The  acidity  of  the  undiluted,  as  well  as  of 
the  diluted,  stomach  contents  is  then  determined  by  titration  (p.  377),  and 
from  the  differences  in  these  two  values  conclusions  may  be  drawn  as  to 
the  degree  of  dilution ;  or,  since  the  amount  of  water  which  was  added 
is  known,  as  to  the  residual  amount  of  stomach  contents  which  was  not 
expressed.  The  following  is  the  method  of  calculation  according  to 
Matthieu  : 

Let  a  =  acidity  of  the  undiluted  gastric  contents. 

Let  6  =  acidity  of  the  diluted  gastric  contents. 

Let  X  =  amount  of  the  test-meal  remaining  in  the  stomach  after 
expression. 

Let  300  c.c.=  the  amount  of  water  introduced  into  the  stomach  for 
dilution. 

Then  ax  =  b  (.t  +  300). 
X  {a  —  b)  300  b. 

300  b 

X  = ■ 

.      a—b. 

For  the  next  step  in  the  procedure  it  is  necessary  to  have  a  clinical 

method  for  the  determination  of  the  fat  in  the  fluids  to  be  examined. 

The  usual  method,  according  to  Soxhlet  (extraction  with  ether),  is  too 

detailed  and  lengthy  to  be  suited  for  clinical  purposes.     On  the  other 

hand,  the  writer  has  found  that  the  butyrometric  method  of  Gerber^  for 

^  That  sedimentation  and  separation  do  not  take  place  even  when  tlie  flour  soup 
remains  quietly  in  a  glass  is  a  further  proof  that  even  the  slightest  peristaltic  movements 
of  the  stomacli  cause  the  homogeneous  character  of  the  meal  to  be  maintained,  and  com- 
pletely exclude  any  sedimentation  which  might  be  caused  by  the  addition  of  tlie  gastric 
juice. 

^Matthieu  and  Remond,  Soc.  de  biol.  de  Paris,  Dec,  1890,  and  Arch.  f.  Verdauungs- 
krankh.,  vol.  i.,  p.  348. 

^  Die  praktische  Milchpriifung,  Bern,  K.  J.  Wyss,  1900. 

26 


402    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 


fat-determination,  which  is  often  employed  in  the  examination  of  milk, 
answers  all  the  demands  of  simplicity  and  exactness.  He  will  there- 
fore next  describe  this  method  of  fat-determination,  which  has  not  been 
used  before  for  clinical  purposes.  The  principle  is  as  follows  :  The 
solutions  in  which  the  fat  is  to  be  determined  are  mixed  with  a  definite 
amount  of  concentrated  sulphuric  acid  and  a  very  small  volume  of  amyl 
alcohol  and  thoroughly  shaken  ;  since  the  mixture  becomes  quite  hot,  the 
action  of  the  sulphuric  acid  tends  to  decompose  the  organic  substances,  with 
the  exception  of  the  fat,  to  such  an  extent  that  a  thin 
solution  results  ;  from  this  the  total  amount  of  fat 
dissolved  in  the  amyl  alcohol  can  be  separated  in  the 
form  of  a  clear  layer  by  means  of  centrifugalization. 
The  volume  of  the  fat-amyl-alcohol  layer  is  then  read 
off  in  a  butyrometer  specially  constructed  by  Gerber. 
The  readings  on  the  graduated  scale  are  calculated  as 
fat  per  cent,  by  weight.  The  butyrometer,  made  of 
hard  glass,  is  about  20  cm.  long.  Its  shape  may  be 
seen  from  Fig.  146.  The  apparatus  has  the  disad- 
vantage that  centrifugalization  cannot  be  performed 
with  the  ordinary  clinical  centrifuge,  which  has  too 
small  a  radius  ;  this  necessitates  the  employment  either 
of  a  much  larger  centrifuge  or  of  one  designed  espe- 
cially for  this  purpose,  such  as  can  be  obtained  from 
Hugershof,  in  Leipzig. 

The  butyrometer  is  filled  by  means  of  pipets,  also 
especially  designed  for  the  purpose.  Of  these  are  re- 
quired a  10  c.c.  (for  the  sulphuric  acid),  a  1  c.c.  (for 
the  amyl  alcohol)  and  an  11  c.c.  (for  the  milk,  the 
flour  soup,  or  stomach  contents). 

The  process  is  as  follows  :    10  c.c.  of   sulphuric 
acid  (specific  gravity  1.820  to  1.825  at  15°  C.)  (cor- 
responding to  90  to  91  per  cent,  acid)  are  added  to 
the   butyrometer  by  means   of   the  pipet,   and  upon 
this  is  stratified  1  c.c.  of  pure  amyl  alcohol  (specific 
gravity  0.815  at  15°  C),  and  then  11  c.c.  of  the  flour 
soup  or  stomach  contents.     The  butyrometer  is  then 
carefully  closed  by  means  of  a  rubber  stopper,  and 
thoroughly  shaken.     On  account  of  the  heat  the  tube 
must  be  covered  with  a  cloth.      It  is  finally  centrifu- 
which   process  the  graduated   end  of  the  butyrometer 
the   center.       By  the   centrifugalization    the   fat   and 
from   the    mixture,    and    lie   as   a   clear,    transparent 
is   now  darkly  colored.     Centri- 
height    of   the    alcoholic 
not    undertaken    imme- 


FiG.  14r..— Butyr- 
ometer with  rubber 
stopper. 


galized,   during 

must  lie  toward 

alcohol  separate 

layer  on  top  of  the  solution,  which  is   now 

fugalization    is    carried    on    as    long    as    the 

layer    increases.       In    case    the    operation    is 


diately,  the  butyrometer  must  be  placed  in  water  at  a  temperature 
of  at  least  70°  C.,  in  order  to  prevent  the  hardening  of  the  fat.  In 
order  to  obtain  exact  results  the  reading  should  be  made  Avhile  the  fluid 


EXAMINING   THE  STOMACH  WITH  AID   OF  STOMACH  TUBE.  403 

is  still  warm.  For  the  purpose  of  reading,  the  rubber  stopper  must  be 
pushed  into  the  mouth  of  the  butyrometer  so  that  the  upper  surface  of 
the  layer  of  fat  (with  its  under  meniscus)  comes  to  lie  at  the  zero  point 
of  the  scale.^  The  scale  (empirically  graduated)  is  then  read  off  at  the 
point  corresponding  to  the  lower  meniscus  of  the  fat-layer.  The  cen- 
trifugalization  should  be  repeated,  particularly  by  those  who  are  inexpe- 
rienced in  the  method,  in  order  to  insure  the  accuracy  of  the  estimation. 
If  'the  estimation  be  correct,  the  second  centrifugalization  must  give 
exactly  the  same  reading  as  the  first.  Gerber  found  that  this  method 
for  the  determination  of  fat  is  exact  for  milk  to  about  0.1  per  cent. 
Control  experiments  which  were  undertaken  at  the  writei-'s  suggestion, 
in  order  to  compare  the  results  from  this  instrument  with  those  from  the 
Soxhlet  apparatus,  have  shown  that  this  degree  of  accuracy  holds  good 
for  the  flour  soup  before  and  after  the  action  of  stomach  digestion. 

The  writer  must  here  make  reference  to  the  presence  of  a  lipolytiG 
enzyme  in  the  gastric  juice,  which  has  been  of  late  carefully  studied  by 
F.  Volhard.^  The  thought  presents  itself  that  perhaps  in  an  examina- 
tion of  the  digested  stomach  contents,  since  a  part  of  the  digested  fat 
may  have  been  split  in  the  stomach,  the  amount  of  fat  after  siphonage 
cannot  serve  as  an  indicator  for  the  amount  of  the  residual  test  meal. 
The  separated  glycerin  and  butyric  acid  (if  butter  fat  be  employed) 
are  both  soluble  in  water,  and,  if  they  are  not  absorbed  by  the  stomach, 
consequently  remain  in  the  watery,  instead  of  in  the  alcoholic,  layer, 
and  thus  escape  estimation.  The  action  of  the  enzyme  in  this  connec- 
tion was  studied  by  the  writer's  assistant.  Dr.  Seller,  and  his  results, 
recently  published  in  the  Archiv  fur  Minische  3Iedicin  (1904-05), 
show  that  the  amount  of  fiit  decomposed  is  so  slight  that  it  may  practi- 
cally be  neglected.  The  flour  soup  is  expressed  after  one  hour,  and 
Seller  has  shown  that  the  lipolysis  in  this  length  of  time  is  quite  incon- 
siderable. Furthermore,  almost  all  of  the  fatty  acids  contained  in  but- 
ter fat  are  insoluble  in  water,  so  that  they  pass  almost  entirely  into  the 
alcoholic  layer  of  the  butyrometer.  The  butyric  acid,  which  is  soluble 
in  water,  is  present  in  such  exceedingly  small  quantities  that  it  may  be 
disregarded.  Owing  to  the  relatively  small  amount  of  glycerin  con- 
tained in  the  fat,  it  follows  that  even  if  there  be  considerable  lipolysis, 
the  loss  in  the  alcoholic  layer  due  to  the  solution  of  the  glycerin  in 
water  is  so  slight  that  it  is  practically  unimportant.  In  other  words, 
the  fatty  acids  liberated  by  lipolysis  in  butyroraetry  may  be  read  off  as 
fat,  and  the  result  will  be  fairly  accurate. 

Although  lipolysis  does  not  interfere  with  the  butyrometric  determi- 
nation, Voihard  has  shown  that  if  the  hydrochloric  acid  of  the  gastric 

'  Tn  centrifugalizing  it  will  be  found  more  practical  to  introduce  the  rubber  cork  so 
that  the  upper  level  of  the  fluid  reaches  only  to  about  the  80  mark  of  the  butyrometer 
scale,  since  the  fat  accumulates  most  readily  "in  the  conical  part  between  the  neck  and  the 
body  of  the  butyrometer.  By  observing  this  precaution,  moreover,  the  disturbing  layer 
of  insoluble  substances  (cellulose,  etc.)  collecting  below  the  fat  may  be  kept  back  in  the 
wide  portion  of  the  butyrometer  by  cautiously  bringing  the  instrument  into  the  vertical 
position  when  the  rubber  cork  is  pushed  in. 

2  Mlinck.  med.   Woch.,  1900,  parts  5  and  G  ;  ZeiL  f.  kliii.  Med.,  vols.  xlii.  and  xliii. 


404    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

juice  be  small  in  amount,  the  acidity  clue  to  the  liberation  of  the  fatty 
acids  by  lipolysis  may  markedly  influence  the  total  acidity ;  it  would 
consequently  be  incorrect  to  refer  this  total  acidity  entirely  to  hydro- 
chloric acid.  The  simplest  method  for  avoiding  this  error  is  to  employ 
the  filtered  gastric  contents  for  the  titration  of  the  acidity.  With  the 
exception  of  the  quantitatively  unimportant  butyric  acid,  the  fatty  acids 
are  insoluble  in  water,  and  so,  since  they  remain  upon  the  filter,  the 
acidity  of  the  filtrate  may  be  referred  directly  to  hydrochloric  acid. 

It  is  also  to  be  remarked  that  it  is  advisable  to  determine  the  amount 
of  fat  in  the  undigested  flour  soup,  as  well  as  the  amount  in  the  ex- 
pressed meal.  This  can  be  done  without  any  especial  trouble.  This 
is  particularly  advisable  because,  on  account  of  the  varying  content 
of  water  in  butter,  we  cannot,  by  weighing  the  amount  of  butter  put 
into  the  soup,  assume  the  weight  of  the  fat-content. 

Next  follow  the  technical  conditions  which  must  be  insured  in  the 
use  of  Matthieu's  determination  of  the  residue  contents  and  Gerber's 
butyrometric  fat-determination  in  order  to  be  able  to  draw  exact  con- 
clusions concerning  gastric  digestion. 

Performance  of  the  Mettiod. 
After  a  thorough  rinsing  of  the  stomach  the  patient  is  given  in  the 
morning  the  300  gm.  of  flour  soup,  prepared  according  to  the  method 
already  described.  It  must  be  eaten  with  a  spoon.  The  remaining  50 
c.c.  are  retained  for  the  determination  of  fat.  After  one  hour  the  con- 
tents are  expressed,  and  300  c.c.  of  water  introduced  for  the  purpose  of 
the  determination  of  the  residue.  The  undiluted  stomach  contents  and 
those  expressed  after  dilution  are  titrated  for  their  acidity,  and  from 
these  two  results  the  amount  of  stomach  contents  remaining  after  the 
first  expression,  or  the  residue,  is  calculated  according  to  the  formula  of 
Matthieu.  Next,  the  amount  of  fat  in  the  undiluted  stomach  contents 
and  also  in  that  portion  of  the  soup  which  was  retained  as  a  control  is 
determined  butyrometrically  according  to  the  method  given  above.  The 
undiluted  stomach  contents  still  remaining  can  be  used  for  whatever 
qualitative  or  quantitative  determinations  may  be  deemed  advisable. 
Qualitative  examinations  in  this  case  normally  show  the  same  results  as 
in  the  use  of  the  ordinary  test  meal.  Free  hydrochloric  acid  should  be 
present ;  lactic  acid  should  not.  The  flour-soup  meal  is  very  well  suited 
for  the  determination  of  the  pathologic  formation  of  lactic  acid,  because 
it  is  free  from  this  substance.  The  titrations  are  best  carried  out  upon 
unfiltered  gastric  contents  (compare  p.  377).  Besides  the  total  acidity, 
the  excess  or  deficit  of  acid  may  also  be  titrated.  If  the  qualitative 
reaction  shows  considerable  amounts  of  lactic  acid,  the  determination  of 
the  hydrochloric  acid  must  be  made  by  Liitke-Martius'  method,  or  that 
of  the  hydrochloric  acid  and  the  organic  acids  by  Hehner-Maly's.  Of 
course,  all  other  advisable  examinations  can  also  be  made  upon  the 
expressed  gastric  contents — namely,  the  qualitative  and  quantitative 
tests  for  pepsin  and  rennin  (pp.  391  and  394)  and  the  ordinary  tests 
for  starch  digestion  (p.  371). 


EXAMINING   THE  STOMACH   WITH  AW   OF  STOMACH  TUBE.  405 


Calculation  of  the  Results* 

The  following  calculatious  are  possible  from  a  consideration  of  the 
residue,  from  the  acidity  of  the  gastric  filtrate,  and  from  the  difference 
between  the  amount  of  the  fat  found  in  the  ingested  flour  soup  and  that 
found  in  the  expressed  contents. 

By  the  addition  of  the  value  x,  found  in  the  calculation  of  the  res- 
idue (p.  401),  to  the  amount  of  contents  expressed  after  one  hour,  there 
is  obtained  the  volume  of  the  contents  which  were  actually  present  in 
the  stomach  at  the  end  of  that  period.  This  we  designate  as  To  (a 
total  gastric  contents  after  one  hour).  From  the  absolute  fat-content 
of  To  found  butyrometrically,  there  can  be  determined  how  much  of 
the  volume  To  can  be  ascribed  to  the  ingested  flour  soup ;  provided  the 
expressed  contents  present  a  thoroughly  mixed  emulsion  whose  homo- 
geneity has  suffered  no  disturbance.  Since  the  results  of  v,  Mering's 
investigations  prove  that  absorption  of  water  from  the  stomach  plays  no 
considerable  role,  and  since  the  absorption  of  fat  in  the  stomach  may 
also  be  neglected,  the  percentage  relation  of  the  fat  to  the  stomach 
contents  is  disturbed  neither  by  the  motility  of  the  stomach  nor  by  the 
absorption  of  water,  but  only  by  the  secretion  of  gastric  juice.  The 
amount  of  fat  remaining  in  the  stomach  serves,  therefore,  as  a  measure 
for  the  amount  of  flour  soup  also  remaining ;  ^  for  example,  if  300  c.c. 
of  flour  soup  with  a  content  of  4  per  cent,  fat,  or  altogether  12  gm. 
of  fat,  were  introduced  into  the  stomach,  and  the  determination  of  fat 
for  To  showed  a  fat-content  of  3  gm.,  we  can  conclude  that  the  amount 
of  ingested  soup  which  remained  at  the  end  of  the  period  was  equal  to 
TT  X  300  =  5  X  300 — i.  e.,  75  c.c.  We  designate  this  amount  as  Sii 
(soup). 

Since  we  can  neglect  the  absorption  of  water  and  the  amount  of  the 
saliva  which  was  swallowed,  the  volume  To  —  8u  is  equivalent  to  the 
volume  of  gastric  juice  present  in  the  expressed  contents.  This  we 
designate  as  Ma  (gastric  juice).  For  example,  if  the  amount  To  =  150 
c.c,  and  the  amount  8u  =  75  c.c,  then  150  —  75,  or  75  c.c,  will  be  the 
volume  of  gastric  juice  contained  in  To.  If  the  acid  content  of  To  has 
been  determined,  it  is  possible  from  these  data  to  j)roceed  furtlier,  and 
to  calculate  what  acidity  was  possessed  by  the  pure  gastric  juice  as  it 
was  excreted  from  the  nmcous  lining  of  the  stomach.^ 

If  75  c.c  of  pure  gastric  juice  are  present  in  the  stomach  contents 
whose  volume  amounts  to  150  c.c,  with  2  per  cent,  acidity,  then  the 
acid  content  of  the  pure  gastric  juice  (J/«)  nmst  evidently  be  4  per 
cent.  In  a  similar  way  the  enzyme  content  of  the  pure  gastric  juice 
can  be  calculated  if  it  has  been  quantitatively  determined  for  the  mixed 
stomach  contents. 

In  order  to  avoid  misunderstandings  in  regard  to  the  value  of  all 
these  calculations,  attention  must  be  called  to  the  following  points  : 

'  The  saliva  which  has  been  swallowed  can  be  very  well  neglected. 
^  In  the  content  of  this  secretion  is  included  any  exceptional  osmosis  caused  by  the 
ingestion  of  the  flour  test  meal. 


406    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

The  flour  soup  contains  such  small  quantities  of  soluble  carbohy- 
drates and  salts  that  such  osmotic  effects  can  be  in  evidence  only  when 
the  absorption  of  the  soluble  products  of  the  digestion  of  the  flour  soup 
is  interfered  with. 

Naturally  the  volume  Ma  is  not  identical  with  the  total  volume  of 
gastric  juice  which  has  been  secreted  up  to  the  time  of  expression. 
An  unknown  amount  of  the  gastric  juice  mixed  with  the  food  has  been 
passed  on  into  the  duodenum  before  expression.  Xevertheless  the  cal- 
culation gives  interesting  results  as  to  the  volume  of  the  secretion  inde- 
pendent of  the  percentage  acidity  of  the  pure  gastric  juice,  since  it 
shows  us  the  relation  of  the  amount  of  the  gastric  juice  present  in  the 
stomach  at  a  given  time  to  the  amount  of  test  meal  present  in  the 
stomach  at  the  same  time.  As  later  examples  will  show,  this  relation 
is  approximately  constant  under  normal  conditions.  The  gastric  juice 
and  flour  soup  are  contained  in  the  volume  To  in  approximately  equal 
parts.  From  this  it  is  evident  that  variations  in  this  relation  are  of 
pathologic  and  diagnostic  interest. 

Concerning  the  conclusions  as  to  the  motility  of  the  stomach  which 
may  be  drawn  from  these  results,  the  following  is  to  be  noted  :  The 
difference  between  the  volume  of  soup  introduced  and  that  recovered 
by  expression  (namely,  the  volume  300 — Su)  can  be  considered  as  a 
measure  of  tlie  motility  of  the  stomach.  Really  this  value  does  not  cor- 
respond to  the  total  motor  power  of  the  stomach,  for  an  unknown 
amount  of  secreted  gastric  juice  has  also  been  passed  on  into  the  duo- 
denum. At  the  same  time  it  is  probably  a  more  reliable  measure  of 
stomach  motility  than  the  value  of  the  total  stomach  contents,  which 
is  used  in  the  older  methods  for  the  same  purpose.  For,  as  already 
mentioned,  the  expressed  contents  contain  under  normal  conditions 
about  equal  amounts  of  soup  and  gastric  juice,  so  that  it  is  easy  to 
judge,  when  variations  from  this  normal  occur,  whether  a  hypersecre- 
tion or  diminished  secretion  is  present.  This  gives  the  actual  value 
of  the  motility  already  mentioned. 

The  calculations  from  the  results  of  the  examination  can  be  presented 
algebraically  as  follows  : 

Let  To  =  the  amount  of  the  expressed  contents,  including  residue. 
(For  calculation  of  the  latter  compare  p.  401.) 
F  =  the  fat-content  of  the  flour  soup  in  per  cent. 
f=  the  fat-content  of  the  expressed  contents  in  per  cent. 
Su  =  the  amount  of  soup  contained  in  the  expressed  contents. 


Then, 


Su  _  / 
To       F 


Su  = 


f.To 
'  F 


From  this  value  the  amount  of  gastric  juice  may  be  obtained  from 
the  formula  3Ia  =  To  —  Su. 


EXAMINING   THE  STOMACH  WITH  AID   OF  STOMACH  TUBE.   407 

The  determination  of  the  acidity  of  the  pure  secretion  may  be  cal- 
culated as  follows  : 

Let  a  =  the  acidity  of  the  expressed  gastric  contents  in  per  cent. 
A  =  the  acidity  of  the  pure  secretion  in  per  cent. 
To  =  the  amount  of  the  expressed  contents  (including  the  residue). 
Ma  =  the  amount  of  secretion  contained  in  the  expressed  contents. 

m,  a         M         -.     .        aTo 

Then,       —  =  ---    and  A  =  -—-- 
'       A         To  Ma 

By  a  similar  formula  the  enzyme  content  of  the  pure  secretion  can 
be  calculated  quantitatively. 

The  Objections  to  this  Method  and  the  Improvements  in  the  Procedure. 

Almost  immediately  upon  the  publication  of  the  method  just  described,  its 
accuracy  was  attacked  by  various  authors  who  had  not  sufficiently  tested  it. 
The  chief  objection  made  was  that  the  mixture  of  the  test  meal  and  gastric  juice 
separated  into  layers  within  the  stomach,  so  that  a  homogeneous  mixture  of  the 
fats  and  other  contents  did  not  occur,  and  that  consequently  the  fat  in  the 
expressed  contents  could  not  be  taken  as  an  indicator  for  the  test  meal  left  in  the 
stomach.  This  objection  was  based  upon  the  observation  that  if  the  test  meal  be 
expressed  in  two  portions,  one  corresponding  to  the  upper,  and  the  other  to  the 
lower,  layer,  there  will  frequently  be  a  diflference  in  the  amount  of  fat  contained 
in  the  two  cases.  This  observation  was  founded  upon  fact.  A  complete  homo- 
geneity of  the  gastric  contents  is  not  usually  present  after  the  introduction  of  the 
test  meal.  At  the  writer's  suggestion  this  question  has  been  carefully  studied  by 
Dr;  Seller,  who  published  his  results  in  a  recent  article.^  Dr.  Seller  found  that 
these  differences  were  not  great  (0.15-0.25  per  cent,  fat  as  an  average),  and  that 
they  were  not  due  to  a  separation  in  layers  by  the  influence  of  gravity,  but  to  the 
fact  that  the  gastric  mucus  never  mixes  homogeneously  with  the  gastric  contents, 
and  that  the  gastric  juice  does  not  do  so  immediately.  The  amount  of  fat  in  the 
expressed  contents  will  consequently  depend  upon  the  location  of  the  tip  of  the 
stomach  tube.  On  the  other  hand,  even  a  moderate  gastric  peristalsis  seems 
able  to  prevent  a  separation  into  layers  by  the  action  of  gravity.  The  basis  for 
these  statements  is  given  in  Seller's  article,  to  which  the  reader  is  referred.  The 
same  work  also  shows  that  these  differences  in  the  quantities  of  fat  contained  in 
different  portions  of  the  gastric  contents  may  be  diminished,  if  we  make  use  of 
gravity,  by  causing  the  patient  to  change  his  position  every  five  minutes  during 
the  length  of  time  the  test  meal  remains  in  the  stomach. 

From  a  consideration  of  these  facts,  the  following  modifications  in  the  prac- 
tical application  of  the  method  are  advised  in  order  to  secure  the  most  accurate 
results : 

1.  Every  five  minutes  during  the  time  of  the  test  the  patient  must  change 
his  position,  varying  between  the  sitting,  the  dorsal,  and  the  left  lateral  position. 
By  this  means  the  gastric  peristalsis  is  markedly  aided  in  producing  a  homo- 
geneous mixture.  The  right  lateral  position  is  to  be  avoided,  since  it  might 
mechanically  aid  the  escape  of  some  of  the  gastric  contents. 

2.  In  order  to  gain  an  idea  of  the  homogeneity  of  the  gastric  contents,  it 
should  be  expressed  in  two  portions,  the  first  being  obtained  before  a  deep  intro- 
duction of  the  tube,  and  representing  the  upper  layer,  and  the  second  corre- 
sponding to  the  lower  layer.  The  first  portion  should  be  smaller  in  volume,  so 
that  any  existing  difference  between  its  composition  and  that  of  the  lower  layer 
will  be  the  more  striking. 

3.  Only  those  portions  of  each  layer  which  are  free  from  mucus  should  be 

>  Deutsch.  Arch.  f.  klin.  Med.,  1904-05. 


408    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 


employed  for  butyrometry.     If  collections  of  mucus  are  visible,  they  should  be 
removed  with  forceps. 

4.  As  a  rule,  a  mean  may  be  taken  from  the  results  of  the  two  tests.  This  will 
be  the  more  accurate  the  less  the  diflference  between  the  fat-percentages  obtained 
in  the  two  tests. 

5.  If  the  butyrometric  results  of  the  two  tests  vary  so  much  that  they  are 
open  to  suspicion,  the  results  should  be  interpreted  only  like  those  of  the  older 
and  less  accurate  tests. 

6.  In  reference  to  the  accuracy  of  taking  the  mean  of  the  two  tests,  the  fol- 
lowing fact  should  be  borne  in  mind :  The  same  diflference  in  the  fat-percentages 
of  the  two  layers  has  quite  a  different  significance  in  the  calculation,  according 
to  whether  the  expressed  contents  contain  a  high  or  a  low  fat-percentage.  For 
example,  if  the  two  layers  contain  2.3  and  2.6  per  cent,  of  fat,  a  difference  of  0.3 
per  cent,  this  is  so  slight  (one-eighth  to  one-ninth  of  the  total  amount  of  fat) 
that  the  average  may  be  taken  without  question.  Should  we  find  fat-percentages 
of  0.9  and  1.2,  however,  we  again  have  a  diflference  of  0.3  per  cent.,  but  this 
time  it  amounts  to  one-third  to  one-half  of  the  total  amount  of  fat,  and  the 
average  percentage  is  subject  to  criticism. 

Normal  Results  with  the  Use  of  This  Method  as  a  Foundation  for  Interpretatioa 
of  Pathologic  Results.  Examples  for  Diagnostic  Use  and  the  Value  of  the 
Method. 

As  normal  results,  the  following  figures  found  by  Dr.  Seller  by 
experiments  upon  normal  individuals  may  be  given  : 


Number. 

Amount  of 

soup 
introduced. 

Total  stomach 
contents,  includ- 
ing the  residue, 
after  1  hour. 
To. 

Content  of  soup 

in  the  stomach 

contents. 

Contents  of 

gastric  juice 

in  the  stomach 

contents. 

Ma. 

Acidity  of  the 

pure  juice. 
Per  cent.  HCl. 

1 

2 

3 

300 
300 
300 

250 
250 

124 

158 

57 

72 
83 
30 

52 
75 

27 

3.5 
4.4 
3.5 

Average 

4 

5 

113 

113 

108 

62 

44 

56 

51 

69 

52 

3.6 

3.2 
4.2 

Average 

110 

50 

60 

3.7 

If  we  consider  300  c.c.  of  flour  soup  as  the  standard  amount  ingested, 
then  we  can  calculate  from  these  and  other  experiments  the  average 
value  of  To  after  the  expression  in  one  hour  to  be  a  little  more  than  100 
This  volume  is  divided  normally  into  approximately  equal  parts 


c.c 


of  secretion  and  soup.  Nevertheless  it  is  the  common  experience  with 
the  ordinary  test  meal  that  the  amount  of  the  expressed  contents  varies 
greatly  even  under  apparently  physiologic  conditions,  so  that  only  con- 
siderable variations  from  the  normal  are  to  be  considered  pathologic. 
It  is  to  be  noticed  that  the  relation  of  the  amount  of  secretion  to  that 
of  soup  is  far  more  constant  under  normal  conditions  than  the  amount 
of  To.  Free  hydrochloric  acid  should,  as  already  mentioned,  always  be 
present.  The  acidity  for  the  normal  pure  gastric  juice  varies  between 
3.2  and  4.4  per  cent.  These  figures  stand  between  those  which  Pawlow 
obtained  for  the  normal  gastric  juice  of  the  dog  (5  per  cent.)  and  those 


EXAMINII^G   THE  STOMACH  WITH  AID   OF  STOMACH  TUBE.  409 

which  Schiile  and  Troller  found  in  human  gastric  juice,  which  they 
caused  to  be  secreted  reflexly  by  chewing  certain  substances  (1.8  to  3.6 
per  cent.).  That  the  vahies  of  Troller  and  Schiile  are  upon  the  whole 
less  than  the  author's  is  explained  by  the  fact  that  the  mere  chewing  of 
substances  which  cannot  be  considered  as  food  (citron  rind,  mustard) 
cause  a  slighter  secretion  than  an  actual  meal. 

It  is  perhaps  best  to  make  the  diagnosis  of  hyper-  or  hypo-acidity 
depend,  not  upon  the  acidity  of  the  total  expressed  gastric  contents,  but 
upon  the  hydrochloric  acid  content  of  the  pure  gastric  juice.  Values 
which  vary  greatly  from  normal  figures  may  then  be  considered  as 
expressions  of  a  hyper-  or  hypo-acidity.  It  may  perhaps  also  be  best  to 
speak  of  hyper-  and  hyposecretion  if  the  volume  of  gastric  juice  amounts 
to  considerably  more  or  less  than  that  given  above  as  normal.  As  a  basis 
for  this  estimate  we  should  not  take  the  absolute  amount  of  gastric  juice 
found  in  the  stomach  after  an  hour,  but,  better,  the  amount  of  gastric 
juice  in  proportion  to  that  of  the  soup  still  present  in  the  stomach.  It 
is  this  relative  amount  which  is  of  value  for  judging  the  secretory 
power  of  the  stomach,  because,  while  at  every  moment  a  mixture  of 
gastric  juice  and  soup  is  being  removed  into  the  intestine,  still  the  rela- 
tive amount  of  soup  and  gastric  juice  expression  is  not  influenced  by 
the  motility.  Seiler  is  quite  right  to  call  this  relation  of  the  volume  of 
secretion  to  that  of  the  flour  soup  remaining  in  the  stomach  the  secretion 
quotient.  This  is  normally  not  far  from  1.  Considerable  variations 
above  1  ^vould  argue  for  the  diagnosis  of  hypersecretion  ;  below  1,  for  the 
diagnosis  of  hyposecretion. 

The  motility  of  the  stomach  may  then  be  said  to  be  normal  if,  after 
the  ingestion  of  300  c.c.  of  meal  soup,  not  more  than  100  to  150  c.c. 
can  be  expressed  at  the  close  of  one  hour,  of  which  about  one-half  con- 
sists of  soup.  Therefore,  the  ratio  of  the  amount  of  juice  to  that  of 
soup  recovered,  as  expressed  by  the  secretion  quotient,  must  be  con- 
sidered in  the  estimation  of  the  motility.  For  example,  if  the  amount 
of  soup  remaining  is  absolutely  normal,  but  a  relatively  greater  amount 
of  juice  is  found,  this  amount  of  soup  points  not  to  a  normal,  but  rather 
to  a  hypernormal  motility.  So  a  normal  amount  of  soup  with  diminished 
secretion  points  to  a  decreased  motility.  The  ratio  of  the  amount  of 
soup  removed  during  one  hour  from  the  stomach   into  the  intestine  to 

the  amount  of  soup  ingested, ^ ,  may  be   called  the  motility 

quotient.  This  varies  normally  between  three-quarters  and  nine-tenths, 
and  must  be  interpreted,  as  has  been  said,  by  the  consideration  of  the 
secretion  quotient. 

It  is  evident  from  the  above  that  it  is  possible  to  discover  by  this 
method  a  numl)er  of  conditions  which  must  have  completely  escaped  the 
older  methods  of  investigation.  By  it,  it  is  possible  to  decide  whether 
an  increase  in  the  amount  of  the  expressed  stomach  contents  points  to  a 
hypersecretion  or  to  a  motor  disturbance.  It  is  also  possible  to  dis- 
criminate more  exactly  than  before  between  hypersecretion  and  hyper- 
acidity, since  the  volume  of  secretion,  as  well  as  the  acidity  of  the  pure 


410    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

gastric  juice,  can  be  calculated.  Experience  with  this  method  has  showed 
us  already  that  stomach  disturbances  are  decidedly  more  complicated 
than  had  heretofore  been  imagined.  The  more  exact  differentia- 
tions it  enables  us  to  make  will  in  the  future  increase  our  therapeutic 
possibilities.  It  has  shown  us,  for  example,  that  there  are  cases  of 
hypersecretion  with  hypo-acidity,  and  cases  of  hyposecretion  with  hyper- 
acidity. This  condition  is  possibly  due  to  an  abnormal  watery  osmosis, 
to  which  we  have  previously  referred,  and  which  we  have  traced  to  an 
insufficient  absorption  of  the  soluble  products  of  digestion  (see  p.  406, 
footnote).  These  conditions  by  the  old  methods  gave  apparently  normal 
results,  because  in  such  cases  the  amount  of  secretion  and  the  acidity  of 
the  gastric  juice  in  mixed  gastric  contents  completely  neutralized  each 
other  in  the  determination  of  the  total  acidity.  To  these  belong  in 
greater  part  those  cases  diagnosed  usually  as  sensory  neuroses,  in  which, 
in  spite  of  disturbances  of  digestion,  the  examination  of  the  stomach 
contents  by  means  of  the  usual  methods  produces  completely  normal 
results.  A  case  which  apj^eared  remarkable  to  the  writer  gave  the  follow- 
ing results  :  With  otherwise  normal  conditions  (motility  and  the  amount 
of  secretion),  the  acidity  calculated  for  the  pure  gastric  juice  was 
abnormally  low,  while  the  contents  expressed  from  a  fasting  stomach 
showed  a  large  amount  of  decidedly  hyperacid  gastric  juice.  The  con- 
dition here  can  evidently  be  explained  only  by  the  fact  that  the  intro- 
duction of  food  into  the  stomach  caused  an  inhibition  of  the  secretion 
instead  of  stimulation.  That  the  present -simple  and  insecurely  founded 
classification  of  the  symptomatology  of  the  diseases  of  the  stomach  into 
increased  or  decreased  secretion  and  excessive  or  diminished  motility 
must  suifer  decided  alteration  may  be  shown  by  the  following  scheme  of 
some  functional  diagnoses  which  we  are  in  the  position  to  make  by  means 
of  the  new  method  : 

A.  Cases  with  Sufficiext  Motility. 

1.  Hypersecretion  with  hyperacidity  and  hypermotility. 

2.  Hypersecretion  with  hypo-acidity  and  normal  motility. 

3.  Xormal  amount  of  secretion  with  hypo-acidity  and  hyper- 

motility. 

4.  Hyposecretion,  hyperacidity,  and  normal  motility. 

5.  Hyposecretion,    hypo-acidity,   and    normal    or    increased 

motility. 

B.  Cases  with  Ixsuffictext  Motility. 

6.  Diminished  motility,  hypo-acidity,  and  hyposecretion, 

7.  Diminished  motility,  nearly  anacidity,  and  hypersecretion. 
More  extended  experience  will  certainly  tend  to  give  still  more  com- 
binations. 

From  the  preceding  recapitulation  it  is  evident  how  poorly  founded 
is  the  attempt  of  certain  authors  to  ascribe  the  conditions  of  hyper- 
acidity and  hypersecretion  to  primar}''  motor  disturbances,  even  narrow- 
ing the  cause  to  pyloric  stenosis,  a  view  which  has  often  led  to  gastro- 
enterostomy in  cases  where  such  an  operation  was  not  at  all  justifiable. 
These  more   exact   functional   diagnoses    in    stomach  disturbances   are 


EXAMINING   THE  STOMACH  WITH  AID   OF  STOMACH  TUBE.   411 

important  also  in  a  therapeutic  connection.  Above  all,  they  indicate 
clearly  whether  it  is  best  to  influence  the  motility  (laxatives,  regular 
expression  of  stomach  contents)  or  to  affect  the  secretion  (belladonna 
preparations,  alkalies,  by  employment  of  means  for  stimulating  the 
secretion  directly  by  means  of  the  appetite,  according  to  Pawlow  [meat 
extract,  bitters] ). 

Further  Value  of  the  Butyrometric  Method  of  Examination  as  Applied  to  the  Testing 
of  Amylolysis,  Absorption  of  Carbohydrates,  Proteolysis,  and  Absorption  of  Proteids 
fay  the  Stomach. 

What  has  already  been  said  concerning  the  advantages  of  the  butyrometric 
method  of  the  examination  of  the  stomach  contents  by  means  of  the  flour-soup 
meal  has  not  exhausted  the  possibilities  of  this  method.  It  is  well  suited,  for 
instance,  to  the  quantitative  testing  of  the  digestion  of  starch.  In  fact,  the  fol- 
lowing method  is  much  more  exact  than  those  previously  employed,  although  it 
must  be  confessed  that  it  has  not  been  as  yet  practically  worked  out.  The 
expressed  stomach  contents,  as  well  as  the  undigested  flour  soup  which  was 
retained  as  a  control,  are  examined  butyrometrically  for  their  fat-content.  Then 
equal  volumes  of  both  of  these  fluids  are  measured  off",  each  thrown  uijon  a  sej}- 
arate  filter,  and  washed  with  water  so  long  as  the  filtrate  still  shows  a  starch  or 
sugar  reaction.  This  is  to  remove  the  soluble  products  of  the  starch  digestion. 
In  the  residue  on  the  filter  in  each  case  the  starch  content  relatively  to  the  con- 
tent of  the  insoluble  carbohydrate  is  determined,  and  the  difference  in  the  two 
amounts  calculated  for  the  unit  of  the  fat-content  shows  how  much  of  the  starch 
has  been  transformed  in  the  stomach  into  soluble  carbohydrates — i.  e.,  has  been 
digested. 

The  soup  meal  can  again  be  employed  for  the  determination  of  the  power  of 
absorption  of  the  gastric  mucosa  for  soluble  carbohydrates.  Equal  amounts  of 
the  expressed  and  retained  flour  soup  are  hydrolyzed,  and  in  each  the  sugar  tested 
quantitatively.  The  amount  of  fat  in  the  two  fluids  must  also  be  determined 
butyrometrically.  The  content  of  sugar  which  is  found  in  the  expressed  con- 
tents serves  as  a  measure  of  the  total  soluble  and  insoluble  carbohydrates  whicb  were 
contained  in  the  stomach  and  not  absorbed.  If  we  therefore  subtract  this  amount, 
calculated  for  the  unit  of  fat-content,  from  the  sugar  of  the  undigested  flour  soup, 
expressed  in  the  same  way,  there  will  be  obtained  the  amount  of  the  absorbed 
carbohydrate  in  terms  of  the  unit  of  fat-content. 

In  order  to  understand  this  value  correctly  it  must  be  emphasized  that  the 
carbohydrates  which  are  introduced  by  this  method  into  the  stomach  do  not  for 
the  most  part  occur  in  a  preformed  absorbable  form,  so  that  the  power  of  absorp- 
tion, as  found,  appears  at  the  same  time  as  a  function  of  the  digestion  of  carbo- 
hydrates. If .  one  wishes  to  determine  the  amount  of  the  absorption  by  itself, 
as  by  the  v.  Mering  method  of  determination,  it  must  be  considered  how  much  sol- 
uble carbohydrate  is  contained  in  the  ingested  flour  soup  and  how  much  of  car- 
bohydrate was  transformed  into  a  soluble  condition  during  the  digestion. 

The  interpretation  of  the  relations  of  carbohydrate  digestion  and  absorption 
may  be  shown  in  the  following  way  : 

Let  Cj  =  the  carbohydrate  of  the  undigested  flour  soup. 

Let  C\  =  the  carbohydrate  of  the  undigested  flour  soup  minus  the  soluble 
carbohydrate. 

Let  6*3^  the  carbohydrate  of  the  expressed-meal  soup. 

Let  C  ^  =  the  carbohydrate  of  the  expressed-meal  soup  minus  the  soluble  car- 
bohydrate. Then  C^  —  C  ^  =  a  measure  of  the  carbohydrate  that  has  been 
digested — i.  e. ,  rendered  soluble. 

And  C\  —  C3  ^  a  measure  of  the  absorbed  carbohydrate. 

Cj —  Cj  carbohydrate  absorbed 

(Ci  —  Cj)  +  (Cj  —  C  J       carbohydrate  originally  soluble  and  that  dissolved 


412     EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

the  absorbed  fractions  of  the  carbohydrate  originally  soluble  and  dissolved  during 
the  digestion. 

This  latter  fraction,  in  an  analogous  manner  to  the  secretion  and  motility 
quotient,  may  be  called  the  absorption  quotient  of  the  carbohydrate.  It  will  give 
us  data  analogous  to  those  obtained  by  the  method  of  v.  Mering.  It  has  the 
advantage  over  his  method  that  the  observation  takes  jslace  under  physiologic 
conditions — namely,  with  a  test  meal  physiologically  constituted  and  palatable, 
while  by  his  method  the  examination  occurs  under  conditions  which  are  somewhat 
abnormal. 

Finally,  the  butyrometric  determination  can  be  used  to  test  the  digestion  and 
absorption  of  proteids  under  natural  conditions.  Here  also  the  method  must  be 
more  thoroughly  worked  out  technically,  but  the  plan  of  the  examination 
appears  to  be  clearly  outlined.  The  process  is  entirely  analogous  to  that  for 
testing  the  carbohydrate  digestion.  After  the  fat  in  the  undigested  flour  soup,  as 
well  as  in  the  expressed  stomach  contents,  has  been  determined,  each  fluid  is  fil- 
tered, and  washed  free  from  soluble  proteids  with  water.  In  all  four  tests  the 
nitrogen  content  as  determined  by  the  Kjeldahl  method  serves  as  a  measure  of  the 
total  proteids,  including  proteoses  and  peptones.  All  of  these  values  must  be  cal- 
culated for  the  unit  of  fat-content. 

Let  iVj  =  the  nitrogen  content  of  the  undigested  flour  soup. 

Let  iVj  ~  t^®  nitrogen  content  of  the  undigested  flour  soup  minus  the  nitro- 
gen of  the  soluble  proteids. 

Let  N ^  =  the  nitrogen  content  of  the  expressed  stomach  contests. 

Let  N  ^  =  the  nitrogen  content  of  the  expressed  stomach  contents  minus  the 
nitrogen  of  soluble  proteids. 

Just  as  in  the  calculation  of  the  carbohydrate  digestion,  N ^  —  iV^  =  a  meas- 
ure of  the  proteids  digested — i.  e. ,  of  the  nitrogen  which  has  become  soluble. 

iVj  —  A'g  =  a  measure  of  the  proteid — i.  e.,  nitrogen  absorbed. 

JVj  —  iVg  absorbed  N  

(N^  —-^2)  +  (-^"2  ~  -^'^  -^  soluble  and  that  dissolved 

the  measure  of  that  part  of  the  soluble  nitrogen,  both  that  preformed  and  that 
made  soluble  by  digestion,  which  was  absorbed.  This  may  be  called  the  absorp- 
tion quotient  of  the  proteids. 

Concerning  the  Teclinic  of  the  Necessary  Determination  of  Carbohy- 
drate in  These  Examinations. — This  determination  can  be  carried  out  accu- 
rately only  if  the  carbohydrate  is  completely  transformed  into  dextrose  and  as 
such  determined.  For  this  purpose,  according  to  the  method  of  Pollitz,  20  c.c. 
of  the  stomach  contents  or  flour  soup  are  treated  with  dilute  sulphuric  acid  until  the 
appearance  of  the  positive  Congo-red  reaction,  then  further  diluted  with  40  to 
50  c.c.  of  dilute  sulphuric  acid  (5  c.c.  of  dilute  sulphuric  acid,  specific  gravity 
1160,  diluted  up  to  1  liter  with  water),  and  the  mixture  heated  for  eight  hours 
at  108°  to  110°  C.  in  a  Lintner  pressure  flask  upon  a  parafiin  bath,  until  a  color 
is  no  longer  obtained  when  iodin  is  added  to  a  small  portion. 

The  task  of  determining  sugar  in  a  fluid  of  this  kind  is  not  very  simple,  on 
account  of  the  content  of  proteid  and  albumose.  In  order  to  obtain  an  exact 
determination  the  proteids  must  be  completely  removed  ;  this  is  true  of  the  polar- 
ization test  (p.  515)  or  of  the  Soxhlet-Allih'n  methods  with  modifications.  The 
polarimetric  method  is  inaccurate,  because  the  proteids  cause  rotation  to  the  left  ; 
and  the  reduction  tests,  because  the  proteids  hinder  the  filtration  of  the  suboxid 
formed.  We  usually  have  not  enough  material  for  the  areometric  fermentation 
test.  After  many  experiments  the  writer  has  found  that  the  removal  of  the  pro- 
teids, as  well  as  the  albumoses  and  peptones,  can  be  best  accomplished  by  the 
filtration  of  the  mixture,  thorough  washing  with  water,  and  final  treatment  of  the 
filtrate  and  washings  with  a  solution  of  phosphotungstic  acid  '  until  no  further 
precipitation  occurs.     The   solution  must  not  contain   hydrochloric   acid.     We 

1  One  part  of  phosphotungstic  acid  diluted  with  20  parts  of  water  and  acidified  with 
sulphuric  acid. 


EXAMINING   THE  STOMACH   WITH  AW   OF  STOMACH  TUBE.  413 

cannot,  therefore,  employ  hydrochloric  acid  either  for  the  hydrolysis  or  for  the 
acidification  of  the  phosphotungstic  acid  solution. 

After  the  precipitation  of  the  proteids,  the  phosjihotungstic  acid  must  be 
removed  from  the  filtrate.  ^  This  is  best  accomplished  by  adding  barium  carbonate 
so  long  as  an  effervescence  takes  place.  The  filtrate  from  this  precipitate  should 
be  neutral  and  free  from  proteids,  and  can  be  employed  for  the  determinations  of 
sugar  according  to  Soxhlet-Allihn,  colorimetric,  or  iodometric  methods. 

Where  it  is  simi^ly  a  question  of  the  determination  of  the  insoluble  starch  in 
the  expressed  meal  in  comparison  with  that  in  the  ingested  flour  meal,  the  starch  can 
be  approximately  determined  colorimetrically  as  iodostarch  according  to  the  usual 
method  of  Ambuhl.'-  But  since  the  stomach  contents  always  contain  erythrodextriu 
in  soluble  condition,  and  since  this  substance,  when  iodin  is  added  to  the  expressed 
meal,  causes  a  dirty  brownish-violet  color  instead  of  a  pure  blue,  the  colorimetric 
determination  of  the  starch  nuist  be  undertaken  after  the  soluble  starch  derivatives, 
especially  the  erythrodextriu,  have  been  removed.  This  can  best  be  accomplished 
by  repeatedly  washing  the  expressed  contents  with  small  amounts  of  water  in  the 
centriftige.  It  must  be  mentioned  that  the  exact  separation  of  the  solid  from  the 
soluble  constituents  by  means  of  the  centrifuge  is  successful  only  when  the 
expressed  contents  have  been  extracted  with  five  volumes  of  ether  for  the  separa- 
tion of  the  fat  (by  means  of  the  separatory  funnel,  p.  375).  One  cubic  centi- 
meter of  the  undigested  and  of  the  expressed  flour  soup  are  exactly  measured  off" 
by  means  of  a  pipet  divided  into  y^^  c.  c. ,  washed  with  water,  and  then  with  ether 
until  a  test  of  the  substance  remaining  shows  a  pure  blue  color.  The  remaining 
part  is  boiled  for  ten  minutes  with  about  500  c.c.  of  water,  during  which  the 
greater  part  of  the  starch  passes  into  solution.  After  cooling,  diluted  Lugol's 
solution  is  added  drop  by  drop  to  both  tests  luftil  the  blue  color  does  not  become 
more  intense.  The  shades  of  color  of  the  two  fluids  are  then  compared  colorimet- 
rically, and  it  is  determined  in  a  measuring  cylinder  how  much  the  darker  fluid 
must  be  diluted  in  order  to  correspond  exactly  to  the  shade  of  the  other.  The 
rates  of  dilution  necessary  for  this  purpose  gives  directly  the  ratio  of  the  amount 
•of  starch  in  the  ingested  to  that  in  the  expressed  meal. 

Special  Examination  of  the  Stomach  for  **  Raw  Motility." 

Those  cases  in  which  the  ability  of  the  stomach  to  em2)ty  itself  is  impaired, 
and  where  jiyloric  stenosis  is  not  present,  are  frequently  spoken  of  as  insutficiency 
or  motor  weakness  of  the  stomach.  We  have  learned  from  v.  Mering  and 
Marbaix  that  the  emptying  of  the  stomach  is  regulated  by  the  intestine  rather 
than  by  the  stomach  itself,  since  nutritive  substances  reaching  the  intestine  effect  a 
reflex  closure  of  the  pylorus  (v.  Mering' s  reflex)  until  the  intestine  has  completed 
its  work.  It  consequently  seems  to  the  writer  to  be  inadmissible  to  regard  the  emp- 
tying of  the  stomach  as  a  jjure  question  of  strength,  as  would  be  suggested  by  the 
term  insufficiency  or  motor  weakness  of  the  stomach,  since  even  a  well-developed 
and  efficient  stomach  does  not  empty  itself  if  it  is  opposed  by  the  intestine. 
Actual  weakness  of  the  stomach  nevertheless  does  occur,  and  in  order  to  differen- 
tiate it  from  the  more  frequent  forms  of  disturbed  motility  which  proceed  from 
the  intestine,  a  special  method  of  examination  is  necessary,  which  the  writer  will 
now  give,  and  wlaich  he  has  careftilly  tested  in  recent  years.  The  motor  activity 
of  the  stomach  nuist  be  examined  under  conditions  in  which  v.  Mering' s  reflex 
does  not  occur.  As  v.  Mering  and  Marbaix  have  shown,  such  a  condition  is 
present  when  the  stomach  contains  water  alone,  since,  under  physiologic  con- 
ditions without  obstruction,  the  water  is  emptied  into  the  intestine  within  a  short 
time.  We  must  consequently  determine  the  length  of  time  required  by  the  stomach 
to  empty  itself  of  a  definite  quantity  of  water — a  half  liter,  for  example. 

Since  we  have  to  do  with  stomachs  which  do  not  empty  themselves  well,  the 

'  It  is  only  in  the  determination  by  means  of  the  polarisco])e,  whicli  for  this  purpose 
is  hardly  accurate  enough,  that  tlie  phosphotungstic  acid  need  not  be  separated,  since  it 
has  no  effect  on  the  plane  of  polarized  light. 

^  Cf.   Schu'eiz,  Ixbenfimittelbiu:h,  Bern,  Verlag  v.  Neukoinni  and  Zimmerniann,  1899. 


414    EXAMINATION  OF  THE  STOMACH  AND  STOMACH  CONTENTS. 

test  must  be  jDreceded  by  a  thorough  cleansing  of  the  organ.  The  patient  then 
drinks  the  prescribed  quantity  of  water,  the  gastric  contents  are  then  expressed  in 
a  half-hour,  and  the  quantity  passed  onward  into  the  intestine  is  thus  determined. 
Since  it  is  usually  impossible  to  empty  the  stomach  completely,  we  must  first 
determine  how  much  water  is  left  behind  from  the  cleansing  irrigation,  and  add 
this  to  the  quantity  drunk  by  the  patient,  if  correct  results  are  to  be  obtained. 
After  the  expression  of  the  gastric  fluid  we  must  also  determine  how  much  has 
escaped  expression.  These  facts  are  best  determined  colorimetrically  in  the  follow- 
ing way:  After  the  cleansing  irrigation,  about  50  c.c.  of  a  distinctly  colored  solu- 
tion of  methylene-blue  are  introduced  into  the  stomach  through  the  tube,  the 
stomach  is  gently  massaged,  and  a  small  portion  of  the  contents  are  expressed. 
The  mixture  removed  will  be  pale  blue  in  color.  Another  50  c.c.  of  the  same 
solution  are  now  diluted  with  water  until  the  same  shade  of  pale  blue  is  obtained ; 
the  amount  of  water  added  must  obviously  be  the  same  as  that  left  in  the  stomach 
by  the  cleansing  irrigation.  A  half- hour  after  the  introduction  of  the  50  c.c.  the 
fluid  is  expressed,  and  the  residue  determined  as  before.  After  we  have  expressed 
all  the  fluid  possible  (fluid  a),  100  c.c.  of  water  are  introduced  into  the  stomach, 
the  stomach  massaged  slightly,  and  the  water  again  expressed  (fluid  b).  We  now 
determine  how  much  of  the  fluid  a  must  be  added  to  100  c.c.  of  water  in  order  to 
obtain  the  same  shade  as  that  of  the  fluid  last  expressed  (fluid  b).  The  required 
amount  of  the  fluid  a  will  equal  the  quantity  of  the  residue  in  the  stomach  which 
could  not  be  expressed.  The  entire  amount  in  the  stomach  at  the  end  of  the  half- 
hour  will  be  found  by  adding  this  residue  to  the  expressed  fluid  a.  In  case  the 
expressed  fluid  a  is  no  longer  colored,  the  residue  escaping  expression  may  be 
directly  determined,  as  in  the  first  instance,  by  adding  some  of  the  original  solution 
of  methylene-blue. 

This  test  for  ' '  raw  motility ' '  must  be  carried  out  with  the  patient  in  the  upright 
position,  since  gravity  interferes  too  much  with  the  expression  if  the  patient  be 
lying  down. 

Special  Examination  of    the   Stomach  for  Pyloric  Stenosis. 

Pyloric  stenosis  is  diagnosed  much  too  frequently  nowadays  when  the  stomach 
fails  to  empty  itself  properly.  In  reality  the  case  may  be  simply  a  functional 
disturbance  of  v.  Mering's  reflex  or  a  condition  of  motor  weakness.  Moritz  has 
shown  that  the  stomach  is  an  excellent  sedimenting  ajjparatus,  and  that  in  all 
forms  of  impaired  motility  firm,  indigestible  substances  (fruit  kernels  and  other 
vegetable  constituents)  may  remain  in  it  for  days,  since  they  are  never  elevated 
to  the  level  of  the  pylorus  on  account  of  their  high  specific  gravity.  We  are 
consequently  not  justified  in  diagnosing  a  pyloric  stenosis  off'hand  from  the 
presence  of  such  old  substances  in  the  retained  gastric  contents.  A  little  reflec- 
tion will  also  show  that  the  retention  of  indigestible  substances  of  a  specific 
gravity  low  enough  to  enable  them  to  float  may  be  utilized  to  diagnose  a  pyloric 
stenosis  the  caliber  of  which  is  not  sufficient  to  allow  of  their  passage.  This  is 
the  basis  of  the  procedure  the  writer  recommends,  by  which  it  is  possible  to 
diagnose  the  existence  and  caliber  of  a  pyloric  stenosis  by  the  administration  of 
little  balls  of  cork.  The  patient  to  be  examined  for  pyloric  stenosis  is  made  to 
swallow  a  ball  of  cork  1  cm.  in  diameter.  If  the  cork  ball  be  found  in  the 
stool  the  following  day,  the  pylorus  must  be  large  enough  to  have  allowed  it  to 
pass.  On  account  of  its  low  specific  gravity,  the  cork  ball  may  easily  be  found, 
since  it  readily  floats  when  water  is  added  to  the  stool.  Certain  precautions  must 
be  observed,  however,  in  carrying  out  this  test.  After  swallowing  the  cork  the 
patient  should  lie  in  bed  for  a  half-day,  preferably  upon  the  left  side,  so  that  the 
ball  may  be  floated  upward  into  the  neighborhood  of  the  pylorus.  If  the  stomach 
is  markedly  loop-like,  it  may  be  sufficient  to  have  the  patient  lie  upon  the  left 
side  for  a  short  time,  under  the  supposition  that  the  cork  ball  is  immediately  floated 
toward  the  pylorus  and  remains  there.  The  writer  has  not  yet  employed  cork 
balls  larger  than  1  cm.  in  diameter,  for  fear  they  might  stick  in  the  esophagus. 
To  what  extent  the  caliber  of  the  ball  may  be  increased  remains  a  subject  for 
further  study. 


LOCAL  EXAMINATION  OF  THE  RECTUM.  415 


EXAMINATION    OF    THE   INTESTINE  AND    FECES. 

Inspection,  palpation,  auscultation,  and  percussion  of  the  abdomen, 
and  their  help  in  the  examination  of  the  intestine,  have  already  been 
considered  upon  pages  301  et  seq.,  304  et  seq.,  286  et  seq.,  196  et  seq., 
and  215  et  seq. 

Hence,  we  will  now  discuss  only  the  local  examination  of  the  rectum 
(digital  and  speculum  examination),  the  testing  of  the  intestinal  func- 
tions, and  the  examination  of  the  feces. 


LOCAL    EXAMINATION   OF   THE   RECTUM. 

DIGITAL    EXAMINATION    OF   THE   RECTUM. 

The  examiner  ordinarily  employs  the  index  finger,  well  lubricated, 
and,  of  course,  with  a  carefully  cut  nail.  The  patient  may  be  in  the 
dorsal  decubitus  with  the  legs  widely  separated,  resting  upon  the  small 
of  the  back  (the  latter  is  advisable,  so  that  the  examiner's  elbow  shall 
not  prevent  his  palpating  the  anterior  rectal  wall).  If,  as  is  sometimes 
more  convenient,  we  examine  with  the  patient  in  the  lateral  position, 
the  knees  should  be  well  drawn  up  to  allow  room  for  the  examiner's 
arm  in  all  directions.  The  knee-chest  position,  which  has  recently  been 
so  frequently  employed  by  the  gynecologists,  is  also  to  be  recommended, 
since  it  displaces  the  intestinal  coils  upward  and  facilitates  the  palpation 
of  the  pelvic  viscera.  For  different  purposes  and  under  different  con- 
ditions these  positions  can  be  varied  and  the  examiner's  hand  changed ; 
the  important  thing  is  that  the  entire  circumference  of  the  rectum  must 
be  palpated,  and  we  must  be  able  to  reach  up  with  the  finger  as  far  as 
possible.  The  anal  opening  should  be  inspected  before  performing  the 
digital  examination,  as  we  can  thus  often  recognize  the  presence  of  hem- 
orrhoids, prolapsus,  fistula  in  ano,  or  fissures. 

The  finger  should  be  introduced  slowly  and  carefully  with  a  gentle 
screw-like  motion,  so  as  not  to  cause  pain  or  injury.  Beginners  often 
make  the  mistake  of  not  following  the  axis  of  the  rectum  after  intro- 
ducing the  finger,  especially  when  they  try  to  palpate  as  high  up  as  pos- 
sible. They  will  then  fail  to  reach  up  very  far,  and  so  may  even  believe 
that  they  have  found  a  stenosis,  though  none  is  present.  The  anatomic 
position  of  the  rectum  should  be  remembered  and  this  error  will  be  pre- 
vented. The  direction  is  first  a  little  forward  from  the  anal  opening, 
then  backward  into  the  hollow  of  the  sacrum,  and  finally  to  the  left 
toward  the  sigmoid  flexure.  While  advancing  the  finger  we  must 
remember  to  keqi  it  always  in  the  middle  of  the  funnel  formed  by  the 
mucous  membrane.  If  feces  are  present  they  will  be  the  best  guide  as 
to  the  direction  in  which  to  advance  the  finger.  The  height  to  which 
the  palpating  finger  may  reach  depends  upon  various  factors  ;  thick, 
short  fingers  on  the  part  of  the  examining  physician,  or  much  fat  on  the 
part  of  the  patient,  are  the  chief  obstacles.     Sometimes  the  pain  of  the 


416  EXAMINATION   OF  THE  INTESTINE  AND  FECES. 

examination  or  the  spasmodic  contraction  of  the  sphincter  Mill  prevent 
an  effective  examination.  Only  in  exceptional  cases  is  it  allowable  to 
introduce  two  fingers.  The  introduction  of  the  whole  hand  under  anes- 
thesia (after  Simon)  has,  so  far  as  we  know,  been  discarded  as  too  dan- 
gerous a  method. 

Digital  examination  reveals  first  of  all  the  more  crude  anatomic 
changes — carcinoma  of  the  rectum,  other  tumors  and  ulcerations  of  the 
rectum,  rectal  polyps  which  are  not  situated  too  high  up,  an  invagina- 
tion which  has  reached  down  as  far  as  the  rectum.  Large  internal 
hemorrhoidal  masses  may  also  be  felt ;  but  unless  thrombosed  it  requires 
considerable  dexterity  to  differentiate  them  with  certainty  from  the  nor- 
mal inequalities  of  the  rectal  mucous  membrane.  Superficial  ulcerative 
processes  are  quite  as  difficult  to  appreciate  by  palpation. 

In  a  case  of  intestinal  obstruction,  considerable  distention  of  the  rectum 
points  strongly  to  fecal  rather  than  some  other  type  of  intestinal  obstruc- 
tion. If  fecal  masses  have  pushed  down  into  the  rectum  and  the  gen- 
eral symptoms  of  obstruction  have  improved,  our  prognosis  immediately 
becomes  more  favorable,  even  before  any  feces  have  been  evacuated.  An 
extremely  painful  digital  examination  would  suggest  inflammatory 
changes  of  the  rectum.  If  slimy,  purulent,  or  bloody  masses  adhere  to 
the  finger  when  withdrawn,  this  diagnosis  is  still  more  strongly  sug- 
gested. A  microscopic  examination  of  the  material  adhering  to  the 
withdrawn  finger  will  sometimes  aid  in  the  diagnosis  of  tubercular  or 
dysenteric  changes,  and  perhaps  be  more  serviceable  than  the  examina- 
tion of  the  feces,  especially  if  the  rectum  has  been  just  cleaned  of  fecal 
matter  by  an  enema  (pus,  tubercle  bacilli,  ameba?).  (Compare  Exami- 
nation of  Feces,  p.  427.) 

A  careful  rectal  examination  is  important  in  diseases  of  the  nervous 
system.  The  amount  of  distention  of  the  rectum,  the  sphincter  tonus, 
and  the  sensitiveness  of  the  rectal  mucous  membrane  tell  of  the  condi- 
tion of  the  rectal  activity  (function).  This  information  is  the  more 
important,  as  the  character  of  defecation  and  the  shape  of  the  stools 
depend  not  only  upon  the  rectum,  but  upon  the  influence  of  the  bowel 
above. 

In  examining  the  rectum  we  must  also  try  to  obtain  information  regarding  the 
condition  of  the  neighboring  organs — the  prostate  and  seminal  vesicles  in  the 
male,  the  uterus,  tubes,  and  ovaries  in  the  female.  A  careful  rectal  examination 
will  generally  obviate  the  necessity  of  a  vaginal  examination  in  a  virgin. 

EXAMINATION  WITH  THE  SPECULUM. 

With  the  aid  of  a  so-called  rectal  speculum  the  examiner  can  see  the  inner 
surface  of  the  rectum  directly.  Eectal  specula  are  made  quite  like  vaginal  spec- 
ula— tubular,  bivalve  or  duck-bill-shaped,  or  many  valved.  They  may  also  con- 
sist of  two  separate  spoons.  The  speculum  should  first  be  warmed  and  well  oiled, 
and  then  carefully  introduced  into  the  axis  of  the  rectum.  With  an  ordinary 
head  mirror  a  good  light  can  be  reflected,  and  the  rectal  mucous  membrane  at  the 
end  of  the  speculum  carefully  examined.  The  position  of  the  patient  will  be 
varied  according  to  the  part  of  the  rectum  to  be  examined,  either  the  lateral, 
the  usual  dorsal  gynecologic  position,  or  sometimes  the  knee-chest  position.  The 
advantage  of  the  knee-chest  position  is  that  the  rectum  is  relieved  by  the  intes- 


LOCAL  EXAMINATION  OF  THE  RECTUM.  417 

tines  dropping  forward,  and  so  is  more  accessible  to  examination.  In  difficult 
cases  tlie  speculum  examination  should  always  be  tried  in  this  position.  The 
speculum  should  be  introduced  very  carefully  and  slowly.  The  many-valved 
specula  must  be  furnished  with  an  obturator  before  being  introduced,  for  other- 
wise they  easily  pinch  and  injure  the  mucous  membrane. 

Examination  with  a  speculum  is  difficult  on  account  of  the  limitation  of  the 
field  of  vision,  and  the  fact  that  the  parts  are  usually  in  an  abnormal  position 
and  under  abnormal  tension.  The  results  are  therefore  rather  meager.  Peristal- 
sis of  the  rectum  is  often  caused  by  the  irritation  of  the  speculum,  especially  in 
inflammatory  affections,  so  that  it  is  very  difficult  to  adjust  the  instrument.  Pal- 
pation reveals  many  of  the  changes,  and  others  (inflammatory,  superficial  ulcers) 
are  just  the  most  difficult  to  recognize  with  a  speculum,  for  the  pressure  of  the 
instrument  causes  considerable  congestion,  altering  the  color,  and  in  the  case  of 
ulcers  oftentimes  brings  on  hemorrhage,  which  covers  the  field  of  vision  again  and 
again  even  if  sponged  off'  continuously.  The  bivalve  duck-billed  speculum  usu- 
ally affords  a  better  view,  but  its  employment  always  requires  the  aid  of  an 
assistant. 

A  detailed  description  of  the  possibilities  of  speculum  examination 
of  the  rectum  by  means  of  a  complicated  "  Rectoscope  "  provided  with 
electric  illuminating  appliances  may  be  found  in  the  recent  monograph 
of  J.  Schreiber,  Die  Rector amanoskopie,  Berlin,  Hirschwald,  1903. 

INSUFFLATION  OF  THE  RECTUM. 

Insufflation  of  the  rectum  is  best  accomplished,  as  described  on  page  306,  with 
a  Davidson  syringe.  It  aids  in  determining  the  position  of  the  sigmoid  flexure 
and  of  the  colon.  When  inflated  they  can  be  seen  to  stand  out  against  the  ante- 
rior abdominal  wall,  separate  from  the  surrounding  parts,  and  may  be  mapped 
out  by  percussion  and  palpation.  The  position  of  abnormal  tumors,  especially  in 
relation  to  their  origin  in  the  colon,  the  sigmoid  flexure,  or  the  kidney  (compare 
p.  310),  can  often  be  determined  by  the  aid  of  this  method.  It  does  not  tell  very 
much  about  the  condition  of  the  rectum  itself,  even  for  the  diagnosis  of  stenosis 
of  the  rectum.  For  moderate  stenoses— which  are  just  the  ones  so  difficult  to 
diagnose — offer  no  obstruction  to  insufflation,  while  very  pronounced  or  imperme- 
able stenoses  can  be  easily  enough  diagnosed  without  insufflation.  This  method  is 
of  little  value  even  for  determining  the  seat  of  such  obstruction.  If  it  is  impos- 
sible to  introduce  any  considerable  quantity  of  air  into  the  rectum,  a  low  position 
of  the  obstruction  has  generally  been  assumed;  but  if  the  stenosis  is  pronounced, 
there  will  be  so  much  abdominal  distention  that  it  will  prevent  the  distention  of 
the  rectum  even  if  the  obstruction  is  high  ujj. 

INJECTIONS  OF  WATER  INTO  THE  RECTUM   AND 
RECTAL   LAVAGE. 

Introducing  fluids  to  determine  the  rectal  capacity  or  the  seat  of  a  stenosis  is 
even  less  valuable  than  inflation  because  the  rectum  is  generally  less  tolerant  of 
fluids  than  of  air.  By  irrigating  the  rectum  and  then  picking  out  any  suspicious 
tragments  from  the  wash  water  to  be  examined  microscopically,  we  can  sometimes 
find  cells  from  a  high-seated  carcinoma.  It  is  best  to  cleanse  the  rectum  thoroughly 
with  an  enema  and  to  administer  a  mild  laxative  the  day  before^ 

SOUNDING  OF  THE   RECTUM. 

If  an  obstruction  is  situated  low  down,  a  rectal  bougie  will  give  no 

more    satisfactory    results  than    an   ordinary  digital    examination.     If 

seated  higher  up,  we  can   never  tell  accurately   whether  the   bougie  is 

impeded  by  a  pathologic  stenosis  or  by  some  physiologic  obstruction,  as 

27 


418  EXAMINATION  OF  THE  INTESTINE  AND  FECES. 

is  very  often  the  ease.  The  elastic  metal  intestinal  tubes  constructed 
with  a  spiral  spring  have  been  advocated  by  F.  Kuhn  ^  for  rectal  work. 
Their  practical  value  has  hardly  been  proved. 

EXAMINATION  OF  THE  INTESTINAL  FUNCTIONS. 
EXAMINATION  OF  THE  MOTILITY  OF   THE  INTESTINES. 

Inspection  and  auscultation  of  the  abdomen  will  tell  something 
about  the  motility  of  the  intestines  (see  p.  302  et  seq.  and  p.  286).  We 
must  also  depend  as  well  upon  the  examination  of  the  feces  (see  422 
et  seq.).  Of  course,  conclusions  in  regard  to  the  intestinal  motility  are 
given  by  the  passage  of  flatus  as  well  as  by  the  passage  of  feces.  The 
intestinal  motility  is  certainly  not  directly  proportional  to  the  frequency 
of  passing  flatus,  for  this  depends  to  a  far  greater  degree  upon  the  pro- 
duction of  gas  in  the  intestine ;  yet,  at  the  same  time,  a  free  and  abun- 
dant passage  of  gas  indicates  good  intestinal  motility,  while  a  complete 
inability  to  evacuate  any  flatus,  which  is  so  annoying  to  the  patient  on 
account  of  the  associated  distention,  proves  some  impairment  in  intes- 
tinal motility.  This  latter  condition  (see  p.  422)  is  important  in  the 
types  of  ileus  where  solid  or  fluid  evacuations  still  take  place  (fecal 
matter  coming  from  below  the  obstruction),  but  where  the  absence  of 
evacuated  gas  presents  such  a  contrast  as  to  furnish  a  very  significant 
symptom  of  obstruction. 

To  obtain  more  information  about  the  intestinal  motility,  certain  substances, 
such  as  charcoal,  milk,  or  lycopodium,  are  ingested  at  a  definite  time,  and  the 
stools  watched  to  determine  the  interval  required  for  these  substances  to  appear. 
Charcoal  will  be  recognized  by  the  black  color,  milk  by  the  light-yellow  color, 
and  lycopodium  by  the  characteristic  tetrad  shapes  of  its  spores  under  the  micro- 
scope. The  charcoal  and  the  lycopodium  should  be  administered  directly  after 
eating,  but  the  milk  between  meals,  as  far  apart  as  posssible.  Of  course,  the 
character  of  the  gastric  motility  must  be  taken  into  account  in  judging  of  the 
results  of  this  test. 

EXAMINATION    OF    THE    CHEMISTRY    OF    THE    INTESTINE    AND 
OF  ABSORPTION  IN  THE  INTESTINE. 

The  careful  examination  of  the  feces  will  aid  in  determining  the 
intestinal  chemistry,  especially  with  reference  to  the  utilization  of  the 
food  (see  p.  438) ;  but  even  so,  we  are  not  able  to  estimate  the  influ- 
ence of  the  length  of  time  the  food  remains  in  the  intestine.  Examin- 
ing the  feces  for  any  digestive  enzymes  will  be  of  no  assistance  in 
judging  the  intestinal  chemistry,  because  most  of  the  enzymes  are 
destroyed  in  the  intestinal  canal,  as  is  explained  on  p.  445.  The  exam- 
ination of  the  chemical  changes  brought  about  by  intestinal  bacteria  is 
as  yet  impracticable.  Even  the  tiresome  process  of  a  complete  meta- 
bolic investigation  (see  the  fundamental  examinations  of  v.  Noorden  ^) 
does  not  always  allow  of  but   one  deduction  in  judging  of  intestinal 

iSee  Berlin.  Min.  WocL,  1898,  No.  2,  p.  27. 

2  Gnindrhs  einer  Methodik  den  StnffwechseU,  Berlin,  1892 ;  Lehrbuch  der  Path.  desStoff- 
wechsels,  Berlin,  1893;  Zeits.f.  Min.  Med.,  1890,  p.  137. 


EXAMINATION  OF  THE  INTESTINAL  FUNCTIONS.  419 

digestion,  because  it  furnislies  results  both  of  stomach  and  intestinal 
digestion.  The  same  difficulty  also  applies  to  the  conclusions  which  may- 
be drawn  regarding  metabolic  changes,  since  these  also  are  affected  by 
variations  in  the  absorption  and  motility  of  the  whole  gastro-intestinal 
tract.  Neither  are  we  justified  in  deducing  from  the  amount  of  urea 
eliminated  the  absolute  degree  of  metabolism,  nor  the  sum  total  of  the 
digestive  processes  taking  place  in  the  organism. 

EXAMINATION  OF   THE  INTESTINAL   DIGESTION   BY  MEANS  OF  THE 
GLUTOID  CAPSULES. 

For  a  long  time  the  writer  lias  been  interested  in  the  problem  of  obtaining 
some  direct  evidence  in  regard  to  the  chemical  activity  of  the  intestines,  especially 
with  reference  to  proteid  digestion.  For  the  small  intestine  he  has  employed  the 
glutoid  capsules,  which  are  made  from  gelatin  (glutoid)  hardened  with  formaldehyd. 
They  either  do  not  dissolve  in  the  gastric  juice  at  all,  or  only  after  a  considerable 
time,  but  they  are  rather  quickly  soluble  in  the  intestinal  juices.^  They  take  the 
place  of  the  pills  coated  with  keratin  to  prevent  the  action  of  the  gastric  juice, 
which  formerly  were  employed  but  which  have  not  proved  successful.  These  glu- 
toid capsules  may  be  utilized  to  diagnose  the  condition  of  the  intestinal  digestion — 
i.  e.,  the  pancreatic  function.  They  are  filled  with  some  substance  which  will  not 
diflPiise  through  the  capsule-wall,  and  whose  absorption  may  be  studied  from  an  ex- 
amination of  the  saliva  or  the  urine.  Substances  containing  iodin  are  best  adapted 
for  this  purpose.  Iodoform  has  given  the  author  the  best  results.  It  is  absorbed 
both  from  the  stomach  and  the  intestines  in  a  veiy  short  time,  within  from  one- 
quarter  to  one  and  one-quarter  hours.  After  the  ingestion  of  0.15  gm.  of  iodoform, 
a  marked  iodin  reaction  can  be  obtained  in  the  saliva  or  in  the  urine  (especially 
well  in  the  former)  with  chloroform  and  nitric  acid  (see  p.  501).  Iodoform  has 
another  great  advantage  in  that  it  cannot  penetrate  the  glutoid  capsules. 

Salol  answers  veiy  well  for  the  same  purpose,  for,  within  one  to  one  and  one- 
half  hours  after  the  ingestion  of  0. 5  gm.  of  salol  salicylic  acid,  it  can  be  demon- 
strated in  the  urine  with  ferric  chlorid  as  salicyluric  acid  (see  p.  502).  So  that  nor- 
mally after  the  glutoid  capsule  has  been  dissolved  by  the  pancreatic  juice,  the  iodin 
reaction  will  be  demonstrable  in  the  saliva  at  the  latest  within  one  and  one-quarter 
hours  if  0. 15  gm.  of  iodoform  has  been  administered,  and  the  salicyluric  reaction 
can  be  demonstrated  in  the  urine  within  one  and  one-half  hours  after  the  admin- 
istration of  0.5  gm.  of  salol.  For  diagnostic  purposes  glutoid  capsules  with  0.15 
gm.  of  iodoform  and  2. 3  degrees  of  hardening  are  the  best  adapted.  For  children, 
capsules  containing  0. 15  gm.  of  iodoform  may  be  used,  or  0.05  gm.  of  iodoform  and 
0. 25  gm.  of  salol,  so  as  to  test  for  the  salicyluric  reaction  in  the  urine.  Adults 
should  take  2  or  3  of  these  capsules  in  order  to  obtain  sufficient  salol.  The 
following  remarks  refer  to  capsules  of  the  above-mentioned  degree  of  hard- 
ening. 

In  order  to  make  the  conditions  as  constant  as  possible  in  regard  to  the 
length  of  time  that  the  capsules  remain  in  the  stomach  and  in  regard  to  the 
degree  of  digestive  stimulation,  it  is  advisable  to  administer  them  with  an  Ewald 
test  breakfast  (p.  367).  Experience  has  shown  that  normally,  under  the  best 
conditions  possible — i.  e.,  normal  gastric  motility,  normal  intestinal  digestion,  and 
normal  intestinal  absorption — the  iodin  reaction  may  be  expected  to  appear  in  the 
saliva,  and  the  salicyluric  reaction  in  the  urine,  in  from  four  to  six  hours.  If 
one  wishes  to  test  the  accuracy  of  the  capsules  obtained  from  the  shops,  he  must 
prove  that  the  reactions  are  obtained  within  this  length  of  time  in  healthy 
individuals.  Only  rough,  approximate  differences  in  the  time  of  the  reaction  are 
of  diagnostic  importance,  so  that  it  is  sufficient  to  examine  the  saliva  after  six, 

^  Deutsch.  med.  Woch.,  1897,  No.  1  ;  Correspondenzbl.  f.  Schiveizer  Aerzie,  1898,  No.  10; 
Deutseh.  Arch.  f.  klin.  Med.,  vol.  Ixi.,  1898. 


420  EXAMINATION  OF  THE  INTESTINE  AND  FECES. 

eight,  ten,  and  twenty-four  hours.  If  we  wish  to  make  the  test  as  accurate  as 
possible,  it  is  perhaj^s  advisable  to  administer  the  caj^sules  in  the  morning,  upon 
an  empty  stomach,  and  then  four  hours  later  allow  the  patient  to  eat  as  usual. 
The  si^ecimens  of  saliva  and  urine  may,  of  course,  be  saved  and  all  examined 
afterward. 

Before  drawing  conclusions  in  regard  to  the  intensity  of  the  pancreatic 
digestion — i.  e. ,  the  rapidity  with  which  the  contents  of  the  capsule  are  absorbed — 
we  must,  of  course,  be  sure  that  within  six  hours  the  capsules  are  dissolved 
neither  by  the  gastric  juice  nor  by  any  chemical  agency  in  the  intestine  other 
than  the  pancreatic  secretion.  This  condition  obtains,  for  it  has  been  proved  that 
these  capsules  can  resist  a  strong  gastric  digestion  for  at  least  seven  to  eight  hours, 
and  the  putrefactive  changes  in  the  intestine  for  twenty-four  hours.  AVhen  they 
are  introduced,  together  with  an  Ewald  test  breakfast,  into  a  stomach  with  normal 
motility,  they  do  not  remain  in  the  stomach  longer  than  one  hour,  but  swell  up  in 
the  gastric  contents  and  are  readily  floated  through  the  pylorus.  Before  we  can 
obtain  trustworthy  data  in  reference  to  intestinal  digestion,  we  must  necessarily 
know  that  the  stomach  em^Dties  itself  within  the  normal  period  of  time.  A  delayed 
reaction  can  never  be  accurately  referred  to  impaired  intestinal  digestion  unless  the 
function  of  the  stomach  has  been  previously  tested  carefully  by  means  of  the 
stomach  tube.  In  this  connection  no  method  of  gastric  examination  is  admissible 
in  which  the  stomach  tube  is  not  employed.  If  there  is  motor  insufficiency 
of  the  stomach,  a  retarded  reaction  is  to  be  ascribed  to  the  delay  of  the  caj^sule 
within  the  stomach,  whether  it  has  been  dissolved  there  or,  later  on,  in  the 
intestine. 

Individual  differences  in  the  rapidity  of  the  excretion  of  the  iodin  and  sali- 
cylic acid  are  not  responsible  for  any  particular  error  in  the  experiment,  because 
as  soon  as  these  substances  get  into  the  circulation  the  reaction  appears  in  the 
saliva  very  quickly.  Another  factor  in  the  experiment  which  is  important  is  the 
rapidity  with  which  the  iodoform  is  absorbed  after  the  capsule  has  been  dissolved 
by  the  pancreatic  juice.  The  glutoid-capsule  test  gives  us,  therefore,  the  result- 
ant of  the  power  of  the  pancreatic  digestion  and  the  absorptive  power  of  the 
intestine.  If  we  wish  to  determine  the  latter  alone,  we  can  repeat  the  test  on 
another  day,  when  we  are  sure  that  the  saliva  no  longer  gives  an  iodin  reaction, 
administering  the  iodoform  plain,  not  enclosed  in  a  glutoid  capsule,  but  with  a 
glass  of  water,  on  an  empty  stomach.  From  v.  Mehring'  s  experiments  we  know 
that  the  result  will  largely  depend  on  the  absorbing  power  of  the  intestine.  Absorp- 
tion is  usually  rapid,  provided  the  stomach  is  normal,  so  that  when  the  hardened 
glutoid  capsules  are  used  the  result  depends  almost  entirely  on  the  intensity  of 
the  pancreatic  digestion. 

The  results  obtained  from  this  method  of  examination  are  interesting.  Even 
when  the  stomach  contents  contained  no  free  hydrochloric  acid  or  pepsin,  the  reac- 
tion was  not  delayed  so  long  as  the  gastric  motilitj'  was  good.  The  remarkably  good 
state  of  nutrition  of  such  patients,  and  the  result  of  such  a  test,  prove  that  the 
intestinal  digestion  may  perform  vicariously  the  entire  gastric  function.  In  cases 
of  diarrhea  due  only  to  an  increased  peristalsis,  without  any  marked  disturbance 
of  intestinal  digestion,  the  reaction  is  either  normal  or  even  somewhat  hastened. 
In  other  types  of  diarrhea  characterized  by  an  involvement  of  the  intestinal 
chemistry  or  intestinal  absorption,  the  reaction  is  either  absent  or  distinctly 
delayed.  In  the  former  case  the  undigested  capsules  are  often  found  in  the 
feces,  together  with  microscopically  visible  undigested  food  remnants.  This 
method  also  aids  in  diiferentiating  an  icterus  due  to  occlusion  of  the  ductus  choled- 
ochus  at  its  point  of  entrance  into  the  intestine  from  one  where  the  obstruction 
to  the  bile  flow  is  higher  up  near  the  liver.  In  the  former  case  the  digestion  of 
the  capsules  maybe  interfered  with  because  the  pancreatic  duct  is  simultaneously 
plugged.  Of  course,  the  pancreas  may  have  a  separate  exit  of  its  own,  besides 
the  one  in  common  with  the  choledochus.  The  test  also  aids  in  the  diagnosis  of 
pancreatic  aflections — e.  g.,  in  several  cases  of  carcinoma  of  the  jjancreas  which 
we  have  observed,  a  negative  result  has  supported  a  presumptive  diagnosis  of 
such  a  position  for  the  tumor.     Circumscribed  carcinoniata  of  the  pancreas  do 


EXAMINATIfjy   OF  THE  12^'TESTIXAL  FUNCTIONS.  421 

not  necessarily  occlude  the  duct,  however,  so  that,  of  course,  a  positive  result  of 
the  glutoid  reaction  will  not  exclude  cancer  of  the  pancreas. 

BOAS'  METHOD    OF  OBTAINING  INTESTINAL  JUICE,  i 

Boas  has  shown  that  it  is  often  possible,  both  in  healthy  and  sick  persons,  to 
obtain  enough  of  the  secretion  in  the  upper  part  of  the  small  intestine  for  an 
examination  of  the  pancreatic  juice,  bile,  and  succus  entericus.  This  method 
depends  upon  the  fact  that,  as  Boas  and  others  have  found,  the  pyloric  sphincter 
can  often  be  overcome  easily  by  a  very  moderate  straining,  so  that  the  duodenal 
contents  enter  the  stomach.  As  the  duodenum,  like  the  empty  stomach,  often 
contains  preformed  secretion,  it  is  sometimes  possible  to  force  this  into  the  stom- 
ach by  the  patient  straining  gently.  The  examiner  can  help  a  little  by  massage 
of  the  duodenal  region.  The  technic  of  the  procedure  is  as  follows  :  The  stom- 
ach tube  is  first  introduced  and  the  stomach  washed  with  a  1  per  cent,  solution 
of  sodium  carbonate.  With  the  patient  in  the  dorsal  decubitus  position,  the 
region  under  the  right  costal  arch,  between  the  mammary  and  parasternal  lines, 
is  massaged  from  right  to  left  for  several  minutes,  and  then,  after  the  tube  has 
been  introduced,  the  patient  expels  the  gastric  contents  in  the  ordinary  way  by 
the  help  of  coughing  or  straining.  With  such  a  method  we  can  often  obtain  40 
to  50  c.c.  of  a  neutral,  alkaline,  or  weakly  acid  fluid.  The  acid  reaction  is  due 
partly  to  the  irritation  of  the  tube  and  partly  to  the  presence  of  preformed  gas- 
tric juice.  The  fluid  is  usually  stained  strongly  with  bile.  We  can  prove  that 
it  is  duodenal  by  demonstrating  a  typical  proteolytic,  lipolytic,  and  diastatic 
action.  The  presence  of  trypsin  can  be  very  easily  proved  ;  but  the  demonstra- 
tion of  the  lipolytic  and  of  the  diastatic  enzymes  has  not  been  universally  suc- 
cessful. For  examination  the  fluid  must,  if  necessary,  be  rendered  distinctly 
alkaline  as  soon  as  possible  by  the  addition  of  a  weak  sodium  carbonate  solution 
(so  as  to  prevent  any  of  the  trypsin  being  destroyed  by  pepsin).  Trypsin  can  be 
most  easily  demonstrated  by  digesting  in  the  alkaline  fluid,  at  incubator  tempera- 
ture, a  flake  of  fibrin  stained  with  Magdala-red.  The  fibrin,  which  is  dissolved 
by  the  typical  digestion  process,  colors  the  fluid  red. 

Arthus  and  Huber  have  announced  another  method  ^  for  demonstrating  the 
action  of  trypsin.  Fresh  fibrin  is  prepared  by  whipping  freshly  drawn  horse 
blood,  and  then  washing  the  coagulum  with  water  until  it  becomes  colorless.  It 
is  finally  completely  covered  and  allowed  to  stand  for  twenty-four  hours,  at  40° 
C,  in  a  2  per  cent,  solution  of  sodium  fluorid,  then  filtered.  We  thus  obtain 
a  solution  of  fibrin  in  sodium  fluorid  which  will  keep  for  months.  The  fluid 
which  is  to  be  examined  for  trypsin  is  first  diluted  with  an  equal  volume  of  a  2 
per  cent,  solution  of  sodium  fluorid,  and  one  volume  of  this  dilution  is  added  to 
two  to  three  volumes  of  the  fibrin  solution,  and  the  whole  mixture  digested  for  a 
considerable  time  at  40^^  C.  If  trypsin  is  present  in  the  fluid,  crystals  or  crusts 
of  tyrosin  will  form  on  the  walls  of  the  vessels.  The  crystals  may  often  be  recog- 
•  nized  by  the  naked  eye.  In  addition  to  their  shape  (see  Fig.  173),  they  are 
characterized  by  their  appearing  light  on  a  dark  background  in  the  polarizing 
microscope  (with  crossed  nicols).  One  advantage  of  this  procedure  is  that  the 
digestive  mixture  remains  sterile  for  an  unlimited  length  of  time,  owing  to  the 
antiseptic  qualities  of  the  sodium  fluorid. 

Griitzner-Gamgee  recommended  the  following  method  to  demonstrate  lipolytic 
activity  :  An  emulsion  of  10  parts  of  oil,  5  parts  of  gum,  and  35  parts  of  water  is 
prepared  ;  also  a  neutral  solution  of  litmus,  which,  in  test  tubes  of  12  mm. 
diameter,  appeats  violet  against  white  paper.  Ten  cubic  centimeters  of  such  a 
litmus  solution  and  5  drops  of  the  emulsion  are  placed  in  several  of  these  tubes  ; 
and  increasing  quantities — e.  g.,  2,  4,  8,    16,  and  32  drops — of  the  fluid  to  be 

^  Boas'  "Ueber  Darmsaftgewinnung  beim  Menschen,"  Centralbl.  f.  hlin.  Med.,  vol.  x., 
1889,  No.  6,  p.  97.  The  f^arae,  Zeitn.  f.  kiln.  Med,  1890,  vol.  xvii.,  p.  lo5  ;  also  Tschelenofi; 
"  Ueber  Darmsaftgewinnung  beim  Menschen,"  Corresprmdenzbl.  j.  Scliweizer  Aerzte  1889, 
No.  6,  p.  161. 

2  Arch,  de  Physiol.,  1894,  p.  622. 


422  EXAMINATION   OF  THE  INTESTINE  AND  FECES. 

examined  are  added  to  the  successive  test  tubes.  They  are  then  immediately  set 
in  a  water  bath  at  37°  C.  After  a  few  moments  the  different  tubes  are  compared. 
If  any  fat-splitting  ferment  is  present,  the  color  of  the  fluid  will  have  turned 
redder  the  larger  the  amount  of  solution  added. 

To  demonstrate  diaatatic  action,  increasing  amounts  of  the  fluid  to  be  exam- 
ined are  added  to  a  thin  starch  paste,  and  the  whole  kept  at  38°  C.  If  a  minimal 
amount  of  iodin  is  then  added  to  this  mixture  and  no  violet  color  appears  (see  p. 
371),  we  obtain  evidence  that  a  diastatic  action  has  taken  place.  Again,  the 
presence  of  dextrose,  as  shown  by  Trommer's  test,  will  prove  the  same  thing 
(see  p.  482  et  seq.). 

Although  it  is  an  interesting  fact  that  intestinal  juice  may  be  obtained  in  this 
manner,  the  procedure  is  not  sufficiently  developed  to  enable  us  to  study  intesti- 
nal digestion  in  this  way,  and  it  seems  improbable  that  it  ever  will  be,  since 
the  results  obtained  are  dependent  upon  entirely  too  many  factors  which  are 
difficult  of  estimation.  If  a  juice  containing  active  trypsin  be  obtained,  the  most 
that  can  be  said  is  that  it  demonstrates  a  patulous  condition  of  the  pancreatic 
duct,  just  as  does  the  reaction  with  glutoid  capsules  (p.  419). 

EXAMINATION    OF   THE   FECES; 

FREQUENCY  OF    MOVEMENTS?  DIARRHEA;    CONSTIPATION; 
AMOUNT  OF  FECES. 

There  is  considerable  variation  in  the  frequency  of  the  bowel  move- 
7fients  within  the  bounds  of  health.  Some  absolutely  healthy  people  have 
a  movement  of  the  bowels  only  once  in  two  or  three  days,  others  have 
several  every  day.  There  is  no  sharp  line  of  distinction  in  either  direc- 
tion between  the  pathologic  and  physiologic.  The  term  constipation  is 
usually  restricted  to  a  condition  of  infrequent  movements  which  is  asso- 
ciated with  certain  other  difficulties  or  which  does  not  bear  a  proper 
relation  to  the  quantity  of  food  taken ;  in  the  same  way,  the  term 
diarrhea  is  employed  only  when  the  movements  are  not  only  frequent, 
but  also  liquid.     Infants  normally  have  two  or  three  movements. 

Other  things  being  equal,  the  frequency  of  the  movements  depends 
upon  the  amount  of  fluid  ingested.  In  starving  individuals  the  number 
is  reduced  to  a  minimum;  and  in  many  and  most  varied  diseases  a 
more  or  less  developed  state  of  starvation  may  be  developed.  For 
instance,  an  individual  who  vomits  everything  is  practically  starving. 
In  the  same  way,  a  gastric  case  or  that  of  any  other  severely  ill  indi- 
vidual, who  takes  little  on  account  of  lack  of  appetite  or  because  he 
cannot  retain  anything,  is  to  be  considered  as  a  starvation  case. 

Diseases  which  lead  to  constipation  are  :  gastric  and  intestinal  catarrh 
(especially  chronic),  gastric  dilatation,  intestinal  obstruction  of  various 
sorts,  peritonitis,  meningitis  and  other  diseases  which  increase  the 
cerebral  pressure.  Sometimes  constipation  becomes  a  more  or  less 
independent  disease  (chronic  constipation),  the  nature  of  which  has  not 
yet  been  explained. 

A  complete  absence  of  movements  is  generally  characteristic  of  some  kind  of 
intestinal  obstruction.  Not  infrequently,  however,  fecal  material  may  be  evacuated 
from  the  section  of  the  intestine  below  the  obstruction.     Continuous  diarrhea  is 

*  Consult  J.  Schmidt  and  J.  Strassburger,  Die  Faces  des  Menschen,  Berlin,  Hirsch- 
wald,  1901. 


EXAMINATION  OF  THE  FECES.  423 

characteristic  of  some  types  of  obstruction,  especially  in  invaginations,  in  complete 
axis  rotation,  or  in  case  something  is  jammed  in  the  gut.  But  these  movements 
are  really  not  fecal  in  character  ;  they  consist  of  serous  or,  often,  bloody  masses 
from  the  lower  intestinal  segment,  due  to  the  venous  congestion  at  the  seat  of 
lesion.  The  character  of  the  movements,  and  especially  the  absence  of  the  j)as- 
sage  of  gas,  should  be  sufficient  to  justify  the  diagnosis  of  obstruction. 

Diarrhea  occurs  in  acute  and  chronic  gastric  and  intestinal  catarrh, 
in  certain  types  of  chronic  peritonitis,  in  intestinal  tuberculosis,  intestinal 
amyloid  degeneration,  cirrhosis  of  the  liver,  cholera,  typhoid  fever, 
dysentery,  many  other  infectious  diseases,  and  uremia. 

The  daily  quantity  of  the  feces  passed,  other  things  being  equal,  is 
directly  proportional  to  the  amount  of  food  ingested.  The  volume  of  the 
individual  movements  is  generally  inversely  proportional  to  the  number. 

There  are,  however,  numerous  exceptions  to  the  first  of  these  state- 
ments— e.  5'.,  in  patients  who  vomit  often,  much  less  is  evacuated  in  the 
movements  than  is  ingested.  Again,  in  severe  forms  of  diarrhea,  espe- 
cially cholera,  much  more  is  evacuated  than  is  ingested,  because  in  addi- 
tion to  the  food  residue  there  are  the  secretions  and  exfoliation  of  the 
intestinal  mucous  membrane.  The  admixture  of  blood  may  also  increase 
the  quantity  of  the  feces. 

In  diarrhea  the  individual  movements  vary  in  volume  and  frequency 
according  to  whether  the  disease  is  localized  in  the  upper  or  lower  intes- 
tine. In  diseases  of  the  lower  part  of  the  colon  (dysentery  is  a  type) 
the  individual  evacuations  are  not  very  voluminous,  but  they  are  very 
frequent,  on  account  of  the  continuous  reflex  tenesmus.  In  diseases  of 
the  upper  intestine  each  evacuation  is  more  profuse,  but  they  do  not 
occur  so  frequently — e.  g.,  typhoid — because  there  is  not  the  same  per- 
sistent desire  to  empty  the  rectum.  These,  so  to  speak,  "profuse" 
diarrheas  may  be  found  in  involvement  of  the  upper  portion  of  the  colon 
as  well  as  of  the  small  intestine. 

After  a  period  of  marked  constipation  quite  incredible  quantities 
of  feces  are  often  passed. 

CONSISTENCE  AND  SHAPE  OF  FECES;  STRATinCATION  OF 
LIQUID  MOVEMENTS. 

The  normal  consistence  and  shape  of  feces  is  well  known.  The  con- 
sistence is  hard  in  constipation,  fluid  in  diarrhea.  Between  these 
extremes  are  all  sorts  of  intermediate  steps — e.  g.,  small  fecal  balls  like 
sheep  dung,  which  occur  in  intense  constipation,  from  the  tightly  packed 
fecal  matter  becoming  friable.  On  the  other  hand,  dry  fecal  masses 
may  be  of  very  unusual  volume  in  constipation  if  a  large  quantity  of 
feces  stagnate  in  the  rectum  and  distend  it  mechanically.  In  intestinal 
stenosis  but  a  short  way  above  the  anus  the  fecal  masses  have  a  dimin- 
ished transverse  diameter ;  but  if  the  stenosis  is  high  up  the  fecal 
matter  changes  its  shape  again  below  the  obstruction.  Leichtenstern 
has  justly  called  attention  to  the  fact  that  a  small  caliber  of  the  fecal 
masses  may  be  found  also  in  inanition  (starvation  feces)  and  in  rectal 
tenesmus. 


424  EXAMINATION  OF  THE  INTESTINE  AND  FECES. 

Very  liquid  diarrheal  movements  often  stratify  themselves  with  the 
liquid  constituents  in  an  upper  layer,  and  the  solid  food  residue  in  the 
lower.  Frequently^  however,  the  formation  of  layers  is  due  simply  to 
an  admixture  with  urine. 

COLOR  AND    GENERAL   APPEARANCE   OF   THE  STOOLS. 

The  normal  color  of  the  stools  of  an  adult  is  dark  brown.  This 
color  is  not  due  to  biliary  pigment,  but  to  its  secondary  products 
(urobilin,  etc.).  Infants'  stools  are  normally  light  yellow  or  golden 
yellow,  because  they  contain  unaltered  bilirubin. 

The  color  of  the  feces  varies  more  or  less  according  to  the  nature  of  the  food. 
A  milk  diet  gives  a  light  color  to  the  stools  ;  abundant  consumption  of  red  wine, 
blueberries,  blackberries,  or  black  cherries,  on  the  other  hand,  gives  them  a  dark 
color.  Food  rich  in  chlorophyll  (vegetables)  generally  produces  a  green  or  olive 
shade  in  the  stool.  Drugs  may  also  change  the  color  of  the  feces.  Extractum 
ligni  Campechiani  produces  a  reddish-brown  color  in  the  stools.  Calomel  is  apt 
to  color  them  greenish.  According  to  Wassilieflf  and  Hoppe-Seyler,  this  colora- 
tion is  not  due  to  the  formation  of  sulphur  compounds  of  mercury,  as  was  for- 
merly believed,  but  to  the  antiseptic  action  of  the  calomel,  which  prevents  the 
transformation  of  the  bile  pigments  into  urobilin,  and  also  to  the  sublimate  de- 
rived from  the  calomel,  which  changes  the  bilirubin  to  biliverdin.  After  the  use 
of  bismuth  the  stools  are  generally  of  a  blackish  color.  Quincke  ^  has  proved  that 
this  color  is  not  due  to  the  formation  of  metallic  sulphur,  as  was  formerly  thought 
to  be  the  case,  but  rather  to  a  reduction  of  the  bismuth  salt  to  bismuth  suboxid,  as 
in  Nylander's  test  for  sugar.  Not  infrequently  bismuth  stools  are  colored  green, 
very  much  like  those  after  calomel,  a  phenomenon  which  Quincke  explains  by 
assuming  that  the  bismuth  also  checks  the  transformation  of  the  bile  pigments  to 
urobilin.  He  claims  that,  contrary  to  the  general  belief,  the  stools  after  the  use 
of  iron  are  not  black  from  ferrous  sulphate.  He  maintains  that  immediately  after 
evacuation  they  present  no  abnormal  color,  but  become  grayish  brown  to  grayish 
black  only  after  standing  and  upon  the  surface  being  exposed  to  the  air.  He 
believes  that  this  phenomenon  is  due  to  the  oxidation  of  organic  iron  combinations 
when  exposed  to  the  air.  Patients  to  whom  we  administer  iron  are  usually  the 
ones  in  whose  dark-colored  stools  there  is  often  an  admixture  of  blood,  so  that  we 
should  remember  Quincke's  reasoning.  The  character  of  the  stools  after  the  ad- 
ministration of  methylene-blue  gives  evidence  of  the  processes  of  reduction  going 
on  in  the  intestinal  canal  itself.  When  freely  evacuated  they  are  usually  of  the 
ordinary  color,  due  to  the  reduction  of  the  methylene-blue,  but  within  a  few 
moments  they  become  bluish  green  on  the  surface.  This  coloration  gradually  pene- 
trates the  mass.     If  the  stool  is  preserved  under  oil  no  such  color  appears. 

Under  pathologic  conditions  the  stool  may  be  abnormally  colored 
by  the  addition  of  blood.  The  stool  is  abnormally  light  in  color  in 
acholia  (deficient  production  of  bile  with  absence  of  icterus)  and  in 
retention  of  bile  due  to  occlusion  of  the  biliary  passages  (in  icterus). 
Such  stools  present  a  peculiar  grayish-white  appearance  (clay-colored). 
This  is  due  not  only  to  the  deficiency  in  amount  of  bile,  but  also  to  an 
abundance  of  unabsorbed  fat. 

NothnageP  distinguishes  uncolored  feces  from  acholic  stools.  The  former 
occur  not  only  without  any  icterus,  but,  in  contradistinction  to  the  latter,  without 

1  Munch,  med.  Woch.,  1896,  No.  36. 

*  Die  Erkrankungen  des  Darmes  und  Peritoneums,  p.  1 8. 


EXAMINATION  OF  THE  FECES.  425 

any  demonstrable  disturbance  of  fat-absorption.  Nothnagel  and  v.  Jakscb  sus- 
pect that  in  these  cases,  instead  of  urobiHn,  colorless  reduction  products  are  formed 
in  the  intestine  from  bilirubin  (leucourobilin  of  Nencki).  This  subject  has  not  as 
yet  been  very  closely  studied  from  a  chemical  standpoint.  Nevertheless  this  pos- 
sibility is  certainly  suggested,  because  v.  Jaksch  succeeded  in  extracting  with  acid 
alcohol  very  considerable  quantities  of  urobilin  from  such  so-called  acholic  stools, 
and  because  such  stools  often  darken  considerably  when  exposed  to  the  air,  an 
effect  evidently  to  be .  ascribed  to  oxidation.  Quincke  claims  that  the  normal 
color  of  such  stools  is  reproduced  when  calomel  is  administered,  merely  because 
the  latter  inhibits  the  reduction  of  the  urobilin,  which  is  ordinarily  caused  by 
putrefactive  processes  in  the  intestine. 

In  diarrhea  the  movements  are,  generally  speaking,  light  colored 
because  the  pigment  is  distributed  through  a  much  larger  volume,  but 
sometimes  (especially  in  intestinal  catarrhs)  they  may  contain  the  bile 
pigment  and  vary  in  color  from  green  to  yellow.  (See  p.  445  for  the 
demonstration  of  bile  pigment  in  the  stools.)  The  presence  of  un- 
changed bile  pigments  in  the  stools  is  always  pathologic,  except  in  infants 
(see  above). 

We  sometimes  find  undigested  food  particles  in  the  stools.  This  is 
of  no  diagnostic  significance  so  far  as  indigestible  constituents  are  con- 
cerned, such  as  seeds,  stones,  and  the  skins  of  fruits.  But  if  the  stools 
contain  considerable  macroscopic  evidence  of  substances  which  are 
ordinarily  so  changed  by  the  intestinal  digestion  as  not  to  be  recognized, 
— e.g.,  bits  of  meat,  casein  flocks,  etc. — we  naturally  attribute  this 
peculiarity  to  some  digestive  disturbance.  This  condition,  found  in 
stomach  and  intestinal  disorders,  was  formerly  described  as  "  lientery." 
If  there  is  a  fistulous  communication  between  the  stomach  and  intestine 
or  between  a  loop  of  the  upper  and  a  loop  of  the  lower  intestine,  more 
or  less  undigested  food  will  appear  in  the  stools.  (See  p.  438  et  seq. 
for  the  microscopic  examination  of  the  movement  with  reference  to  the 
utilization  of  the  food.)  If  excessive  decomposition  processes  take 
place  in  the  intestine,  the  diarrhea  movements  will  exhibit  a  peculiar 
foamy  consistence.  In  infantile  diarrhea  the  stools  are  often. of  a  green- 
ish color,  due  to  the  abnormal  decomposition  of  the  bile  pigment ;  or 
if  there  are  many  flocks  of  casein,  they  may  have  a  crumby  or  lumpy 
appearance  instead  of  their  normal  smooth  character. 

With  reference  to  the  admixture  of  mucus,  blood,  and  pus  in  the 
stools,  see  the  following  pages. 


ODOR   OF   THE    STOOLS- 

The  odor  of  normal  liuman  feces  is  well  known.  It  is  due  chiefly 
to  indol  and  skatol,  and  j^erhaps  also  to  methyl  mercaptan.  The  nor- 
mal stool  of  an  infant  emits  only  a  very  faint  odor,  which  is  not  pecu- 
liarly fecal.  In  intestinal  catarrh,  however,  the  odor  of  infants'  stools 
may  be  very  foul.  The  odor  of  diarrheal  movements  varies  greatly, 
sometimes  abnormally  strong,  sometimes  noticeably  slight.  Nearly 
odorless  stools  very  frequently  follow  the  use  of  strong  cathartics. 
(Compare  the  characteristics  of  certain  types  of  movements  on  p.  443.) 


426  EXAMINATION    OF  THE  INTESTINE  AND  FECES. 

EVIDENT   ADMIXTURES   OF    MUCUS    IN   THE    STOOLS. 

A  noticeable  admixture  of  mucus  in  the  stool  will  be  recognized 
here,  as  in  other  excreta,  usually  by  its  peculiar  cousistence  and  trans- 
parency. In  a  doubtful  case  the  addition  of  dilute  acetic  acid  will  cloud 
the  portions  containing  mucus.     The  mucus  in  the  feces  is  a  true  mucin. 

Even  a  normal  stool  contains  some  mucus,  and  sometimes  in  small 
masses  which  can  be  recognized  macroscopically.  Greater  amounts  of 
mucus  indicate  some  catarrhal  condition  of  the  intestinal  mucus  mem- 
brane. 

In  catarrh  of  the  small  intestine  the  mucus  is  evenly  distributed  in 
the  solid  or  semisolid  feces,  and  may  be  recognized  by  the  slimy  con- 
sistence of  the  whole  stool  or  by  the  presence  of  small,  evenly  distrib- 
uted shreds  or  tiny  transparent  lumps.  We  must,  however,  be  careful 
not  to  confuse  bits  of  swollen  vegetable  tissue  with  lumps  of  mucus. 
The  former  are  frequently  found  in  a  normal  stool,  and  can  be  easily 
recognized  microscopically  by  their  cellular  structure  (see  Fig.  141). 
Large  shreds  of  mucus  in  a  watery  stool  are  found  especially  in  catarrh 
of  the  large  intestine.  The  large  lumps  of  mucus  which  sometimes  coat 
solid  fecal  masses  are  also  derived  from  the  large  intestine.  Mucus  pas- 
sages are  also  observed  in  catarrh  of  the  large  intestine  between  nor- 
mal movements  (colico  mucosa,  enteritis  membranacea).  These  peculiar 
whitish  ribbon-  or  tube-like  formations  are  passed  frequently  and  wdth 
rather  violent  pains,  probably  due  to  the  violent  peristalsis  needed  to  tear 
them  from  the  wall  of  the  large  intestine.  The  laity  often  mistake  these 
formations  for  tapeworm.  Admixtures  of  small  kernels  or  tapes  of 
mucus  are  observed  in  the  watery  stools  of  cholera  (rice-water  stools, 
see  p.  443).      With  reference  to  the  chemical  test  for  mucin,  see  p.  446). 

VISIBLE    ADMIXTURE    OF    BLOOD   IN    THE    STOOL. 

The  blood  contained  in  the  stool  may  exhibit  itself  in  different  ways. 
Sometimes  a  microscope  is  required  to  demonstrate  it ;  at  others  it  may 
be  recognized  macroscopically  by  a  red  or  blackish  color. 

In  the  latter  event,  various  deductions  in  regard  to  the  seat  of  the 
hemorrhage  may  be  made  from  the  color  and  arrangement  of  the  blood 
admixture.  For  instance,  solid  feces  coated  externally  with  blood  would 
indicate  a  hemorrhage  only  in  the  lower  portion  of  the  intestine,  where 
the  feces  are  already  solid  and  shaped  (hemorrhoids).  Conversely,  solid 
feces  evenly  tinged  throughout  would  point  toward  a  hemorrhage  in  the 
stomach  or  the  upper  part  of  the  intestine.  The  admixture  of  blood 
even  in  liquid  stools  is  usually  more  evenly  distributed  if  the  hemor- 
rhage is  in  the  upper  part  of  the  intestine.  But  the  liquid  movements 
from  the  large  intestine  (dysenteric  meat-water  stools,  see  p.  444),  may 
also  contain  evenly  mixed  blood.  The  color  of  the  blood  in  liquid 
stools  sometimes  forms  a  good  criterion  for  determining  the  seat  of 
hemorrhage.  The  higher  the  hemorrhage  is,  the  more  altered  is  the 
original  blood  color,  due  to  intestinal  decomposition  and  intestinal  diges- 
tion. In  hemorrhage  from  the  stomach,  gastric  digestion  may  also  exert 
some  change.     Profuse  hemorrhage  from  the  stomach  does  not  always 


EXAMINATION  OF  THE  FECES.  427 

cause  hematemesis,  so  that  we  may  first  suspect  the  condition  from  the 
appearance  of  the  stools,  which  may  be  nearly  black  and  of  a  tar-like 
consistence.  Profuse  typhoid  hemorrhages  sometimes  show  an  alteration 
of  the  blood  ;  usually,  however,  it  is  still  distinctly  red,  because  it  gen- 
erally comes  from  the  lower  portion  of  the  small  intestine,  and  a  stool 
follows  a  hemorrhage  quickly.  The  bloody,  serous  diarrheal  stools  with- 
out true  fecal  matter  are  of  great  diagnostic  importance  in  certain  types 
of  obstruction,  especially  invagination  (see  p.  423).  In  doubtful  cases 
a  microscopic  examination  may  determine  the  presence  of  blood  in  the 
feces  ;  but  the  red  blood-corpuscles  are  often  found  considerably  changed 
and  hard  to  recognize.  Sometimes  they  may  be  destroyed  completely, 
and  then  the  question  as  to  whether  blood  is  present  or  not  must  be 
decided  by  a  chemical  or  spectroscopic  examination. 

PUS  IN  THE  STOOL. 
A  very  considerable  admixture  of  pus  or  pure  pus  stools  are  always 
due  to  perforating  abscesses.  A  slight  amount  of  pus  in  the  stool,  which 
often  can  be  demonstrated  only  microscopically,  and  which  is  frequently 
associated  with  blood  or  mucus,  may  be  due  to  catarrhal  changes,  but  is 
generally  due  to  ulcerative  processes  of  the  mucous  membrane  (tubercu- 
losis, dysentery).  Lumps  of  pus  (even  when  microscopic)  immediately 
suggest  an  ulcerative  process.  It  may  be  very  difficult  to  demonstrate 
pus  in  the  stool,  because  the  pus  corpuscles  are  sometimes  destroyed  by 
the  digestion  and  the  intestinal  decomposition.  Experiments  bearing 
directly  on  this  point  have  shown  us  that  intestinal  decomposition  may 
destroy  pus  corpuscles  within  a  comparatively  short  time,  so  that  it  is 
impossible  to  recognize  them.  The  nuclei  may  resist  the  decomposition 
for  a  considerable  length  of  time,  but  they  are  difficult  to  recognize  in 
this  isolated  condition,  especially  as  they  are  polymorphous  ^  and  differ 
in  no  way  from  the  cell  nuclei  of  any  animal  food,  which  may  persist 
after  digestion.  Moreover,  even  in  normal  stools  individual  white 
blood-corpuscles  may  be  found  as  a  result  of  the  normal  transmigration 
through  the  mucous  membrane.  The  demonstration  of  pus  is  sometimes 
difficult  even  in  perforation  of  perityphlitic  abscesses  into  the  intestine, 
because  decomposition  in  the  abscess  has  already  begun  to  change  the 
character  of  the  pus,  and  this  change  may  be  complete  in  the  intestine. 

The  undigested  lumps  of  casein  found  in  the  diarrheal  movements  accompany- 
ing a  milk  diet  must  not  be  confounded  with  bits  of  pus.  Although  impregnated 
with  fecal  pigment,  the  former  sometimes  assume  a  pus-like  appearance  ;  they  may 
easily  be  recognized  microscopically  by  the  fat-drops  which  they  contain. 

NEOPLASTIC   FRAGMENTS    EST   THE   STOOL. 

Larger  or  smaller  pieces  of  tumor  are  not  infrequently  cast  off  in  carcinoma  of 
the  rectum  or  of  the  intestine  higher  up.  These  fragments  attract  attention 
chiefly  in  a  liquid  stool  by  their  grayish- red  color  and  solid  consistence.'^ 

^  Pus  cells  have  polyraorphous  nuclei,  and  are  called  polynuclear  leukocytes.  (See 
Examination  of  Blood.) 

^  A  bit  may  be  teased  apart  or  frozen  and  sectioned  and  then  examined  microscopic- 
ally, or  the  fragments  may  be  placed  in  a  4  per  cent,  watery  solution  of  formaldehyd 


428  EXAMINATION  OF  THE  INTESTINE  AND  FECES. 

As  it  is  often  impossible  to  recognize  the  finer  details,  the  essential  point  is  to 
detect  the  numerous  nuclei  arranged  according  to  the  character  of  the  cell  constitu- 
ents. Fragments  of  adenomatous  polyps  are  sometimes  found  in  the  stools.  They 
may  occur  independently  or  they  may  be  located  in  the  neighborhood  of  carci- 
nomatous and  tuberculous  ulcers  of  the  intestines. 

GALL-STONES,  PSEUDOGALL-STONES,  BILIARY  GRAVEL,  PAN- 
CREATIC STONES,  INTESTINAL  CONCRETIONS,  INTESTINAL 
SAND   IN    THE   STOOLS- 

Cholelithiasis,  an  attack  of  biliary  colic,  may  be  followed  by  the 
appearance  of  gall-stones  from  time  to  time  in  the  stools,  or  they  may 
appear  without  any  previous  biliary  colic.  In  searching  for  them  the 
stool  should  be  thoroughly  mixed  with  water  and  washed  and  rubbed 
through  a  sieve.  To  be  certain,  we  should  examine  the  movements 
during  at  least  fourteen  days  after  the  cessation  of  the  attack  of  colic. 

Gall-stones  are  concretions  which  form  in  the  biliary  passages,  from  the  size  of 
a  pinhead  to  that  of  a  pigeon's  egg,  or  even  larger.  They  consist  chiefly  of  chol- 
esterin  and  calcium  bilirubin,  in  varying  proportions.  Besides  these  there  are 
present  subordinate  amounts  of  biliverdin,  bilicyanin,  biliftiscin, 
bilihemin,  and  calcium  carbonate.  Cholesterin  gives  a  light,  and 
calcium  bilirubin  a  dark,  color  to  the  concretion.  The  color  varies, 
according  to  the  predominance  of  one  or  the  other  of  these  con- 
stituents, between  white  and  dark  brown  or  dark  olive  green. 
Fig.  147— Wood  Sometimes  they  are  soft  enough  to  be  readUy  cut  or  crushed, 
cell  from  the  seed  but  often,  on  the  Contrary,  are  very  hard.  The  cross-section 
BLTOzero)!  ^^^^^^  usually  shows  distinct  concentric  layers  of  crj^stalline  consistence, 
sometimes  of  different  colors.  In  other  cases  the  surface  may 
present  very  beautiful  facet  formations,  so  that  tetrads  and  rhombic  or  multi- 
angular  shapes  result.  Sometimes  the  surface  is  irregularly  granular,  a  point 
of  diagnostic  importance.  If  facets  are  distinctly  shaped  we  may  be  sure  of  the 
presence  of  multiple  concretions,  and,  in  all  probability,  of  their  origin  in  the  gall- 
bladder. Round  stones  occur  singly  and  also  in  numbers.  Very  large  stones 
(larger  than  hazelnuts)  hardly  ever  reach  the  intestine  per  vias  naturales,  but 
probably  always  by  perforation  of  th6  bile  passages. 

We  must  be  careful  not  to  confound  other  solid  constituents  of  the  feces  with 
gall-stones — e.  g. ,  woody  bits  of  plants,  especially  from  the  cores  of  pears.  These 
similar  formations  have  been  termed  pseudogall-stones}  The  microscopic  examina- 
tion of  a  small  fragment  scratched  off  with  a  knife  from  such  a  formation  shows 
characteristic  wood  cells  (Fig.  147).  The  chemical  examination  (see  below)  would 
also  prevent  any  mistake.  Besides,  the  wood-like  particles  are  much  harder  than 
even  the  hardest  gall-stones. 

So-called  ^^  biliary  sand,''''  in  the  majority  of  cases,  consists  of  these  small 
pseudogall-stones.  The  existence  of  biliary  sand — i.  e.,  large  numbers  of  the 
smallest  gall-stones — in  the  feces  has  not  been  accurately  proved  as  yet.  Naunyn 
considers  it  impossible,  because  his  investigations  show  that  such  small  concretions 
easily  dissolve  in  the  intestine,  and  because  such  small  concretions  would  not  be 
passed  in  any  such  large  quantities  at  one  time,  but  gradually,  as  they  were  formed. 
Another  kind  of  pseudogall-stones  is  the  concretion  which  consists  of  fats  and 
fatty  soaps  that  are  not  easily  melted.     They  are  found  in  the  stools  after  the  admin- 

(R  Formaldehyd  solul.  venale  (33  per  cent.)  120,  aq.  dest.  ad  1000).  Bits  of  from  \  to 
1  in.  in  thickness  are  sufficiently  hardened  after  one-half  to  one  hour ;  but  it  does  no  harm 
to  leave  them  in  the  solution  up  to  eight  days.  The  pieces  are  then  frozen  in  with  the 
formalin  solution  itself  or  with  clear  water  and  cut ;  the  sections  are  placed  in  50  per 
cent,  alcohol  and  stained  with  aqueous  anilin  dyes.  With  this  method  the  sections  are 
said  to  be  much  better  preserved  than  with  the  ordinary  freezing  process. 

'  Compare  Fiirbringer,  Verhandl.  d.  XL  Conc/r./.  inn.  Med.,  1892,  p.  313. 


EXAMIXATION  OF  THE  FECES.  429 

istration  of  large  amounts  of  olive  oil  in  treating  cholelithiasis.  Hence,  the  over- 
estimation  of  the  therapeutic  value  of  this  oil.  It  is  ditficult  to  understand  this 
error.  These  artificially  j^roduced  concretions  are  characterized  usually  by  their 
transparency  and  soft,  greasy  consistence,  and,  if  the  biliary  passages  are  not 
occluded,  by  their  greenish  color. 

Even  a  careful  and  prolonged  search  may  fail  to  find  the  concretion 
in  certain  cases  of  gall-stone  disease,  sometimes  because  the  stone,  which 
was  jammed  in  the  neck  of  the  gall-bladder  and  so  caused  the  colic, 
has  returned  to  the  bladder  itself.  In  other  cases  the  stones  which  are 
at  fault  have  become  stuck  in  the  ductus  choledochus,  while  the  patency 
of  the  biliary  passage  has  been  re-established  alongside  of  the  stone. 
Finally,  the  concretion  may  have  fallen  to  pieces  in  the  intestine. 
Naunyn's  experimental  investigations  seem  to  prove  that  the  latter  is 
very  often  the  case.  He  believes  that  ordinarily  only  the  more  solid 
gall-stones — for  instance,  those  with  a  solid  cholesteriu  shell — are  found 
in  the  feces.  A  further  explanation  of  the  cases  where  no  gall-stone 
is  found  in  the  feces  after  a  typical  attack  of  colic  is  the  fact  that 
typical  attacks  of  colic  may  be  due  to  inflammation  with  or  without 
gall-stone. 

For  chemical  examination  gall-stones  are  first  dried,  then  powdered,  and  then 
extracted  with  alcoholic  ether  to  dissolve  the  cholesterin.  This  may  be  easily 
recognized  by  allowing  the  solution  to  evaporate  slowly  in  a  watch  glass.  The 
characteristic  glistening  cholesterin  crystals  separate,  and  are  easily  recognized 
under  the  microscope  by  their  sharp,  linear,  rhombic  outline  (see  Fig.  211). 
After  extraction  with  alcohol  and  ether,  the  residue  is  treated  while  cold  with  very 
dilute  potassium  hydroxid.  If  the  powder  contains  calcium  bilirubin  a  yellow 
solution  will  be  obtained,  from  which  Gmelin's  reaction  may  be  obtained  (p.  472). 
Naunyn  claims  that  some  concretions  contain  only  bilirubin,  in  which  case  the 
green  in  Gmelin's  reaction  will  be  absent  and  only  the  blue  ring  will  be  found. 

The  much  rarer  pancreatic  concretions  differ  from  gall-stones  in  not  containing 
bile  coloring  matter,  and,  chemically,  in  consisting  chiefly  of  calcium  carbonate, 
which  dissolves  with  effervescence  in  hydrochloric  acid.     They  seldom  have  facets. 

Intestinal  Stones  or  Fecal  Concretions ;  Incrustations  of  Food  Particles  tvith 
Organic  Salts. — These  play  an  important  part  in  human  pathology  in  exciting 
appendicitis.  They  appear  very  rarely  in  the  stools.  They  consist  almost 
exclusively  of  ammonium  and  magnesium  phosphate,  and  should  be  examined  in 
the  same  way  as  urinary  calculi  (see  p.  563).  Eichhorst  and  Deetz  '  report  cases, 
which  were  not  sufficiently  explained  pathologically,  in  which  large  quantities  of 
intestinal  sand,  consisting  of  finely  granular  mineral  concretions,  were  found.  Per- 
haps these  cases  have  at  times  been  erroneously  considered  of  biliary  origin. 

ANIMAL  PARASITES  IN  THE  STOOLS. 

PROTOZOA. 

Of  the  protozoa  there  bave  been  observed  in  the  human  intestinal  contents 
amebae  (Fig.  150),  sporozoa  of  the  species  Coccidium  (psorosperms),  flagella  of 
the  species  Megastomum  (Fig.  149),  cercomonas  (Fig.  148)  and  trichomonas 
(Fig.  151)  and  infusoria  of  the  species  Balantidium.  The  parasites  of  the  species 
Ameba  have  become  of  considerable  importance  in  the  past  two  decades,  because 
they  have  been  found  to  be  the  cause  of  some  dysenteric  disturbances  (Fig.  150). 
Amebae  are  organisms  with  streaming,  creeping  (so-called  ameboid)  movements. 
They  consist  of  a  protoplasmic  substance  containing  granules  and  vacuoles,  which 
changes  its  shape  in  an  irregular  way  while  moving.      Each  ameba  contains  in  its 

'  Arch.  f.  klin.  Med.,  vol.  Ixx.,  p;irts  3  and  4,  p.  365. 


430 


EXAMINATION  OF  THE  INTESTINE  AND  FECES. 


interior  a  nucleus,  which  is,  however,  not  always  easy  to  see.  Propagation  takes 
place  by  division  ;  the  formation  of  sjjores  has  not  been  definitely  proved.  Some 
amebae  have  permanent  types   (permanent  cysts,    encysted  amebse).     They  are 


Fig.  148.— Cercomonas  hominis:  Length,  9  to  11  m;  width,  5  /x  (Davaine)  (after  Roos). 


small,  round,  with  a  sharp,  often  double,  contour,  and  are  immobile.  The  death 
of  an  ameba  is  indicated  by  the  cessation  of  its  ameboid  movements  (Fig.  150), 
and  it  then  disintegrates  so  rapidly  that  it  is  not  easily  to  be  recognized.    Quincke 


Seen  on  flat. 


Seen  on  side. 


Encysted  form. 


Fig.  149.— Megastoma  entericum :  Length,  15  to  17  m  ;  breadth,  9  to  11  jx  (after  Eoos).    Beutseh. 

Arch./,  klin.  Med.,  voL  li.,  p.  506. 

claims  that  the  permanent  types,  on  the  contrary,  may  remain  visible  in  the  stool 
for  twenty  days.  ^     As  yet  no  one  has  been  able  to  cultivate  amebse,  so  that  it  is 


Fig.  150.— Amebse  of  dysentery  (after  Leuckart)  (Losch). 

difficult  to  obtain  any  light  on  the  .species  of  the  individuals  found.     Amebse  some- 
times occur  in  normal  intestinal  contents.     Large  numbers  are  found  quite  regu- 

^  Quincke  and  Roo?.  Berlin.  Uin.  Woch.,  1893,  No.  45  ;  Janowsky,  Ze?'te.  /.  klin.  3Ied,, 
1897,  xxxii.,  5  and  6  ;  Roos,  Arch.  f.  klin.  Med.,  vol.  li. 


EXAMINATION  OF  THE  FECES. 


431 


larly  in  tropic  dysentery.  Pure  cultures  of  dysenteric  amebae  have  not  as  yet  been 
grown  ;  but  dogs  and  cats  have  been  infected  with  stools  containing  amebae  intro- 
duced per  OS  and  per  rectum.  Streptococci  are  also  very  frequently  found  in 
dysenteric  stools  along  with  the  amebae,  so  that  some  cases  are  due  to  mixed  infec- 
tion. The  amebfe  penetrate  the  base  of  intestinal  ulcers,  and  are  also  found  in 
the  pus  of  dysenteric  abscesses,  which  also  argues  in  favor  of  their  etiologic  sig- 
nificance.    With  Ldsch,  who  discovered  it,  Quincke  suggested  calling  the  ameba 


Fig.  151.— Trichomonas  intestinalis :  Len^h,  without  tail,  11  to  15  ^ ;  width  5.5  to  8  /x  (Marchand) 

(after  Roos). 

which  has  sometimes  been  found  in  the  stools  of  healthy  individuals  Amoeba  intes- 
tinalis vulgaris — the  true  dysenteric  ameba.  Arnceba  coli  (Fig.  150)  and  the  ameba 
of  the  German  dysenteric  disorders  he  names  Arnceba,  coli  rnitis,  placing  it  halfway 
between  the  others.  We  do  not  really  know  whether  these  are  diflferent  species 
or  whether  they  are  varieties  of  varying  virulence. 

The  organisms  can  be  most  readily  recognized  by  their  ameboid  motion,  so  that 
it  is  very  important  to  examine  the  stool  when  freshly  voided  and  contained  in  a 


Fig.  152.— a  movable  stage  which  can  be  heated. 


vessel  which  has  been  warmed  to  40°  C.  Bloody  or  purulent  flakes  are  selected 
from  the  stool  and  examined  microscopically.  More  solid  ma.'^ses  must  first  be 
diluted  with  warm  physiologic  salt  solution.  Dry  preparations  may  be  stained,  and 
the  amebae  are  seen  to  be  much  paler  than  the  deeply  stained  bacteria.  Their 
motility  can  be  preserved  by  employing  a  warm  stage.  The  warm  movable  stage, 
constructed  according  to  the  author's  directions  by  Leitz,  in  Wetzlar,  is  illustrated 
in  Fig.  152.  It  is  a  combination  of  Schulze's  warm  stage  with  a  superimposed 
movable  stage.     The  apparatus  is  attached  to  the  stage  of  the  microscope  by  two 


432  EXAMINATION  OF  THE  INTESTINE  AND  FECES. 

screws,  whicli  are  not  visible  in  the  figure,  and  the  stage  is  heated  by  two  small 
burners  beneath  the  points  a  and  b. 

ENTOZOA. 

DiscoveriiDg  the  eggs  of  one  of  the  intestinal  worms  is  quite  as 
important  from  the  diagnostic  point  of  view  as  discovering  the  organ- 
ism itself.  A  low  power  is  the  best  to  employ  at  first,  and  then  a 
higher  one.  The  stools  should  either  be  liquid  or  washed  with  water. 
It  may  be  necessary  to  scratch  off  particles  of  feces  from  the  edge  of 
the  anal  opening  with  a  microscopic  spatula,  or  to  obtain  some  from  the 
rectum  by  means  of  the  introduced  finger.  The  Oxyuris  vermicularis 
is  not  infrequently  observed  in  this  way.  Larger  quantities  of  feces 
may  be  obtained  by  introducing  a  thick  glass  tube  with  blunt  edges. 
If  the  eggs  cannot  be  demonstrated  upon  the  first  examination,  admin- 
istering some  cathartic  (castor  oil)  will  often  prove  of  service,  as  the 
liquid  intestinal  contents  will  thus  be  more  evenly  mixed.  (For  the  char- 
acteristic peculiarities  of  the  eggs  of  the  different  species,  see  below.)  If 
neither  eggs  nor  bits  of  the  parasite  are  found  after  the  administration 
of  an  ordinary  cathartic,  the  next  procedure  is  to  give  the  patient  some 
anthelmintic — e.  g.,  santonin.  In  case  of  ascarides  this  will  serve  the 
double  purpose  of  diagnosis  and  treatment ;  but  for  tapeworm  the  treat- 
ment is  more  prolonged  and  complicated.  For  diagnostic  purposes  it 
would  be  sufficient  to  administer  about  one-third  of  the  usual  therapeu- 
tic dose — e.  g.,  3  gm.  ext.  filicis. 

Leichtenstern  ^  has  drawn  attention  to  the  diagnostic  importance  of 
Charcot's  crystals  in  the  stool  (see  Fig.  211)  for  the  recognition  of 
intestinal  worms.  These  crystals  occur  in  the  feces  with  every  variety 
of  entozoa,  and  often  in  very  large  amounts.  They  appear  to  bear 
some  relation  to  the  metabolism  of  the  worms. 

See  Blood  Examination  (p.  650)  with  reference  to  the  almost  con- 
stant occurrence  of  Charcot's  crystals  and  eosinophilic  leukocytosis  in 
the  various  types  of  helminthiasis. 

Round  Worms, 

Nematodes  Ascarides. — The  only  ascaris  which  occurs  frequently  in  the 
human  intestine  is  the  Ascaris  lumbricoides  (Fig.  153).  The  diagnosis  of  ascaris 
is  generally  very  easily  made,  either  from  the  eggs  or  from  the  worms  themselves. 
The  latter  are  10  to  15  cm.  long,  white  to  dirty  brown  in  color.  They  are  evacu- 
ated with  the  feces  from  time  to  time,  and  sometimes  may  be  vomited.  The  as- 
carides eggs  are  passed  in  so  great  numbers  with  the  feces  that  the  examination  of 
bits  of  feces  from  about  the  anal  orifice  is  usually  sufficient.  They  differ  from 
all  other  entozoa  eggs  in  their  peculiar,  irregularly  wavy  albuminous  shell  (see  Fig. 
153,  c).  This  envelope  may,  however,  be  absent.  The  largest  diameter  of  the 
eggs  is  about  0.05  to  0.06  mm. 

Oxyuris  vermicularis  (Fig.  154). — This  small  intestinal  worm  inhabits 
chiefly  (but  not  exclusively)  the  large  intestine.  It  is  3  to  12  mm.  long.  It  causes 
very  annoying  itching  in  the  anal  region,  and  should  be  searched  for  in  almost  any 
case  of  pruritus  ani.  Either  the  small  thread-like  worms  are  found  in  the  feces  or  on 
the  skin  in  the  vicinity  of  the  anus,  or  else  the  eggs  are  found  microscopically  in  the 
bits  of  feces  which  adhere  to  the  anal  orifice.  The  eggs  are  0. 05  mm.  long,  and  some- 

1  Deutsch.  med.  Wock,  1892,  p.  582. 


EXAMINATION   OF  THE  FECES. 


433 


what  symmetric.  Leichtenstern  has  ^jroved  that  oxyuris  never  lay  eggs  in  the 
intestine,  but  always  migrate  through  the  anal  orifice  for  that  purpose.  Hence,  for 
diagnostic  purposes,  it  is  of  no  use  to  examine  the  stools  for  the  eggs.  Even  the 
eggs  found  at  the  anal  orifice  are  more  or  less  accidental.  In  the  majority  of  cases 
the  only  way  to  demonstrate  the  presence  of  oxyuris  is  to  find  the  worm  itself 

Ankylostoiniim.  Duodenale. — If  viewed  with  the  naked  eye,  this  worm 
(Fig.  155)  closely  resembles  oxyuris.     It  inhabits  the  small  intestine,  and  is  6  to 


Fig.  153.— Ascaris  lumbricoides  :  a,  Body  :    b,  head;  c,  eggs  (after  v.  Jaksch). 

18  mm.  long  (Heller).  The  male  is  always  smaller  than  the  female.  The  eggs  are 
•oval,  0.05  mm.  long,  0.023  mm.  broad,  and,  unlike  those  of  oxyuris,  are  evacuated 
in  the  feces.  Ankylostoma,  as  found  in  the  stool,  are  usually  of  a  reddish  tinge, 
due  to  the  coloring-matter  of  the  blood  sucked  from  their  host.  They  are  hooked 
so  firmly  to  the  intestinal  wall  that  they  rarely  appear  in  the  stools  unless  some 
anthelmintic  has  been  administered.  For  this  reason  the  diagnosis  must  be 
based  upon  the  history,  upon  the  appearance  of  severe  consecutive  anemias,  and 


Fig.  154.— Oxyuris  vermicularis  and  egg:  a,  Natural  size  ;  b,  egg  (after  Heller). 

principally  upon  the  demonstration  of  the  eggs  in  the  stools.  Ankylostomum  in- 
duces a  very  severe  anemia.  It  occurs  in  certain  vicinities  among  miners,  work- 
men in  tunnels,  and  brickmakers.  In  the  tropics  it  is  called  tropic  or  Egyptian 
•chlorosis. 

[Since  the  publication  of  Stiles'  masterly  monograph,^  the  importance  of  this 

^  Hygienic  Laboratory,  Bulletin  No.  10,  Feb.,  1903.     (Report  vpon  the  Prevalence  and 
Geographic  Distribution  of  Hook-worm  Disease  (Uncinariasis  or  Ankylostomiasis). 

28 


434 


EXAMINATION  OF  THE  INTESTINE  AND  FECES. 


parasite  in  the  Southern  States  has  been  attested  by  numerous  observers.     Na 
clinician  here  should  fail  to  familiarize  himself  with  the  general  features  of  the 


Fig.  155.— Ankylostomum  duodenale:  a,  Male  (natural  size):  b,  female  (natural  size);  c,  male 
(enlarged) ;  d,  female  (enlarged) ;  e,  head ;  /,  eggs  i  after  v.  Jaksch). 

worm,  its  eggs,  and  embryos.     The  appended  diagrams  (Figs.  156  and  157)  are 
copied  from  the  above-mentioned  soui'ce. — Ed.] 


<2- 


FiG.  156.— New  World  hook-worm  ( Un- 
cinarin  Americana) ;  natural  size  :  1,  Male  ;  2, 
female;  3,  the  same  enlarged  to  show  the 
position  of  the  anus  (a),  the  Tulva  (v),  and 
the  mouth  (m)  (after  Stiles). 


Fig.  157.— Four  eggs  of  the  New  Wt.rlii  hook- 
worm (  Vncinaria  Americana),  in  the  one-,  iwo-,  and 
four-cell  stages.  The  egg  showing  three  cells  is  a 
lateral  view  of  a  four-cell  stage.  These  eggs  are 
found  in  the  feces  of  patients,  and  give  a  positive 
diagnosis  of  infection.  Greatly  enlarged  (after 
.Stiles). 


Tricocephalus  Dispar  (Fig.  158). — This  is  a  round  worm,  4  to  5  cm.  long, 
which  inhabits  the  cecum  and  colon.     The  eggs  are  easily  recognized  and  fre- 


EXAMINATION  OF  THE  FECES. 


435 


quently  found  in  the  stools.  Ordinarily  it  is  a  very  harmless  parasite,  but  if  pres- 
ent in  very  large  numbers  it  may  produce  very  grave,  even  fatal,  enteritis,  as 
has  been  shown  by  Leichtenstern  and  Moosbrugger. 

Trichina  Spiralis  (Fig.  159). — In  the  first  stages  of  trichinosis  the  adult  or 
embryo  trichina  may  sometimes,  though  very  rarely,  be  evacuated  in  the  stools, 
and  so  be  utilized  in  establishing  the  diagnosis.  The  full-grown  male  is  1. 5  mm. 
or  less  in  length,  and  the  female  4  mm.  or  less. 

Anguillula  Intestinalis  and  Stercoralis  (Fig.  160). — These  worms,  0.8 
to  2. 2  mm.  long,  are  found  in  the  intestinal  contents  of  patients  with  Cochin-China 


Fig.  158.— Trichocephalus  dispar:  Parasite  (natural  size)  and  egg  (after  Kiichenmeister). 

diarrhea.  Leichtenstern  found  this  worm  among  brickmakers  under  similar  con- 
ditions as  ankylostomum,  sometimes  occurring  with  the  latter  parasite  and  some- 
times alone.  Both  Perroncito  and  the  author  found  it  in  the  workmen  employed 
in  the  St.  Gothard  tunnel.  We  do  not  know  whether  it  has  any  pathologic  sig- 
nificance. Grassi  and  Leichtenstern  ^  believe  that  Anguillula  intestinalis  and  ster- 
coralis are  only  different  stages  of  development  of  one  and  the  same  parasite,  which 
develops  in  the  feces  outside  of  the  human  body  in  the  sexually  ripe  stages  as 
Rhabditis  stercoralis. 

Trematodes  (Flukes). 

Distomum  lanceolatum  and  hepaticum  are  found,  although  very  rarely, 
in  the  biliary  passages.     Their  eggs  have  been  found  several  times  in  the  intes- 


FiG.  159.— Trichina  spiralis  (greatly  enlaged) :  a,  Female  ;  6,  male ;  c,  embryo  (after  Heller). 

final  contents.     They  closely  resemble  the  eggs  of  the  Distomum  pulmonale 
(Fig.  212). 

Cestodes  (Tapeworms). 

The  tapeworms  which  are  important,  so  far  as  the  human  body  is  concerned, 
are  almost  exclusively  the  Taenia  solium,  Taenia  mediocanellata  (saginata),  and 
the  Bothriocephalus  latus.  They  all  inhabit  the  small  intestine.  As  is  well 
known,  tapeworms  consist  of  different  generative  forms  united  to  each  other,  the 
so-called  head,  and  the  sexual  segments  or  proglottides,  which  develop  from  and 
are  attached  to  the  head,  and  in  which  the  eggs  develop  hemaphroditely.  These 
segments  and  free  eggs  are  from  time  to  time  evacuated  with  the  patient's  stools. 
The  diagnosis  of  tapeworm  infection  should  never  be  made  from  the  general 
symptomatology,  but  only  from  the  occurrence  of  proglottides  or  of  eggs  in  the 

^  "  Ueber  Anguillula  Intestinalis,"  Deutsch.  med.  Woch.,  1898,  No.  8. 


436 


EXAMINATION  OF  THE  INTESTINE  AND  FECES. 


feces  (see  above,  p.  432).     The  color  of  the  individual  proglottides,  or  of  a  series 
of  them  as  they  appear,  is  whitish.     Shreds  of  mucus  or  strings  of  vegetable  or 
animal  fiber  are  often   mistaken    by  the  laity  for    tapeworm,    mistakes  which 
merely  emphasize  the  importance  of  the  physician  observ- 
ing the  suspected  material  himself. 

After  the  tapeworm  has  been  passed,  it  is  especially 
important  to  know  whether  the  head  has  been  secured. 
If  not,  the  treatment  is  unsuccessful  and  will  have  to  be 
rei3eated  at  some  future  time.  If  the  small  end  of  the 
tapeworm  has  been  jjassed  without  the  head  being  at- 
tached, we  must  search  carefully  for  the  latter.  This  is 
best  done  by  gently  mixing  the  feces  with  a  large  quan- 
tity of  water  and  straining  through  a  fine  sieve,  or  by 
allowing  the  mixture  to  settle,  and  then  jJouring  off  the 
upper  layers  and  searching  for  the  head  at  the  bottom. 
A  cathartic  should  always  precede  the  anthelmintic,  to 
render  the  search  easier.  If  the  head  has  remained  be- 
hind, fresh  segments  or  other  eggs  will  be  passed  within 
three  months. 

Taenia. — Teenise  differ  from  the  bothriocephalus  in  two 
points.  In  the  first  place,  the  sexual  orifice  is  situated  at 
the  margin  of  the  proglottides  ;  sometimes  on  one  side, 
sometimes  on  the  other  ;  looking  to  the  naked  eye  like 
a  slight  excavation  in  a  blunt  projection.  In  the  second 
place,   the   head  has  round  sucking  disks. 

Tmnia  Solium  (Fig.  161). — In  its  early  stages  this  tape- 
worm inhabits  (as  swine  measles,  Cysticercus  cellulosse) 
the  intermuscular  connective  tissue  of  the  hog.  Man  be- 
comes infected  by  eating  raw  or  insufficiently  cooked  pork. 
The  worm  in  man  may  attain  a  length  of  3  m.  The  head 
is  rounded  and  small,  the  size  of  a  pinhead  (1.3  mm.  in 
diameter),  and  has  a  wreath  of  booklets  in  the  middle  between  4  sucking  disks. 
Continuous  with  the  head  is  a  thread-like  non-segmented  portion  about  3  cm. 
long,  to  which  the  proglottides  are  attached  ;  toward  the  end  of  the  worm  the 
latter  are  large  and  broader.  Each  segment  is  a  little  narrower  at  the  upper  than 
at  the  lower  end.  Full-grown  segments  in  a  relaxed  condition  are  9  to  10  mm. 
long,  4  to  5  mm.  broad,  and  when  fresh  are  somewhat  contracted  and  wavy. 
Each  proglottis  contains  a  uterus  with  comparatively  coarse  dendritic  branches. 


Fig.  160.— Anguillula 
intestinalis  and  stercor- 
alis  :  1,  Larva  (Anguillula 
intestinalis)  ;  2,  male  An- 
guillula stercoralis ;  3, 
female  Anguillula  ster- 
coralis (after  Perroncito). 


Fig.  161. 


-Taenia  solium :  a,  Head  (enlarged) ;  h.  proglottis  (magnified  six  times) ;  c,  egg  (after 

Heller). 


These  details  can  be  seen  best  with  the  naked  eye  by  compressing  a  mature  pro- 
glottis between  two  slides.  The  eggs  are  round,  about  0.035  mm.  in  diameter. 
They  have  a  thick  covering  with  radiating  stripes.  Taenia  solium  in  man  may 
lead  to  an  auto-infection  with  Cysticercus  cellulosae. 


EXAMINATION  OF  THE  FECES. 


437 


Taenia  Mediocanellata  (Saginata)  (Fig.  162.) — The  cysticercus  stage  of  this' 
tgenia  is  found  in  cattle,  probably  also  in  goats  and  sheep.  It  is  comparatively 
rarely  observed  in  meat,  because  it  occurs  in  no  such  great  numbers  as  the 
Cysticercus  cellulosse  of  the  hog.  This  fact  probably  has  some  connection  with 
the  different  modes  of  life  of  the  two  parasites. 

The  adult  segments   Tcenia  mediocanellata,  when  relaxed,  are  16  to  20  mm. 


Fig.  162.- 


-Tctnia  lucdiueaiiellata  :  a,  Head  (enlarged);  6,  head  (natural  size);  c,  proglottis  (mag- 
nified six  times) ;  d,  egg  (after  Heller). 


long,  5  to  7  mm.  broad.  The  uterus  has  five  subdivisions,  and  the  branches  are 
much  more  numerous  than  in  Taenia  solium.  The  entire  taenia  reaches  a  much 
larger  size  than  Taenia  solium  (up  to  6  m.  long)  (saginata— "  stuffed").  The 
head  is  also  much  larger,  2. 5  mm.  broad.  It  has  no  booklets,  and  was  therefore 
formerly  called   Taenia   inermis.       The  eggs  do  not  differ  much  from  those  of 


Fig.  lO;;.— Buthrioceplialus  latus:  a.  Head  (enlarged) ;  b.  iiead  (natural  size) ;  c,  ripe  segment 
(magnified) ;  d,  egg  (after  Heller). 


Taenia  solium.  Once  in  a  while  single  proglotti  creep  out  of  the  anus.  Auto- 
infection  with  the  cysticercus  of  Taenia  mediocanellata  has  been  observed  but 
once. 

Bothriocephalus  Latus  (Fig.  163). 

This  is  the.  largest  of  all  human  tapeworms,  attaining  sometimes  a  length  of 
8  m.  The  mature  segments  are  quadrilateral  and  nearly  square  (about  5  mm.)  ;  the 
growing  segments  are  three  to  four  times  as  broad  as  they  are  long,  10  to  15  mm. 
broad  by  1  to  4  mm.  long.  The  head  is  flat  and  oblong,  1  mm.  broad,  2  mm. 
long,  with  a  slit-like  sucking  groove  at  the  corner  on  each  side.     The  sexual 


438  EXAMINATION  OF  THE  INTESTINE  AND  FECES. 

opening  in  the  proglottides  is  not  at  the  margin,  as  in  the  teniae,  but  in  the  middle 
of  the  surface.  The  uterus  is  situated  around  this  opening,  in  the  shape  of  a 
roset.  The  eggs  have  a  thin  shell,  with  coarse,  granular,  mulberry-like  con- 
tents, and  a  lid  at  the  top,  and  can  thus  be  easily  distinguished  from  the  tenia 
eggs.  They  are  also  larger  than  the  latter  (0.07  mm.  long  and  0.045  mm.  broad). 
In  the  young  ova  it  is  not  always  easy  to  recognize  the  lid,  as  it  is  either  unde- 
veloped or  occupies  only  the  extreme  pole.  With  bothriocephalus  we  usually 
find  longer  pieces  and  not  individual  segments  in  the  stools.  The  segments  do 
not  occur  as  often  as  with  the  teniae.  Hence,  searching  for  the  ova  is  of  especial 
diagnostic  importance.  As  certain  cases  of  pernicious  anemia  are  due  to  the 
action  of  this  parasite,  the  stools  should  be  carefully  examined  in  every  case  of 
severe  anemia  whose  etiology  is  not  plain. 

MICROSCOPIC    EXAMINATION  OF  THE   STOOLS  WITH  REFERENCE 
TO  THE  UTILIZATION  OF  THE  FOOD. 

UTILIZATION  AND  SPLITTING  OF  FAT. 

An  incomplete  utilization  of  the  fats  sometimes  becomes  apparent  even  in  a 
microscopic  examination  of  the  stool.  Stools  which  contain  an  abnormal  quan- 
tity of  fat  appear  gray,  often  glistening.  The  fat  consists  partly  of  a  microscopic 
admixture  and  partly  of  larger  particles,  whose  form  depends  upon  the  manner 
in  which  it  was  administered.  Under  the  microscope  the  fat  is  seen  to  consist 
of  fat-drops  and  of  needle-like  crystals.  (See  Fat-crystals  of  the  Sputum,  Fig. 
211,  a.)  Their  appearance  depends  upon  the  melting-point  of  the  respective 
fats,  and  upon  whether  the  fats  are  found  in  the  stool  unchanged,  split  up,  or 
saponified.  Neutral  fats  may  appear  either  as  drops  or  as  needles.  Fatty  acid 
soaps  usually  ajDpear  as  thick,  short  needles  or  cakes  ;  free  fatty  acids,  as  needles. 

Normal  stools  contain  a  moderate  number  of  fat-needles,  which  represent  the 
fats  that  are  not  so  easily  melted,  and  are  therefore  less  readily  absorbed.  Fat- 
drops  are  not  so  common  except  after  abundant  ingestion  of  milk  or  easily  melted 
fats.  They  usually  signiiy  an  insufiicient  utilization  of  the  fats,  as  does  also  an 
abnormal  prominence  of  fat-needles. 

The  stools  may  be  abnormally  fatty  in  disease  of  the  pancreas,  and  in  cases 
when  the  bile  is  shut  off  from  the  intestine.  But  in  both  cases  emulsified  fat, 
such  as  is  contained  in  milk,  seems  to  be  well  absorbed.  (See  Chemical  Exam- 
ination of  Feces,  p.  446.) 

UTILIZATION  OF  STARCH. 

The  microscopic  appearance  of  starch  is  well  known  (p.  359,  Fig.  141). 
Well-preserved  starch  granules  are  rarely  found  in  the  normal  feces  of  an  adult, 
but  they  may  occur  in  the  movements  of  infants  improperly  fed  with  starches. 

An  abundance  of  starch  granules  in  the  stools  of  adults  is  pathologic,  and  is 
usually  a  sequence  of  diarrhea  or  of  gastric  hyperacidity.  The  absence  of 
pancreatic  juice  does  not  seem  to  produce  pathologic  quantities  of  starch  in  the 
feces,  because  the  starches,  along  with  the  other  carbohydrates,  are  utilized 
very  extensively  by  the  intestinal  bacteria  for  the  formation  of  acids.  Defi- 
ciency of  bile  in  the  intestinal  contents  is  not  responsible  for  any  increase  of 
starch  in  the  stool,  as  the  bile  contains  only  traces  of  a  diastatic  enzyme,  which 
are  of  no  practical  importance. 

UTILIZATION    OF  THE  MUSCLE    FIBERS   AND  OF  THE   OTHER    PROTEIDS  OF 

THE  FOODS. 
Meat  fibers  in  the  movements  are  easily  recognized  microscopically  by  the 
more  or  less  well-preserved  transverse  striation.  (Fig  164,  aa.)  The  more  thor- 
ough the  digestion,  the  less  distinctly  this  appears,  and  the  more  are  the  frag- 
ments rounded  off".  Undigested  muscle  fibers  are  constantly  found  in  the  feces 
of  a  person  upon  a  mixed  diet.  The  amount  becomes  pathologically  increased 
in  diarrhea,  in  fever,  and  in  other  disturbances  of  the  digestive  mechanism. 


EXAMINATION  OF  THE  FECES. 


439 


To  discover  connective  tissue  the  stools  should  be  stirred  with  water  and 
examined  over  some  dark  substance  (black  plate).  (See  Examination  of  Sputum.) 
The  connective-tissue  fragments  may  then  be  recognized  as  white  fibers. 

Ad.  Schmidt^  claims  that  the  macroscopic  appearance  of  muscle  fibers  in 
the  stools  of  a  patient  who  has  ingested  a  test  meal  of  100  gm.  of  very  slightly 
roasted  chopped  meat  demonstrates  some  severe  damage  to  the  intestinal  diges- 
tion. On  the  other  hand,  the  occurrence  of  macroscopically  visible  fragments  of 
connective  tissue  is  indicative  of  insufiicient  gastric  digestion,  because  connective 
tissue,  unless  it  is  cooked  to  pieces,  is  dissolved  only  by  pepsin. 

Coagulated  proteids  and  casein  may  be  found  in  amorphous  masses  in  normal 


/  ... 


Fig.  164.— Microscopic  elements  of  normal  feces :  a,  Muscle  fibers  ;  h,  connective  tissues ;  c, 
•epithelial  cells ;  d,  white  blood-corpuscles ;  e,  spiral  vessels  of  plants ;  J—h,  vegetable  cells ;  i, 
plant  hairs ;  k,  triple  phosphate  crystals ;  I,  stone  cells.  Scattered  among  these  elements  are 
micro-organisms  and  debris  (after  v.  Jaksch). 

stools,  and  more  especially  in  stools  denoting  insufficiently  utilized  food.  The 
coarse,  crumbling  casein  lumps  are  important  diagnostically,  because  they  com- 
pose the  major  part  of  an  infant's  poorly  digested  stool.  An  infant's  normal 
stool  should  be  homogeneous  and  even. 

INDIGESTIBLE    FOOD    RESIDUE. 

In  every  normal  stool  the  constituents  of  the  food  which  are  indigestible 
reappear.  All  cellulose-like  substances  are  not  attacked  by  the  digestive  fer- 
ments, and  only  very  incompletely  by  the  bacteria  of  the  intestine  (plant  hairs 
and  spiral  vessels,  vegetable  cell  formations,  etc.).  (Fig.  164,  e.,  i.,  I.)  Various 
parts  of  a  meat  diet  also  remain  undigested  ;  for  instance,  larger  strands  of  con- 
nective tissue  and  fragments  of  elastic  fibers  (Fig.  164). 

FERMENTATION   OF   THE   FECES   AFTER   EVACUATION. 

Ad.  Schmidt  and  his  pupils  have  recently  endeavored  to  draw  conclusions  in 
relation  to  intestinal  function  from  the  manner  in  which  the  feces  ferment  after 
evacuation — i.  e.,  from  the  gases  which  are  thus  formed.  The  most  important  of 
the  original  communications  is  to  be  found  in  the  Deutsches  Archiv  fiir  klinische 
Medizin.,  vol.  Ixi. 


BACTERIA   OF   THE   FECES. 

Feces  consist  to  a  large  extent  of  the  body  substance  of  micro-organisms. 
Before  Koch's  culture  methods  became  known,  it  seemed  to  be  quite  impossible 
to  isolate  the  bacterial  admixture  of  a  normal  or  pathologic  stool.  But  since 
then,  by  the  isolation  of  individual  varieties,  some  light   has  been  thrown  on 

I  Deutsch.  med.  Work.,  1899,  No.  49,  p.  811. 


440  EXAMINATION  OF  THE  INTESTINE  AND  FECES. 

this  subject.  Bienstock  was  the  first  to  study  the  question  exactly.  He  decided 
that  only  four  kinds  of  bacilli  were  to  be  found  in  the  intestine,  one  of  which 
was  the  specific  decomposer  of  the  proteids  ;  and  that  there  were  no  micrococci, 
because,  being  non-sporebearing,  they  were  destroyed  upon  entering  the  digestive 
tract  by  the  hydrochloric  acid  of  the  stomach.  Later  investigators,  who  worked  with 
anaerobic  culture  methods  and  varied  culture  media,  could  not  corroborate  these 
results  ;  they  showed  that  the  number  of  varieties  was  much  larger.  Although 
at  the  present  time  no  practical  clinical  methods  seem  available,  except  for  the 
demonstration  of  specific  pathologic  varieties,  it  does  appear  probable  that  sooner 
or  later  these  investigations  will  aid  in  our  understanding  of  some  of  the  com- 
plicated problems  of  digestion. 

Mannaberg's  comprehensive  description  may  be  consulted  for  the  better 
known  species  of  normal  intestinal  bacteria  and  fungi. i  By  far  the  majority  of 
the  species  of  bacteria  in  the  feces  belong  to  the  Bacterium  coli  group.  Among 
the  best  known  varieties  are  the  Bacterium  lactis  aerogenes,  the  Bacillus  subtilis, 
Proteus  vulgaris,  Bacillus  butyricus  (Bacillus  amylobacter),  and  others.  Bacteria 
which  elsewhere  we  know  as  the  cause  of  disease,  such  as  the  staphylococci,  are 
found  in  abundance  in  normal  feces.  Only  when  these  bacteria  are  so  very 
abundant  that  they  can  be  demonstrated  without  culture  do  they  become  import- 
ant from  a  diagnostic  standpoint. 

"We  can  obtain  an  approximate  notion  of  the  bacteriologic  condition  of  the 
feces  by  examining  with  an  oil-immersion  lens  a  small  particle  unstained  (if  too 
hard,  mix  with  water).  The  number,  the  shape,  and  the  individual  movements 
of  the  bacteria  should  be  noted.  For  more  accurate  microscopic  examination  a 
dry  specimen  should  be  stained  with  carbolfuchsin  or  after  Gram's  method  (p.  596). 
The  ordinary  plate  culture  media  are  used,  if  necessary,  to  grow  the  individual 
varieties — e.  g.,  bouillon,  gelatin,  and  agar-agar.  Especially  for  the  intestinal 
bacteria,  faintly  acid  beer-wort,  in  the  form  of  agar  plates,  is  recommended.  Several 
varieties  are  said  to  grow  in  this  medium  which  do  not  thrive  upon  the  ordinary 
culture  media.  Here  we  cannot  go  into  the  technic  of  these  nor  of  the  anaerobic 
cultures. 

Escherich's  investigations  on  the  intestinal  bacteria  of  infants  are  of  interest. 
He  found  that  immediately  after  birth  the  meconium  was  fi-ee  from  bacteria.  Four 
to  seven  hours  after  birth  was  the  earliest  that  he  found  any  bacteria.  The  feces 
of  milk  generally  contain  but  two  species  of  bacteria — the  Bacillus  coli  communis, 
which  chiefly  inhabits  the  colon  and  the  lower  segment  of  the  small  intestine,  and 
is  much  in  excess  so  far  as  numbers  go,  and  the  Bacillus  lactis  aerogenes,  which 
grows  in  the  upper  part  of  the  small  intestine.  In  the  stools  of  more  than  half 
of  the  infants  suffering  from  acute  gastric  catarrh  he  also  found  a  spirillum, 
extremely  fine  and  hard  to  stain,  to  which  he  ascribes  a  grave  prognostic  signifi- 
cance. 

PATHOGENIC   BACTERIA  OF  THE  FECES  WHICH   ARE    IMPORTANT  FROM  A 
DIAGNOSTIC   STANDPOINT. 

Bacilli  of  Tuberculosis  (Fig.  213). — In  intestinal  tuberculosis  these  bacilli 
are  found  in  the  feces,  and  are,  therefore,  of  diagnostic  importance.  The  stools 
may,  however,  contain  these  bacilli,  even  though  there  is  no  intestinal  tuberculosis 
(if  the  patients  swallow  their  sputum).  Searching  the  stools  has  even  been  recom- 
mended for  the  diagnosis  of  lung  tuberculosis  in  cases  of  irresponsible  persons  who 
swallow  the  sputum.  Although  in  the  examination  of  sputum  previous  treatment 
with  dilute  potassium  hydroxid  or  digestive  enzymes  is  often  successful  it  is  rarely 
of  use  in  the  examinati<-n  of  feces  (see  p.  596),  because  the  feces  consist  chiefly 
of  indigestible  substances,  which  are  insoluble  in  potassium  hydroxid.  But  it  may 
be  serviceable  in  the  examination  of  mucopurulent  particles  of  the  movement 
which  have  been  isolated  from  the  mass  of  feces.  We  do  not  know  whether  under 
certain  conditions  decomposition  may  destroy  tubercle  bacilli  in  the  intestine.     At 

^  In  the  introduction  to  Xothnagel :  Diseas&s  of  the  Intestines  and  Peritoneum.  It  con- 
tains a  comjalete  index  of  the  literature  on  the  subject. 


EXAMINATION  OF  THE  FECES.  441 

any  rate,  we  cannot  always  demonstrate  tubercle  bacilli  in  the  stools  even  when 
there  is  undoubted  intestinal  tuberculosis.  Perhaps  this  is  on  account  of  the  dilu- 
tion of  the  content  of  tubercle  bacilli  by  the  abundant  particles  of  food.  Tubercle 
bacilli  are  most  readily  found  in  the  purulent  or  bloody  pieces  of  diarrheal  stools. 
Generally  speaking,  direct  searching  through  solid  stools  is  less  promising.  Never- 
theless they  may  quite  frequently  be  demonstrated  in  solid  movements  if,  as  Ham- 
burger recommends,  we  mix  a  piece  of  feces  the  size  of  a  j^ea  with  a  few  centi- 
meters of  water,  then  centrifuge  gently  to  remove  the  coarser  pieces,  dilute  the 
supernatant  cloudy  fluid  with  a  double  volume  of  alcohol,  centrifuge  once  more, 
and  then  after  drying  examine  the  remaining  precipitate,  which  will  consist  almost 
exclusively  of  bacteria.  As  tubercle  bacilli  in  the  feces  may  be  due  to  swallowed 
sputum,  we  can  diagnose  intestinal  tuberculosis  if  bacilli  are  found  in  the  feces 
only,  when  at  the  same  time  attacks  of  diarrhea  occur  with  pus  and  blood  in  the 
stool.  The  tubercle  bacillus  must  be  carefully  distinguished  from  the  smegma 
bacillus,  which  is  said  to  occur  at  the  anal  orifice  and  might  have  become  mixed 
with  the  feces. 

Bacillus  of  Cholera  (Comma  Bacillus)  (Fig.  165). — The  demonstration  of 
cholera  bacilli  is  of  great  importance  in  the  early  diagnosis  of  the  first  cases  of  a 
cholera  epidemic.     The  bacilli  are   constantly  present  in  the  stools  of  cholera 


Fig.  165.— Cholera  bacilli  (X  1000)  (after  Weichselbaum). 

patients,  and  at  times  in  very  great  quantities.  By  demonstrating  their  presence 
the  differential  diagnosis  between  cholera  nostras  and  asiatica,  formerly  so  very 
difficult,  may  be  made  with  certainty  in  an  isolated  case  and  without  first  waiting 
for  an  epidemic.  A  dry  specimen  should  be  prepared  from  one  of  the  little  mucus 
flakes  suspended  in  the  movement,  and  then  stained  in  the  ordinary  way  with 
ftichsin-gentian- violet  or  methyleue-blue.      (See  Examination  of  Sputum.) 

A  microscopic  exaiuination  for  comma  bacilli  is  not  enough  to  make  a  diag- 
nosis absolutely  sure,  because  there  are  other  comma-shaped  bacilli,  as,  for  ex- 
ample, those  of  Finkler  and  Prior,  found  in  cholera  nostras.  Moreover,  a  negative 
microscopic  result  without  any  culture  tests  would  not  permit  the  absolute  exclu- 
sion of  cholera.  For  this  reason  gelatin  plate  cultures  must  be  ju-epared  from  the 
suspected  cholera  stool  in  order  to  render  the  diagnosis  certain.  ■  This  is  done  in 
the  ordinary  -way  described  in  any  text-book  on  I)acteriologic  technic.  After 
twenty-four  to  thirty-six  hours  numerous  liquefSnng  colonies  will  lie  found,  from 
which  gelatin-streak  and  potato  cultures  are  to  be  made.  The  gelatin-streak 
cultures  are  characterized  by  the  fact  that  the  gelatin  on  the  surface  is  liquefied 
very  rapidly,  whereas  in  the  interior  the  liquefaction  occurs  only  as  a  slender  canal 
along  the  line  of  inoculation.  On  jiotato  the  comma  bacilli  grow  rather  slowly  at 
20°  C.  as  a  thin  gray-green  coating.  If  the  comma  bacilli  are  cultivated  in  a 
sterilized  solution  of  1  gm.  of  peptone  and  0.5  gm.  of  NaCl  to  100  gm.  of  water, 


442  EXAMINATION  OF  THE  INTESTINE  AND  FECES. 

and  concentrated  sulphuric  acid  is  then  allowed  to  flow  underneath,  a  red  discol- 
oration will  occur  at  the  line  of  junction  of  the  two  fluids,  due  to  the  indol  con- 
tained in  the  culture.  This  pigment  used  to  be  called  cholera-red,  but  this  name 
is  not  quite  correct,  because  the  same  indol  reaction  occurs  also  with  other  bacteria. 
If  the  culture  is  not  a  pure  one,  the  reaction  is  of  no  diagnostic  importance.  Cholera 
bacilli  are  motile  in  a  hanging  drop. 

The  comma  bacilli  may  sometimes  be  found  in  the  vomitus. 

Competent  data  relative  to  the  bacteriologic  demonstration  of  cholera  bacilli 
are  to  be  found  in  Pfeiffer's  comprehensive  article  in  Deutsche  medicinische  Woch- 
enschrift,  1892,  No.  36. 

In  regard  to  the  differences  between  the  Finkler-Prior  (see  p.  361)  and  other 
comma  bacilli  found  in  certain  cases  of  cholera  nostras,  and  the  true  comma  bacil- 
lus of  Koch,  bacteriologic  manuals  should  be  consulted. 

Various  difficulties  in  making  a  bacteriologic  diagnosis  of  cholera  have  recently- 
arisen  on  account  of  the  discovery  of  numerous  varieties  of  cholera  bacilli.  To 
solve  these  difficulties  Pfeiffer  requires  for  diagnosis  a  biologic  cholera  reaction  of 
the  suspected  culture.  This  is  accomplished  by  injecting  into  the  peritoneal  cavity 
of  young  guinea-pigs  a  lethal  amount  of  the  bacilli  in  question  simultaneously  with 
an  injection  of  a  definite  amount  of  the  serum  of  animals  immune  to  cholera.  If 
they  are  true  cholera  bacilli  they  will  be  dissolved  within  a  short  time  in  the  peri- 
toneal cavity.  Pfeiffer  ^  claims  that  other  bacteria,  no  matter  how  much  they  may 
resemble  cholera  bacilli,  do  not  show  this  purely  specific  reaction. 

If  serum  from  animals  immunized  against  cholera  be  added  to  a  liquid  culture 
of  cholera  bacilli,  the  latter  becomes  non-motile  and  agglutinates  in  lumps,  very 
much  as  do  typhoid  bacilli  when  acted  on  by  typhoid  serum.  (See  Widal's  Serum 
Diagnosis,  p.  675,  ff.)  This  peculiarity  may  be  utilized  in  making  a  differential 
diagnosis  of  cholera. 

Typhoid  Bacilli. — Typhoid  bacilli  have  been  demonstrated  in  the  stools  of 
typhoid  patients  from  the  second  or  third  week  on.  Culture  methods  (isolation 
and  plate  cultures)  are,  of  course,  necessary  for  each  demonstration,  since  the 
typhoid  bacilli  do  not  possess  any  typical  morphologic  peculiarities.  This  demon- 
stration is,  however,  too  complicated  and  takes  too  long  to  be  of  any  practical 
importance  in  the  diagnosis  of  typhoid  fever.  Eisner  ^  has  announced  a  method 
of  isolating  typhoid  bacilli  more  easily  from  the  stools,  and  also  differentiating  them 
from  colon  bacilli.  He  employs  a  faintly  acid  culture  medium  containing  potas- 
sium iodid.  Piorkowski  ^  has  attempted  to  achieve  the  same  result  by  the  em- 
ployment of  plate  cultures  upon  a  medium  to  which  alkaline  urine  has  been  added. 

To  overcome  the  difficulties  of  a  bacteriologic  diagnosis  of  typhoid  bacilli  in 
contradistinction  to  certain  varieties  of  colon  bacilli,  Pfeiffer  *  tried  to  characterize 
the  typhoid  bacilli  by  some  biologic  reaction  with  the  serum  of  animals  immune  to 
typhoid.  This  reaction  as  described  by  Pfeiffer  is  performed  upon  animals  in  ex- 
actly the  same  way  as  the  cholera  reaction  (see  above).  It  may  now  be  replaced 
by  the  convenient  Gruber-Widal  agglutination  reaction  of  typhoid.  (See  later. 
Blood-examination,  p.  675.)  To  be  sure,  the  utility  of  this  procedure  for  recog- 
nizing typhoid  bacilli  has  of  late  been  questioned,  while  the  value  of  the  serum 
reaction  as  a  diagnostic  measure  is  now  hardly  ever  disputed. 

Kruse's  Bacillus  of  Dysentery. — While  tropic  dysentery  seems  to  be  an 
amebic  disease  (see  p.  429),  Kruse  °  has  recently  described  a  peculiar  bacillus  as 
the  exciting  cause  of  non-tropic  epidemic  dysentery.  These  bacilli  are  found  as 
plump  rods  in  the  purulent  jDortions  of  the  stool,  and  grow  readily  upon  artificial 
culture  media,  forming  delicate  leaf-like  colonies  upon  gelatin  plates  within  twenty- 
four  to  forty-eight  hours.     According  to  Kruse,   they  are  found  in  such  large 

i  Zeits.  /.  Byg.,  1895,  vol.  xix.,  p.  75. 

^  Zeits.  f.  Hyg.  u.  Infectionskrankh.,  1895,  vol.  xxi. ;  and  Brieger,  Deutsch.  med.  Woch. 
1895,  No.  50,  p.  835. 

»  Berlin,  klin.  Woch.,  1889,  No.  7,  p.  149. 

*R.  Pfeiffer  and  W.  Kolle,  "Ueber  die  specifische  Immunitiitsreaetion  der  Typhus- 
bacillen,"  Zeils.  /.  Hyg.,  1896,  vol.  xxi.,  part  2.  ^  Deutsch.  med.  Woch.,  1900,  p.  G37. 


EXAMINATION  OF  THE  FECES.  443 

numbers  in  the  fresh  stools  of  dysentery  that  in  plate  cultures  their  colonies  greatly 
exceed  those  of  the  colon  bacilli.  Upon  glucose  agar  they  grow  like  typhoid 
bacilli,  without  producing  gas  either  superficially  or  in  the  depths  of  the  culture 
medium.  Upon  potato  there  is  a  yellowish  growth  along  the  line  of  inoculation, 
surrounded  by  a  clear  area.  They  may  be  differentiated  from  typhoid  bacilli  by 
their  plumpness  and  also  by  their  lack  of  motility  and  the  absence  of  cilia.  They 
do  not  stain  by  Gram's  method.  They  sometimes  exhibit  distinct  polar  granules, 
Kruse  believes  that  the  relation  of  these  micro-organisms  to  dysentery  is  shown  by 
the  fact  that  they  are  agglutinated  by  the  blood-serum  of  a  dysenteric  convalescent 
in  a  dilution  of  1  :  50,  and  sometimes  by  a  dilution  of  even  1  :  1000.  Under  cer- 
tain conditions  the  agglutinative  power  of  the  serum  of  a  dysenteric  convalescent 
may  last  for  a  year.  In  reference  to  the  diagnostic  value  of  the  agglutinative 
reaction,  the  reader  is  referred  to  Lentz's '  article. 

Streptococci. — A  number  of  serious  diseases  have  recently  been  attributed  "^ 
to  an  invasion  of  the  digestive  tract  by  streptococci.  Their  course  is  like  that  of 
typhoid,  cholera,  or  finally,  of  an  acute  enteritis  with  strepticopyemic  localization 
(peritonitis,  endocarditis,  nephritis,  etc.).  These  cases  can  be  easily  diagnosed 
from  a  microscopic  examination  of  the  diarrheal  stools,  which  always  contain  very 
extraordinary  quantities  of  streptococci.  They  may  be  found  in  a  dry  preparation 
stained  with  carbolfiachsin  or  by  Gram's  method  (see  p.  596).  The  vomitus  and 
the  urine  may  sometimes  contain  abundant  streptococci.  The  prognosis  in  these 
cases  is  usually  fatal,  except  in  those  resembling  typhoid,  which  generally  recover. 
(See  pictures  of  streptococci,  Fig.  218). 

Anthrax  Bacilli. — Anthrax  can  sometimes  be  diagnosed  by  the  presence  of 
anthrax  bacilli  in  the  loose,  frequently  bloody,  stools.      (See  Fig.  235). 

CHARACTERISTIC  NATURE  OF    THE  STOOLS   IN    SOME   DISEASES. 

Stools  of  Typhoid  Fever. — Typhoid  fever  is  generally  accompanied  by  loose 
yellow  stools  with  a  consistence  like  pea  soup.  They  usually  settle  in  layers  with 
a  thick  crumbling  sediment  and  a  supernatant,  cloudy,  watery  menstrum.  The 
odor  is  generally  very  strong  and  offensive,  and  possibly  diagnostic.  The  reaction 
is  usually  strongly  alkaline.  In  fact,  the  stools  usually  contain  abundant  micro- 
scopic crystals  of  triple  phosphates  (ammoniomagnesium  phosphate;  see  Figs. 
189  and  190).  Simple  microscopic  examination  does  not  disclose  any  special 
bacteriologic  characteristic.  The  stools  are  frequently  stained  with  blood.  A 
slight  tinge  not  infrequently  precedes  a  profuse  intestinal  hemorrhage  and,  hence, 
is  to  be  carefully  watched  for.  Pus  in  quantities  which  can  be  demonstrated  micro- 
scopically is  only  contained  in  the  stools  of  cases  Avith  severe  and  extensive  ulcer- 
ations. The  diarrheal  stools  of  typhoid  are  usually  very  copious.  Solid  move- 
ments are  not  infrequently  found,  not  only  in  the  beginning,  but  even  throughout 
the  entire  duration  of  the  disease. 

Stools  of  Asiatic  Cholera  and  Cholera  Nostras. — In  mild  attacks  of  Asi- 
atic cholera  and  cholera  nostras  the  stools  may  present  the  character  of  an  ordinary 
diarrhea.  In  severe  cases  they  are  no  longer  fecal  in  color,  but  are  thin  and 
nearly  colorless  or  grayish,  like  water  in  which  tiny  cloudy  flakes  are  suspended 
(rice-water  stools).  The  absence  of  any  brown  coloration  is  probably  due  to 
oligocholia  or  acholia.  The  stools  no  longer  emit  a  fecal,  but  a  sour  semen- 
like odor.  The  reaction  is  alkaline  or  neutral.  In  the  mucous  flakes  we  see, 
under  the  microscope,  intestinal  epithelium  arranged  in  layers,  more  or  less  abun- 
dant cholera  bacilli  (Fig.  165),  and  sometimes  drops  of  fat.  The  stools  may  also 
be  slightly  tinged  with  blood.  Cholera  stools  contain  only  about  2  per  cent,  of 
solids,  and  of  this  a  large  amount  is  sodium  chlorid,  but  very  little  proteids.  The 
stools  are  usually  very  profuse  and  voided  without  any  especial  eflbrt  (not  like 

^  Zeits.  f.  Hyfj.  u.  Infectiomkrankh. ,  vol.  xli.,  1902,  part  3,  p.  559. 

"^  Compare,  e.  y.,  "  Contribution  a  I'etude  du  streptocoque  et  de  I'enterite  strepto- 
coccique.  Quatre  memoires  par  MM.  de  Cerenville,  Tavel,  Eguet  et  Krummbein," 
Ann.  Swisses  de  mecl,  Series  II.,  1895.     C.  Sallmann,  Basel. 


444  EXAMIXATION  OF  THE  INTESTINE  AND  FECES. 

dysentery).  As  the  general  condition  imjDroves  they  gradually  resume  a  fecal 
appearance.  As  is  well  known,  cases  of  cholera  do  occur  without  diarrhea  (^cholera) 
sicca). 

The  stools  of  cholera  nostras  are  much  like  those  in  true  cholera,  except  that 
true  cholera  bacilli  are  absent,  and  that,  corresponding  to  the  milder  natui-e  of  the 
disease,  they  are  more  or  less  stained  by  bile.  Both  the  stools  and  vomitus  in 
cholera  nostras  contain  very  varied  micro-organisms  (Finkler-Prior  bacilli,  strep- 
tococci, and  others,  see  pp.  442  and  443). 

Stools  of  Dysentery  and  Carcinoma  of  the  Rectum. — Dysentery  stools 
present  the  character  of  rectal  diarrhea  (see  p.  423) — i.  e.,  they  are  not  profuse, 
but  voided  so  much  the  oftener.  Soon  after  the  attack  begins  they  lose  their  fecal 
character,  and  are  at  first  slimy,  then  mucopurulent,  and  finally  sanguinopurulent 
or  seropurulent  (meat- water  stools,  white  flux,  red  flux).  We  may  often  see  pecu- 
liar, solid,  reddish  or  white  fi-agments,  which  consist  partly  of  blood-stained  mucus 
(carimculfe  of  older  writers)  and  partly  of  macroscopically  visible  bits  of  exfoliated 
mucus.  The  stools  in  dysentery  may  be  practically  odorless,  but  in  grave  cases 
(gangrenous  flux)  they  emit  a  noticeable  cadaverous  odor.  The  stools  of  carcinoma 
of  the  rectum  sometimes  very  closely  resemble  those  of  dysentery. 

Stools  in  Diseases  of  the  Pancreas. — Considering  the  predominance  of  the 
pancreas  in  the  digestion  of  fats,  it  is  easily  understood  that  in  some  of  the  diseases 
of  this  organ  which  lead  to  its  destruction  or  to  the  occlusion  of  its  ducts,  so-called 
'  \fat-stools "  are  observed.  The  latter  are  characterized  microscopically  and 
chemically  by  their  abnormal  amount  of  fat  (steatorrhea).  We  must,  however,  be 
rather  cautious  in  making  use  of  this  sjnnptom  for  diagnosis,  because,  on  the  one 
hand,  the  stools  may  show"  an  abnormal  amount  of  fat  in  any  case  of  marked  icterus, 
and,  on  the  other  hand,  cases  of  almost  total  destruction  of  the  pancreas  have  been 
observed  when  the  stools  at  the  time  showed  no  abnormal  amount  of  fat.  This  is 
because  emulsified  fat,  even  ^dthout  any  pancreatic  juice,  can  be  veiy  readily 
absorbed,  as  showed  on  p.  438,  w^hile  evidently  the  fat  not  in  emulsion  was  taken 
care  of  by  the  vicarious  action  of  the  bile.  Hence,  fattj^  stools  are  diagnostic  of 
pancreatic  disorders  only  where  there  is  no  jaundice,  and  hence  also  the  absence 
of  fatty  stools  does  not  exclude  destructive  pancreatic  disturbance.  In  making  a 
diagnosis  of  pancreatic  disturbance  fi'om  the  appearance  of  the  stools  we  must  also 
remember  that,  if  the  pancreatic  juice  is  absent,  chemical  examination  shows  only 
insignificant  quantities  of  soaps  in  the  fatty  stools  (p.  446),  the  movements  show 
but'slight  signs  of  putrefaction,  and  the  urine  contains  only  a  slight  amount  of 
indican  (see  p.  475).  In  pancreatic  disease  where  there  is  no  flow  of  pancreatic 
juice  into  the  intestines,  well-liardened  glutoid  capsules  (see  p.  419)  are  found 
undissolved  in  the  intestinal  contents.  The  iodoform-glutoid  reaction  is  there- 
fore absent. 


CHEMICAL    EXAMINATION    OF  THE    FECES. 
REACTION    OF   THE    STOOLS. 

Under  normal  conditions  the  reaction  of  the  feces  mav  be  neutral, 
faintly  acid,  or  faintly  alkaline.  Gamgee  considers  a  faintly  alkaline 
reaction  the  most  frequent.  The  reaction  on  the  surface  of  formed  feces 
often  differs  from  that  in  the  interior.  The  reaction  may  also  change 
upon  prolonged  standing.  An  admixture  of  urine  will  very  soon  pro- 
duce an  alkaline  reaction.  Pathologically  the  reaction  may  become 
either  strongly  acid  or  strongly  alkaline,  according  to  the  kind  of  decom- 
position processes  which  are  occurring  in  the  intestinal  canal.  Typhoid 
and  cholera  stools  are  usually  alkaline.  The  stools  accompanying  a  milk 
or  a  starchy  diet  are  usually,  but  not  always,  acid  in  reaction. 


EXAMINATION  OF  THE  FECES.  445 

PIGMENT    OF  THE  FECES. 

The  color  of  the  feces  of  normal  adults  is  never  due  to  unchanged  bile  pigment 
(bilirubin),  because  the  latter  is  partly  transformed  into  urobilin  in  the  intestine, 
and  i^artly  reabsorbed  and  used  over  again  in  the  organism  (probably  to  help  form 
bile  and  to-  produce  urinary  pigment).  Therefore  the  presence  of  bilirubin  in  the 
feces  always  indicates  some  abnormality  in  the  intestine,  either  some  disturbance 
in  absorption  or  in  the  chemical  processes,  or  else  some  increased  peristalsis.  Bile 
pigment  often  appears  in  diarrheal  stools.  It  can  then  sometimes  be  recognized 
by  its  intense  yellowish  or  greenish  shade.  Chemically,  it  can  be  very  easily 
demonstrated  by  Gmelin's  test  (p.  472j — i.  e.,  by  dropping  a  little  nitric  acid 
directly  uj^on  the  feces  and  noting  the  green,  red,  and  violet  rings  around  the 
drops  of  acid.     The  green  I'ing  is  the  most  characteristic. 

The  normal  jjigment  of  stools  is  urobilin  or  hydrobilirubin.  These  substances 
may  be  easily  extracted  from  the  feces  by  means  of  alcohol  containing  hydrochloric 
acid,  and  then  demonstrated  in  solution  spectroscopically  or  chemically  with  zinc 
chlorid.  (See  Examination  of  the  Urine,  p.  478.)  Ad.  Schmidt  recently  an- 
nounced a  simple  method  of  demonstrating  urobilin  in  the  feces  directly  Avithout 
extraction.^  He  adds  a  little  concentrated  mercuric  chlorid  solution  to  a  small 
amount  of  feces  in  a  porcelain  dish.  If  urobilin  is  present  the  feces  will  turn  red. 
The  reaction  can  be  completed  in  about  a  quarter  of  an  hour.  The  same  test  can 
be  employed  to  demonstrate  the  presence  of  bilirubin,  which  will  turn  green  in 
the  presence  of  the  mercuric  chlorid  solution.  In  the  same  specimen  of  feces 
we  can  therefore  recognize  by  the  contrast  of  color  the  particles  which  contain 
bilirubin  and  those  which  contain  urobilin.  Schmidt  believes  that  the  formation 
of  urobilin  begins  in  the  large  intestine,  or  perhaps  very  low  down  in  the  small 
intestine.  He  was  unable  to  produce  the  change  of  bilirubin  to  urobilin  by 
bacterial  cultures  ;  but  the  fresh  intestinal  wall  itself  in  an  incubator  did  cause  this 
change  to  take  place.  Hence,  it  would  seem  that  the  formation  of  urobilin  is  a 
function  of  the  intestinal  wall. 

BILE  ACIDS  IN  THE  FECES. 
Normally,  the  bile  acids  are  almost  completely  reabsorbed  from  the  intestinal 
canal,  so  that  in  the  feces  only  small  quantities  of  cholic  and  choloidinic  acid  are 
to  be  found.  Very  little  definite  is  known  about  the  presence  of  bile  acids  in  the 
feces  under  pathologic  conditions.  Their  detection  is  a  complicated  process. 
(See  Hoppe-Seyler,  Physiologisch-und  pathologisch-chemische  Analyse,  1893,  p.  47.) 
If  a  large  quantity  of  the  bile  acids  is  present  in  the  feces  they  may  be  detected, 
in  all  probability,  directly  by  extracting  with  dilute  sodium  carbonate  solution 
and  then  performing  Pettenkofer' s  test  (see  p.  475). 

DIGESTIVE  ENZYMES  IN  THE  FECES. 

,  The  enzymes  may  be  extracted  from  the  feces  by  means  of  glycerin  or  of  l)its 
of  fibrin,  which  absorb  the  enzymes  physically.  This  requires  the  addition  of 
antiseptic  substances  to  prevent  putrefaction.  Thymol,  oleum  menthse  piperitse, 
and  oleum  sinapis  volatile  are  well  adapted  for  this  purpose.  The  presence  of  the 
enzyme  can  then  be  demonstrated  by  an  artificial  digestive  test.  To  some  diges- 
tive mixture  we  add  a  little  of  the  glycerin  extract,  or  of  the  fibrin  containing 
the  enzymes.  In  the  latter  case  the  fibrin  itself  may  serve  as  the  object  to  be 
digested,  or  disks  of  coagulated  egg  albumin  (see  ]).  '391)  may  be  used.  These 
digestive  tests  also  require  the  presence  of  small  amounts  of  antiseptic  substances, 
so  as  to  exclude  the  action  of  bacteria.  At  the  conclusion  of  a  digestive  exjieri- 
ment  we  must  examine  microscopically  to  exclude  any  bacterial  action.  The 
action  of  pepsin  is  to  be  tested  in  a  0.2  per  cent,  solution  of  HCl,  that  of  trypsin 
in  0.3  to  0.4  per  cent,  solution  of  Na^CO;,.  Arthus'  method  of  testing  for  trypsin 
may  be  employed  (p.  421).  Both  pepsin  and  trypsin  seem  normally  to  be  de- 
stroyed in  the  intestine. 

v.  Jaksch  generally  found  diastase  and  an   inverting  ferment  in  children's 

*  Verhandl.  des  Cong.  /.  inn.  Med.,  1895. 


446  EXAMINATION  OF  THE  INTESTINE  AND  FECES. 

feces.  Leo  found  the  same  in  adults' .  Xeither  author  was  able  to  demonstrate 
the  i^resence  of  trypsin  in  most  cases,  but  Leo  demonstrated  all  three  ferments  in 
cases  of  diarrhea. 

MUCIN    IN   THE  FECES. 

Stools  normally  contain  considerable  mucin,  which  is  increased  in  catarrhal 
conditions  of  the  intestines.  Sometimes  the  api^earance  and  consistence  of  the 
feces  (see  p.  426)  are  enough  to  show  this.  Chemically,  mucin  can  be  demon- 
strated by  mixing  the  feces  with  water,  adding  an  equal  volume  of  calcium  hy- 
droxid,  in  which  mucin  is  soluble,  and  then  adding  dilute  acetic  acid  to  the  filtrate. 
Cloudiness  indicates  mucin  (v.  Jaksch  method). 

PROTEIN  AND  PEPTONE  OR  PROTEOSES  IN  THE    FECES. 

The  detection  of  these  substances  by  means  of  the  biuret  reaction  must  be  per- 
formed with  special  caution,  because  the  urobilin  which  is  contained  in  the  feces 
also  reacts  to  this  test  (extracting  urobilin  with  alcohol ;  see  p.  467).  Normal 
feces  are  free  from  any  soluble  proteids,  peptones,  and  proteoses,  but  they  can  be 
demonstrated  under  pathologic  conditions,  especially  diarrhea. 

CARBOHYDRATES  IN  THE    FECES. 

Unaltered  starch  is  best  demonstrated  microscopically  (see  p.  438  and  Fig. 
141,  I,  n,  p.  359). 

To  show  the  presence  of  sugar,  feces  are  boiled  with  water,  then  filtered,  and 
the  filtrate  tested  by  Trommer's  test  or  by  the  phenylhydrazin  test  (pp.  482 
and  487). 

QUANTITATIVE   AND    QUALITATIVE  TESTS  FOR  FATS,  FATTY  ACIDS,  AND 

SOAPS  IN  THE  FECES. 

Even  a  microscopic  examination  of  the  stool  will  enable  one  to  form  some 
estimate  of  the  content  of  fat  (p.  438). 

To  estimate  the  amount  of  fat  quantitatively'  and  accurately  a  weighed 
amount  of  the  stool  is  dried  at  100°  C,  then  mixed  with  double  the  quantity  of 
sand,  which  has  been  treated  for  several  days  previously  with  water,  alcohol,  and 
HCl,  and  then  again  with  water.  The  feces-sand  mixture  is  now  extracted  with 
ether,  by  means  of  Soxhlet's  apparatus,  until  no  more  fat  can  be  removed.  This 
usually  requires  between  eight  and  ten  hours.  The  ether  residue  after  thorough 
washing  with  warm  water  indicates  the  amount  of  neutral  fats  and  fatty  acids 
which  are  present.  The  content  of  fatty  acids  is  determined  by  dissolving  a  weighed 
amount  of  the  ethereal  extract  in  alcohol  and  ether  and  then  titrating  with  alco- 
holic i:)Otassium  hydroxid,  with  phenolijhthalein  as  an  indicator. 

To  determine  the  amount  of  the  soaps,  the  feces  are  boiled  with  acidulated 
(HCl)  alcohol,  after  they  have  been  first  extracted  with  ether  in  the  manner  men- 
tioned above  ;  they  are  then  dried  again  and  extracted  once  more  with  ether.  The 
hydrochloric  acid  will  free  the  fatty  acids  from  the  soaps,  and  the  latter  may  then 
be  titrated  in  the  second  ether  extract  as  described  above.  The  amount  of  soap 
present  may  now  be  calculated  from  the  result.  F.  Miiller  has  suggested  a  simpler 
method  when  we  wdsh  to  determine  only  the  neutral  fats  and  the  fatty  acids,  in- 
cluding the  soaps.  He  advises  boiling  the  dried  specimen  directly  with  acidulated 
alcohol  in  order  to  liberate  the  fatty  acids  from  the  soaps.  The  feces  will  then 
contain  only  fatty  acids  and  neutral  fats.  The  former  can  be  titrated  as  above  in 
a  definite  portion  of  the  ether  extract. 

With  these  quantitative  estimates  as  a  basis,  it  is  easy  to  determine  the  quantita- 

^  Cf.  Fried.  Miiller,  "  Untereuchungen  iiber  den  Icterus,"  Zeits.  f.  kUn.  Med.,  vol. 
xii.,  p.  51,  1887  ;  Deucher,  Correapondenzhl.  f.  Schweizer  Aerzte,  1898,  No.  11. 

VoUiard's  work  upon  the  lipolytic  ferment  of  the  stomach  should  be  consulted  for 
the  method  of  estimating  the  neutral  fats  and  the  free  fatty  acids  separately  {Zeits./. 
klin.  Med.,  1901,  vol.  xliii.,  p.  417). 


EXAMINATION  OF  THE  FECES.  447 

tive  variations  of  the  free  fatty  acids  and  soaps  as  compared  with  the  neutral  fats. 
In  healthy  individuals,  and  even  in  cases  of  jaundice,  provided  the  pancreatic 
juice  flows  into  the  intestine,  by  far  the  greater  part  (84.3  per  cent.,  F.  Miiller) 
of  the  fat  is  split  up  into  fatty  acids  or  soaps.  If  the  pancreatic  duct  is  occluded, 
Miiller  found  only  39  per  cent,  of  the  fats  split  up,  as  against  Deucher,  who  found 
80  per  cent.  According  to  Deucher,  the  80  per  cent,  is  composed  almost  exclu- 
sively of  free  fatty  acids,  not  soaps. 

CHEMICAL  AND   SPECTROSCOPIC  TESTS  FOR  BLOOD  IN  THE  FECES. 

Blood  undergoes  a  variety  of  chemical  changes  during  its  passage  through  the 
digestive  tract.  The  most  important  derivatives  which  originate  from  the  hemo- 
globin are  methemoglobin  and  hematin. 

TeichmamnJ 8  hernia  ted  and  Schdnbein-Almen! s  turpentine-guaiac  test  are  the 
most  useful  for  detecting  chemically  the  hemoglobin  derivatives  in  the  feces. 
These  methods  often  give  positive  results  even  when  the  microscopic  examination 
for  blood-corpuscles  fails. 

One  difiiculty  in  utilizing  the  turpentine-guaiac  test  (p.  471)  in  such  compli- 
cated mixtures  as  the  feces  and  the  gastric  contents  (p.  360)  is  that,  according  to 
Weber,  ^  other  substances  can  produce  the  bluish  coloration  of  the  reagent ;  for 
instance,  potato  and  other  vegetable  substances,  preparations  of  iron,  bile,  saliva, 
milk,  and  pus.  By  employing  the  acidulated  ethereal  extract,  Weber  claims 
to  avoid  this  difficulty  :  A  sample  specimen  of  the  feces  or  stomach  contents 
is  well  stirred  with  one-third  its  volume  of  glacial  acetic  acid.  The  mixture  is 
then  shaken  with  ether.  A  little  alcohol  will  hasten  the  clarifying  of  this  ether 
extract.  A  few  cubic  centimeters  are  poured  off,  and  10  drops  of  a  freshly  pre- 
pared tincture  of  guaiac  and  20  to  30  drops  of  oil  of  turpentine  are  added.     If 


Fig.  166.— Direct-vision  hand  spectroscope. 

blood  is  present,  the  mixture  will  turn  violet  blue  ;  if  not,  it  turns  red  brown, 
with  often  a  slightly  greenish  tinge.  The  reaction  is  more  marked  if  we  add 
some  water  and  then  extract  the  blue  pigment  with  chloroform.  In  healthy  indi- 
viduals the  feces  never  react  positively  to  this  test.  Ewald  ^  was  able  to  demon- 
strate an  admixture  of  blood  with  this  method  even  in  gastric  contents  which 
were  not  colored,  especially  in  cancer  of  the  stomach.  Weber  found  the  test 
sensitive  enough  to  demonstrate  blood-pigment  in  the  daily  movement  of  a  healthy 
individual  after  the  ingestion  of  only  3  centimeters  of  blood. 

According  to  Boas,^  the  guaiac  test  for  blood  does  not  always  yield  decisive 
results  in  the  examination  of  the  feces,  since  the  blue  color  is  often  veiled  by  the 
brown  shades  and  rendered  indistinct.  For  this  reason  Boas  recommends  a  con- 
trol test  with  aloin,  as  suggested  by  Klunge,  Schar,  and  Rossel.  According  to 
Rossel,*  the  test  is  performed  as  follows:  5  c.c.  of  the  stool  are  extracted  with 
20  c.c.  of  ether,  in  order  to  remove  the  fat,  which  would  subsequently  interfere 
with  the  test  by  the  formation  of  emulsions.  After  the  removal  of  the  ether, 
3  to  5  c.c.  of  acetic  acid  are  added  to  the  feces,  and  the  mixture  is  again  extracted 
with  ether  in  a  test-tube.  The  acid  ethereal  extract  obtained  in  this  manner  is 
then  employed  for  the  investigation.  A  solution  of  aloin  is  prepared  by  dissolving 
as  much  aloin  as  can  be  placed  upon  the  point  of  a  small  knife  in  froni  3  to  5  c.c. 

'  Berlin,  klin.  Woch.,  1893,  No.  19. 

'  "Ueber  occulte  Magenblutnngen,"  Deut-fch.  med.  Woek.,  1901,  No.  20. 

3  Ibid.,  1903,  No.  47. 

*  Arch.  J.  klin.  Med.,  vol.  Ixxvi.,  p.  505,  1903. 


448 


EXAMINATION  OF  THE  INTESTINE  AND  FECES. 


of  60  to  70  per  cent,  alcohol.  To  the  acetic  acid  ethereal  extract  is  first  added  20  to 
30  drops  of  a  resinous  oil  of  turpentine,  and  then  10  to  15  drops  of  the  solution 
of  aloin;  if  the  stool  contain  blood  the  resulting  mixture  soon  becomes  bright  red, 
and  upon  standing  for  a  time  assumes  a  cherry  color.  If  no  blood  be  present  the 
aloin  solution  remains  yellow  for  at  least  one  to  two  hours,  and  then  acquires  a 
slightly  reddish  tinge.  According  to  Boas,  the  aloin  reaction  may  be  markedly 
accelerated  by  the  addition  of  a  few  drops  of  chloroform.     "With  this  modification 


Red. 


Yellow. 


Green. 


Blue. 


Violet. 


1 

II'    l||J,||yl,X;:!iJ,.id:V.al,H.u,,n™ 

'W^ 


E     1> 


Red. 


Yellow. 


Green. 


Blue. 


Violet. 


Fig.  167. — Important  clinical  spectra  :  1,  Oxyhemoglobin  ;  2,  reduced  hemoglobin ;  3,  methemo- 
globin ;  4,  hematin  in  acid  alcoholic  solution ;  5,  reduced  hematin  in  alkaline  solution ;  6,  hema- 
toporphyrin  in  acid  solution;  7,  urobilin  (after  Salliowski). 


agitation  of  the  mixture  results  in  the  formation  of  reddish  droplets  which  settle 
in  the  bottom  of  the  tube  as  an  intense  red  precipitate.  Under  certain  conditions 
Boas  regards  the  aloin  test  as  more  sensitive  than  the  guaiac  test.  According  to 
Brandberg,  the  oil  of  turpentine  may  be  replaced  by  a  dilute  solution  of  hydrogen 
peroxid. 

An  ordinary  hand  spectroscope  (direct-vision,  after  Browning,  Fig.  166)  is 
sufficient  for  the  spectroscopic  detection  of  the  derivatives  of  the  blood-pigment. 
The  substance  must  be  well  diluted  with  water  and  examined  in  the  sunlight.    The 


URINARY  EXAMINATION.  449 

spectroscope  should  first  be  adjusted  by  moving  the  inner  tube  sothatFraunhofer's 
lines  can  be  easily  seen  if  the  instrument  is  held  toward  a  white  surface  or  the  sky. 
In  order  to  avoid  side  lights  and  to  make  an  examination  with  an  ordinary  test 
tube  we  employ  the  apparatus  ''  B"  (see  figure),  made  of  brass  and  blackened  ou 
the  inside.  This  can  be  shoved  over  the  prism  end  of  the  spectroscope,  and  fas- 
tened by  means  of  the  screw,  s.  The  test  tube,  with  the  substance  to  be  examined, 
is  placed  in  the  cross-tube  C,  and  the  light  is  admitted  through  B. 

The  normal  pigments  of  the  feces,  even  when  considerably  diluted,  frequently 
mask  the  characteristic  spectrum  of  the  hemoglobin  derivatives  by  their  diffuse 
absorption  of  light ;  hence  a  mere  watery  dilution  of  the  feces  is  not  to  be  recom- 
mended in  doubtful  cases.  The  following  method  is  more  desirable  :  Several  cubic 
centimeters  of  the  stool  to  be  examined  are  mixed  with  water  and  acidulated  with 
several  drops  of  sulphuric  acid  until  the  Congo-red  reaction  is  masked  (see  p. 
372).  The  mixture  is  then  filtered,  and  the  filtrate  extracted  with  ether.  The 
extraction  may  be  hastened  by  adding  a  few  drops  of  alcohol.  If  the  feces  con- 
tain blood  the  ether  turns  reddish  brown  and  shows  spectroscopically  the  charac- 
teristic bands  of  acid  hematin  (see  Fig.  167). 

If  the  fluid  to  be  examined  is  alkaline,  we  need  only  to  acidulate  with  a  little 
acetic  acid  to  obtain  the  spectrum  of  the  acid  solution.  Conversely,  the  spectrum 
of  the  alkaline  solution  can  be  easily  obtained  from  the  acid  by  adding  soda 
solution.  Of  course,  the  hemoglobin  of  muscle  fiber  gives  the  same  reaction  and 
the  same  spectrum  as  the  hemoglobin  of  blood,  so  that  we  must  be  careful  to  exclude 
any  mistake  by  seeing  that  the  patient  does  not  ingest  any  large  amount  of  raw  or 
half-cooked  meat. 


URINARY   EXAMINATION. 

AMOUNT  OF  URINE. 

The  daily  volume  of  urine  excreted  by  a  healthy  adult  varies  under 
average  conditions  between  1500  and  2000  c.c'  An  abundant  inges- 
tion of  water  will  considerably  increase,  and  a  diminished  ingestion 
will  correspondingly  diminish,  the  amount.  The  amount  will  vary  in 
inverse  ratio  to  the  insensible  perspiration  ;  hot  weather  diminishes  and 
cold  weather  increases  the  amount.  Profuse  perspiration,  diarrhea, 
and  vomiting  all  decidedly  diminish  the  amount.  In  children  or  abnor- 
mally small  individuals  the  amount  of  urine  is  correspondingly  less. 
The  normal  average  for  such  a  person  can  be  determined  from  the  fol- 
lowing formula,  supposing  the  average  weight  of  a  healthy  adult  to  be 
75  kilos  (165  pounds)  : 

X  :  1500-2000  :  :  a  :  75, 

where  x  represents  the  daily  amount  of  urine  sought  and  a  the 
weight  of  the  individual  in  kilos.  Children,  and  especially  nursing  in- 
fants, on  account  of  the  preponderance  of  liquid  in  their  food,  excrete 
proportionally  a  larger  amount  of  urine  than  is  represented  by  the 
formula. 

]  [In  this  country  the  average  quantity  eliminated  in  twentv-four  hours  would  fall 
considerably  below  this.     The  figures  usually  given  are  1000  to  1500  c.c— Ed.] 
29 


450  URINARY  EXAMINATION. 

According  to  Martin  and  Ruge/  67  per  cent,  of  all  newborn  infants  excrete 
urine  the  first  day  of  life,  but  generally  only  after  the  lapse  of  twelve  or  more 
hours.  The  remaining  33  per  cent,  do  not  void  urine  until  the  second  or  the 
beginning  of  the  third  day.  The  daily  amount  of  urine  of  the  newborn  varies 
between  150  and  200  c.c.  Eancke,  Bischoff,  and  others  estimate  the  excretion  per 
diem  from  the  third  to  the  fifth  year  as  about  700  c.c. 

As  a  rule,  less  urine  is  voided  during  the  night  than  during  the  day  (from  one- 
fourth  to  one-half  as  much). 

According  to  Quincke,'^  this  condition  is  reversed — i.  e.,  more  urine  is  excreted 
during  the  night  than  during  the  day  in  heart  and  kidney  diseases,  in  the  aged 
with  arteriosclerosis,  in  cachexia,  and  in  diabetes  insipidus.  Under  these  condi- 
tions the  amount  voided  at  night  may  be  doubled  that  voided  during  the  day. 
Not  only  the  watery,  but  the  solid  constituents  as  well,  are  thus  increased. 
Quincke  regards  this  phenomenon  as  the  result  of  a  nocturnal  recuperation  of 
the  damaged  organs  (heart  and  kidneys). 

Polyuria  means  an  •  increase,  oliguria,  a  diminution,  in  the  quantity 
of  urine. 

The  quantity  of  urine  in  pathologic  conditions  depends,  first,  upon 
the  condition  of  the  secreting  renal  parenchyma,  and,  second,  upon  the 
rapidity  of  the  blood-current  in  the  kidneys  (Heideuhain).  It  will 
therefore  be  affected  by  a  general  circulatory  disturbance,  as  well  as  by 
disease  of  the  kidneys  alone.  To  alter  it  appreciably  both  kidneys 
must  be  diseased,  for  otherwise  the  healthy  kidney  would  assume  vica- 
riously the  total  function,  as  regularly  occurs  in  unilateral  nephrectomy. 
The  more  acute  the  nephritis,  the  more  the  amount  of  urine  falls  below 
the  normal ;  the  more  chronic  the  course  of  a  nephritis,  the  more  the 
amount  exceeds  the  normal.  Although  as  yet  we  have  no  definite 
explanation  of  the  latter  phenomenon,  it  is  presumably  due  to  a  compensa- 
tory process.^  This  increase  reaches  a  maximum  in  the  true  contracted 
kidney,  where  the  volume  has  been  found  to  be  as  high  as  12  liters 
per  day  (Bartels).  In  regard  to  the  amount  of  secretion,  the  so-called 
chronic  parenchymatous  nephritis  resembles  sometimes  acute  nephritis 
and  sometimes  the  contracted  kidney.  A  similar  variation  in  amount  is 
observed  in  amyloid  kidney.  Diseases  of  the  heart  and  lungs,  leading 
to  passive  congestion,  are  associated  with  a  diminution  in  the  amount 
of  urinary  excretion,  which  clearly  depends  upon  a  slowing  of  the  renal 
circulation.  In  such  disturbances  the  estimation  of  the  amount  of 
urine  is  therefore  of  great  diagnostic  and  prognostic  significance. 

The  increased  excretion  following  convulsions  (especially  in  hyste- 
ria— the  so-called  urina  spastica)  and  after  attacks  of  angina  pectoris 
is  probably  to  be  attributed  to  some  vasomotor  influence.  Many  other 
alterations  in  the  volume  of  the  urine  depend  upon  quantitative  and  quali- 
tative variations  in  the  substances  thus  eliminated,  and  are  primarily  in- 
duced by  disturbances  of  metabolism — e.  g.,  the  polyuria  in  diabetes  mel- 
litus.     We  do  not  know  the  cause  of  the  polyuria  in  diabetes  insipidus. 

1  Vierordt,  Daten  und  Tabellen,  1888. 

^  Arch.  f.  exp.  Path.  u.  Pharm.,  vol.  xxxii.,  parts  8  and  4. 

^The  increase  of  blood-pressure  is  frequently  assumed  as  an  explanation  of  the 
polyuria.  This  assumption  seems  to  the  writer  unwarranted,  since  he  has  observed  cases 
with  long-continued  polyuria  and  typical  contracted  kidneys  in  which  the  autopsy 
revealed  absolutely  no  trace  of  cardiac  change. 


SPECIFIC  GRAVITY  OF  THE   URINE.  451 


FREQUENCY  OF  URINATION. 

Although  varying  decidedly  in  different  individuals,  the  frequency  of  urination 
corresponds  in  general  to  the  amount  of  urine  excreted.  It  is  also  influenced, 
however,  by  any  inflammatory  affection  of  the  urinary  tract  or  by  any  disturb- 
ance of  innervation  of  the  bladder.  The  increased  frequency  of  urination  from 
inflammatory  conditions  of  the  urinary  tract  depends  upon  a  stimulation  of  the 
bladder  reflexes  (pollakiuria,  bladder  tenesmus).  Although  observed  chiefly  in 
affections  of  the  bladder,  and  especially  of  its  neck  or  of  the  urethra,  this  fre- 
quent voiding  of  urine  may  depend  also  upon  kidney  disease,  resulting  either  from, 
a  pathologic  reflex  emanating  from  the  kidney,  or  from  the  irritation  of  an  abnor- 
mal urine  upon  the  mucous  membrane  of  the  bladder.  Diseases  of  the  spinal 
cord  which  either  increase  the  irritability  of  the  bladder  or  weaken  the  sphincter 
are  also  responsible  for  an  increased  frequency  of  urination.  An  abnormally  infre- 
quent urination  depends  upon  some  mechanical  or  nervous  obstacle  to  the  empty- 
ing of  the  bladder.  (See  later,  Examination  of  the  Nervous  System,  Innerva- 
tion of  the  bladder.) 


SPECIFIC  GRAVITY  OF  THE  URINK 

For  the  sake  of  simplicity  the  specific  gravity  of  the  urine  is  ordi- 
narily expressed  in  four  figures,  taking  the  specific  gravity  of  distilled 
water  as  1000  instead  of  1.  Special  aerometers  called  urinometers  are 
employed  for  this  purpose.  Their  scale  is  marked  from  1000  to  1050. 
To  insure  a  correct  reading  the  subdivisions  should  be  sufficiently  wide 
apart.  Many  urinometers  are  not  very  accurately  constructed,  so  that 
it  is  always  well  to  compare  a  new  instrument  with  a  reliable  one ;  at 
least,  it  can  be  ascertained  whether  it  reads  1000  in  distilled  water  at 
the  ordinary  room  temperature,  15°  C.  (60°  F.).  Although  a  very  large 
urinometer  is  more  accurate,  a  smaller  instrument  requires  less  urine, 
which  sometimes  is  a  distinct  advantagre. 

In  the  determination  of  the  specific  gravity  the  urine  is  poured  into 
a  tall  glass  cylinder  (a  urinometer  and  an  appropriate  glass  cylinder  are 
generally  obtained  together),  the  urinometer  is  immersed  in  the  urine, 
and  then  with  the  eye  at  the  level  of  the  surface  of  the  urine  the  sub- 
division is  read  off  which  corresponds  to  the  lowest  part  of  the  curve 
of  the  meniscus.  For  the  sake  of  accuracy  the  cylinder  should  be 
sufficiently  large  to  allow  the  urinometer  free  motion.  The  bulb  of  the 
urinometer  should  not  be  allowed  to  stick  against  the  side  of  the  ves- 
sel, all  bubbles  or  froth  should  be  removed  from  the  surface  of  the 
urine  by  means  of  filter  paper,  and  the  urine  should  be  at  the  ordinary 
room  temperature.  If  the  urine  is  colder  than  15°  C,  one-third  of 
the  urinometer  unit  should  be  subtracted  for  every  degree  of  Centigrade 
below  the  ordinary  temperature ;  if  warmer,  the  proportionate  amount 
should  be  added.  Since  the  specific  gravity  of  individual  specimens 
of  urine  varies  so  decidedly  during  the  day,  it  is  imperative  that  the 
specific  gravity  of  a  mixed  sample  from  the  total  twenty-four-hour 
secretion  be  obtained  if  any  definite  conclusions  are  to  be  drawn  from 
the  results. 

If  the  specimen  is  too  small  to  work  with  in  the  ordinary  way,  it 


452  URINARY  EXAMINATION. 

is  a  simple  matter  to  dilute  it  with  distilled  water  in  a  known  propor- 
tion, to  estimate  the  specific  gravity  of  the  mixture,  and  then  to  calcu- 
late the  specific  gravity  of  the  urine  at  least  approximately. 

The  specific  gravity  of  a  twenty-four-hour  specimen  of  urine 
varies  normally  from  1015  to  1020.  Copious  beer-  or  water-drinking 
may  bring  it  as  low  as  1002  ;  excessive  perspiration  as  high  as  1040. 
The  ingestion  of  food  and  liquids,  or  the  loss  of  water  from  the 
skin  or  from  the  lungs,  is  responsible  for  the  marked  variations 
which  occur  in  single  specimens,  as  well  as  in  the  twenty-four-hour 
specimen. 

Pathologically,  the  specific  gravity  is  influenced  by  the  secreting 
parenchyma  of  the  kidney,  by  the  velocity  of  the  renal  circulation,  and 
by  abnormalities  of  metabolism.  In  acute  nephritis  the  urine  is  con- 
centrated and  of  a  high  specific  gravity  j  in  chronic  nephritis  due  to  a 
true  contracted  kidney,  the  urine  is  profuse  and  of  a  low  gravity.  The 
specific  gravity  usually  varies  inversely  with  the  amount  of  urine.  Both 
under  physiologic  and  pathologic  conditions,  therefore,  a  scanty  urine  is 
more  concentrated  than  a  more  profuse  one.  Diabetes  mellitus  forms  an 
exception  to  the  rule,  since  the  excretion  of  sugar  produces  a  high 
specific  gravity  despite  the  excessive  amount  of  urine ;  this  is  so  charac- 
teristic that  a  diagnosis  is  often  possible  on  this  ground  alone.  Some 
types  of  nephritis  are  also  exceptions  to  the  above  rule,  such  as  those 
showing  a  tendency  to  uremia  and  concomitant  diminution  in  the  excre- 
tion of  solids ;  these  cases  present  a  low  specific  gravity  with  a  small 
amount  of  urine.  Again,  in  some  cachectic  conditions,  even  without 
nephritis,  diminished  metabolism  and  the  lessened  ingestion  of  food  as 
well  as  of  water  produce  a  fall  in  volume  of  urine  and,  at  the  same 
time,  a  low  specific  gravity. 

The  specific  gravity  is  a  pretty  accurate  indication  of  the  amount  of 
solids  excreted  in  the  urine.  The  solids  excreted  in  1  liter  of  urine 
can  be  approximately  represented  in  grams  by  multiplying  the  last  two 
figures  of  the  specific  gravity  by  2.2337.^  A  urine  of  high  specific 
gravity  is  called  concentrated.  The  urea  is  mainly  responsible  for  the 
specific  gravity.  For  this  reason  alone,  apart  from  the  diminished 
secretion  of  water,  a  fever  urine  is  always  concentrated. 

In  reference  to  the  value  of  the  determination  of  the  specific  gravity 
of  the  urine  as  a  substitute  for  the  cryoscopic  urinary  examination, 
see  p.  551. 

TRANSPARENCY  OF    TliE  URINE, 

Freshly  voided  normal  urine  is  absolutely  clear  and  transparent ;  but 
after  it  has  been  standino-  for  some  time  an  indistinct  cloud  of  so-called 
mucin,  "the  nubecula,"  appears  (see  p.  468).  Various  other  insoluble 
substances  may  cloud  pathologic  specimens  of  urine.  (See  the  section 
on  the  Sediment  and  Turbidity  of  the  Urine,  p.  553  et  seq.) 

^  Yierordt,  Daten  unci  Tahellen  zum  Gebrauch  fiir  Mediciner.  1888. 


COLOR   OF  THE   URINE.  453 

COLOR  OF   THE  URINE, 

NORMAL    URINARY    PIGMENT. 

The  color  of  the  urine  varies  normally  within  different  shades  of 
yellow,  the  depth  of  color  increasing  in  direct  proportion  to  the  specific 
gravity.  The  abundant  urine  of  a  drinker  or  of  a  person  with  con- 
tracted kidneys  may  be  as  pale  as  water,  as  contrasted  with  the  scanty 
urine  of  acute  nephritis,  of  passive  congestion,  or  of  fever,  which  is 
almost  always  dark.  In  diabetes  mellitus,  despite  the  high  specific 
gravity,  the  urine  is  exceptionally  pale.  This  is  of  similar  diagnostic 
importance  as  the  great  increase  in  amount.  The  urine  in  anemic  indi- 
viduals is  always  paler  than  normal,  except  in  pernicious  anemia.  There 
the  urine  is  quite  dark,  because  this  disease  is  associated  with  a  rapid 
destruction  of  the  red  corpuscles,  and,  as  is  well  known,  the  urinary 
pigments  are  derived  from  the  hemoglobin. 

The  only  method  of  designating  the  color  of  the  urine  is  to  compare 
it  with  certain  fixed  shades  on  a  chart.  In  Neubauer  and  Vogel's 
book/  unfortunately,  only  a  few  different  shades  are  represented. 
Radde's  "^  scale  can  be  used  for  other  purposes  as  well,  and  is  more  highly 
recommended.  Naturally,  to  obtain  imiformity  of  results,  a  certain 
uniform  thickness  of  the  urine  must  be  observed  in  each  case,  and  the 
specimen  must  be  held  against  a  white  background.  For  the  qualitative 
determination  of  the  normal  urinary  pigment  (urochrome)    see  p.  504. 

COLORING  OF  THE  URINE  BY  PATHOLOGIC  URINARY  PIGMENTS. 

Hemoglobinuria  ;  Hematuria. — Urine  which  contains  blood 
or  hemoglobin  presents  a  red,  brownish-red,  or  sometimes  even  a 
greenish-black  or  black  color.  These  variations  depend  partly  upon  the 
amount  of  admixed  blood,  and  partly  upon  the  degree  of  alteration  of 
the  blood-pigment  in  the  urine.  Urine  containing  hemoglobin  proper 
is  reddish,  while  that  containing  methemoglobin  is  more  brownish.  (See 
Spectroscopic  Demonstration  of  Blood-pigment,  p.  471  et  seq.)  Such 
urines  are  usually  cloudy  on  account  of  the  blood-corpuscles  and  other 
organic  mixtures,  and  in  hemoglobinuria  on  account  of  flakes  of  hemo- 
globin. Upon  standing,  these  elements  all  settle  in  the  form  of  a 
sediment. 

Hematoporphyrinuria  (see  p.  471). — Urine  which  contains 
hematoporphyrin  is  sometimes  excreted  after  persistent  use  of  sulphonal, 
trional,  or  tetronal.  Its  color,  if  the  layer  of  urine  is  thick,  is  a  very 
dark  brown  or  almost  a  black  ;  and  if  thin  a  yellowish  red  to  violet. 

With  jaundice  the  urine  contains  bile  pkpncnU^  and  its  color  varies 
from  a  dark  yellow  or  green  to  a  brown  ov  bhick,  depending  upon  the 
concentration  of  the  urine  and  the  amount  of  bile  pigment,  or  upon  its 

^  Anleitung  znr  qiialitativen  unci  qnantitativen  Analyse  des  Harnes,  older  editions. 
Tn  the  more  recent  editions,  edited  by  Huppert  and  Tiiomas,  that  plate  is  no  longer 
included. 

^  Slenochromatische  Anstalt,  Hamburg,  1877. 


454  URINARY  EXAMINATION. 

chemical  modifications.  When  such  a  urine,  especially  if  strongly 
acid,  is  allowed  to  stand  in  the  cold  for  some  time,  needle-like  crystals 
of  bilirubin  separate  out  and  settle  with  the  rest  of  the  sediment.  (See 
p.  472,  Demonstration  of  Biliary  Coloring  Matter;  also  p.  561  et  seq.) 
The  urine  of  patients  suffering  with  melanotic  ttimor,  a  very  rare 
condition,  contains  melanin  (phymatorrhusin).  It  becomes  dark  brown 
to  black  after  prolonged  exposure  to  the  air,  the  melanin  having  sepa- 
rated from  the  "  melanogen  "  of  the  urine.  As  a  rule,  the  urine  is  per- 
fectly clear,  although  it  may  rarely  become  cloudy  from  a  granular  pre- 
cipitate of  the  melanin.      (See  Demonstration,  p.  477  et  seq.) 

The  large  amount  of  urobilin  in  the  urine  of  some  varieties  of 
icterus  (cirrhosis)  shows  a  similar  dark-brown  color.  (See  Reaction,  p. 
478  et  seq.) 

Various  aromatic  products,  such  as  result  from  decomposition  by 
putrefactive  processes  (peritonitis,  suppuration,  etc.),  are  often  responsible 
for  a  remarkably  dark-colored  urine.  This  color  is  sometimes  seen  even 
in  a  freshly  voided  specimen,  but  more  commonly  appears  after  exposure 
to  the  oxidation  of  the  air.  Either  pyrocatechin,  alkapton,  or  mdican 
may  give  rise  to  a  dark-colored  urine.  If  much  indican  is  present 
there  is  sometimes  a  conspicuous  precipitation  of  indigo  (see  pp.  475 
and  561).  Although  the  bluish  tinge  of  the  indigo  may  be  masked  by 
the  color  of  the  urine,  a  bluish-black  scum,  due  to  the  separation  of  the 
indigo,  generally  a  rises  to  the  surface.  (See  Demonstration  of  Indigo 
and  Indican,  p.  475  et  seq.) 

Indigo  may  be  formed  from  indican  even  before  the  urine  is  voided.  The 
author  once  obtained  a  specimen  of  grass-green  urine  from  an  apparently  healthy 
boy  without  being  able  to  determine  the  precise  condition.  The  chloroform 
extract  showed  that  the  color  depended  upon  the  admixture  of  the  blue  of  the 
indigo  with  the  yellow  of  the  urine. 

MEDICINAL   PIGMENTS    WHICH    COLOR    THE    URINE. 

There  are  so  many  drugs  which  may  be  responsible  for  an  abnormal 
color  of  the  urine  that  it  is  possible  to  mention  here  only  the  most 
important.  At  the  same  time  the  writer  wishes  to  emphasize  the  fact 
that,  if  the  urine  shows  any  peculiar  or  extraordinary  color  not  other- 
wise explainable,  we  should  consider  the  possibility  of  attributing  it  to 
the  administration  of  some  drug. 

Carbolic  acid,  coal-tar  products,  hydroquinone,  resorcin,  pyrocatechin, 
naphthalene,  salol,  the  arbidin  derived  from  the  leaves  of  Uva  ursi,  and 
many  other  aromatic  substances,  when  administered  internally,  and 
sometimes  even  when  employed  externally,  produce  a  dark  olive-green 
to  black  urine.  The  dark  color  frequently  becomes  apparent  only  after 
considerable  exposure  to  the  air  or  after  the  urine  becomes  alkaline.  It 
depends  upon  the  formation  of  colored  compounds  by  the  oxidation  of 
the  excreted  drugs.  Hydroquinone  and  pyrocatechin  are  especially 
prone  to  result  from  such  oxidations,  and  they  cause  the  dark  color  of 
urines  containing  phenol,  salol,  and  arbutin. 


REACTION  OF  THE   URINE.  455 

The  appearance  of  this  color  in  the  urine  should  occasion  no  alarm  unless  one 
of  these  drugs  is  being  used  externally ;  as,  for  instance,  in  the  old  Lister  anti- 
septic employment  of  carbolic  acid.  Then  the  drug  is  evidently  being  absorbed 
in  considerable  and  uncontrollable  amount,  although  not  intended  to  be  absorbed 
at  all.  As  a  product  of  excretion  simply,  the  dark  color  is  of  no  particular  sig- 
nificance. The  dread  of  it  is  largely  due  to  the  frequency  with  which  it  was  met 
after  the  use  of  the  carbolic  spray  of  Lister's  method.  Often  quite  moderate 
doses  of  salol  (30  gr.  (2gm.)  a  day)  will  be  accompanied  by  the  excretion  of  a  black 
urine  without  any  ill  efiects,  while  doses  large  enough  to  cause  toxic  symptoms  may 
cause  no  discoloration.  These  variations  depend  to  a  considerable  extent  upon 
the  degree  of  acidity  of  the  urine,  as  well  as  upon  the  length  of  time  it  is  exposed 
to  the  air. 

The  administration  of  chrysarobin,  rhubarb,  senna  or  cascara  may 
produce  a  yellow  or  reddish-brown  urine,  which  will  become  distinctly 
red  if  the  reaction  is  alkaline.  (This  is  due  to  the  presence  of  chiyso- 
phauic  acid ;  see  p.  503.)  Santonin  is  apt  to  produce  a  safPron-yellow 
or  greenish  color,  which  changes  to  red  if  the  urine  is  rendered  alkaline. 
(See  Test  for  Santonin,  p.  503.)  The  pigment  of  madder,  of  beets,  and 
of  hucMeherries  may  under  certain  conditions  be  excreted  in  the  urine 
(Gorup-Besanez). 

ODOR    OF    THE    URINE, 

Normal  urine  possesses  a  peculiar  faint  odor  which  is  not  particularly 
unpleasant.  The  disagreeable  so-called  urinous  odor  depends  upon  bac- 
terial decomposition  taking  place  either  in  the  urinary  tract  or  after  the 
voiding  of  the  urine.  It  is  often  called  ammoniacal,  since  ammonia  can 
usually  be  demonstrated  in  such  a  specimen.  There  are,  however,  other 
odorous  substances  concerned  besides  ammonia,  as  one  can  appreciate  by 
the  sense  of  smell — e.  g.,  aromatic  decomposition  products  (phenol). 
Decomposing  albuminous  urine  presents  an  odor  so  characteristic  as  to 
justify  a  definite  diagnosis  of  the  presence  of  proteid. 

Decomposition  in  the  urinary  tract,  or  the  absorption  of  hydrogen  sulphid 
from  putrefactive  areas  in  the  body,  will  sometimes  produce  an  odor  of  sulphu- 
retted hydrogen  (hydrothionuria). 

Various  odorous  substances  if  introduced  into  the  body  appear  directly  as  such 
in  the  urine — e.  g.,  the  odorous  substances  of  valerian,  leek,  castor,  crocus  (saffron), 
asafetida,  meat,  bouillon,  and  coffee.  Other  substances  form  characteristic  odorous 
compounds  in  the  body  about  which  little  is  understood,  but  which  are  excreted  in 
urine — e.  g.,  balsams,  especially  the  balsam  of  copaiba,  cubebs,  saffron,  and  the  oil 
of  turpentine.  Even  tiny  doses  of  the  last  impart  a  very  distinct  odor  of  violets. 
The  peculiar  odor  of  the  urine  after  eating  asparagus  is  due  to  methylmerkaptan 
(Nencki). 

REACTION   OF   THE   URINE. 

Normal  urine  has  an  acid  reaction,  due  not  to  free  acid,  but  to  acid 
salts,  especially  dihydrogen  sodium  phosphate,  H^NaPo^.  At  times  the 
reaction  may  be  amphoteric — i.  e.,  the  urine  may  turn  blue  litmus  paper 
red,  and  red  paper  a  faint  blue.  This  is  due  to  the  presence  of  the  acid 
dihydrogen  phosphate  and  the  alkaline  disodium  })hoRphate  in  a  definite 
relationship  of  such  a  nature  that  each  salt  is  capable  of  exerting  its 
influence  upon  the  indicator  without  interference  with  the  other.     This 


456  URINARY  EXAMINATION. 

is  only  possible  provided  the  acid  salt  is  not  present  in  too  great  an 
excess. 

Specimens  of  urine  voided  at  different  times  of  the  day  react  differ- 
ently, a  variation  depending  largely  upon  the  phenomena  of  digestion. 
During  digestion  the  secretion  of  hydrochloric  acid  by  the  stomach 
diminishes  the  acidity  of  the  urine,  which  may  even  become  alkaline. 
This  diminution  of  acidity  is  shown  by  a  more  ready  precipitation  of 
the  earthy  phosphates  and  carbonates,  so  that  the  urine  is  cloudy  when 
first  voided  or  when  heated.  The  more  hydrochloric  acid  secreted  by 
the  stomach,  the  more  decidedly  alkaline  the  urine  simultaneously 
excreted,  so  that  such  a  turbidity  after  eating  oftentimes  suggests  a  diag- 
nosis of  pathologic  gastric  hyperacidity.  It  is  incorrect  to  consider  the 
precipitation  per  se  a  manifestation  of  perverted  metabolism  inducing  phos- 
phaturia.  If  the  acid  contents  of  the  stomach  are  vomited  or  removed 
by  gastric  lavage,  the  acidity  may  be  still  further  reduced  or  the  urine 
even  rendered  decidedly  alkaline,  although  oftentimes  without  vomiting 
or  lavage,  the  degree  of  hypersecretion  alone  is  sufficient  to  cause  quite 
a  marked  permanent  phosphaturia  and  an  alkaline  urine.  Perhaps  the 
acid  is  excreted  in  the  feces  ;  but  thus  far  we  have  no  direct  investigation 
of  this  point. 

The  nature  of  the  food  ingested  will  also  alter  the  reaction  of  the 
urine.  A  vegetable  diet  or  a  liberal  consumption  of  wine  or  of  fruit 
may  cause  the  excretion  of  an  alkaline  urine ;  the  alkalinity  is  occasioned 
by  the  fact  that  the  organic  acids  become  oxidized  in  the  body  to  alka- 
line carbonates.  On  the  other  hand,  a  diet  rich  in  proteid  or  meat  will 
intensify  the  acid  reaction,  because  acids,  especially  sulphuric  acid, 
result  from  the  oxidation  of  proteid  in  the  organism. 

Alkaline  drugs  render  the  urine  alkaline.  All  acids  not  oxidized  to 
carbonic  acid — e.  g.,  the  mineral  and  aromatic  acids — intensify  its  acidity. 
Most  of  the  fatty  series  are  oxidized  to  carbonic  acid,  and  so,  in  moder- 
ate doses,  do  not  usually  increase  the  acidity.  Alkaline  bacterial  fer- 
mentation of  the  urine  outside  the  urinary  tract  is  often  responsible  for 
an  alkaline  reaction,  especially  when  the  urine  is  kept  in  a  warm  place. 

The  following  pathologic  conditions  either  diminish  the  acidity  of  the 
urine  or  render  it  alkaline  : 

1.  Abnormal  conditions  of  gastric  digestion. 

2.  The  admixture  of  alkaline  secretions  from  exudations  of  the  uri- 
nary tract  (cystitis,  gonorrhea,  rupture  of  abscess  into  the  tract). 

3.  The  rapid  absorption  of  transudations  or  exudations,  the  alkaline 
salts  of  which  are  excreted  in  the  urine. 

4.  The  alkaline  fermentation  of  the  urine  within  the  urinary  tract. 
To  understand  the  significance  of  an  alkaline  reaction  of  the  urine, 

it  is  important  to  determine  whether  this  depends  upon  free  ammonia  or 
upon  a  fixed  alkali.  If  red  litmus  paper  placed  near  the  surface  of  the 
urine  is  turned  blue  without  being  immersed,  or  if,  when  a  glass  rod 
dipped  in  dilute  hydrochloric  acid  is  held  over  the  surface  of  the  urine, 
white  fumes  of  ammonium  chlorid  are  produced,  or  if  we  note  a  strong 
ammoniacal  odor,  the  reaction  is  caused  by  a  volatile  alkali,  probably 


SEPARATION  OF  THE   URINES  OF  THE  TWO  KIDNEYS.     457 

ammonia.  Moistened  red  litmus  paper  suspended  for  a  sufficiently  long 
time,  one-quarter  to  one-half  hour,  over  a  normal  acid  urine  will  become 
blue,  showing  that  a  certain  amount  of  ammonia,  even  without  any 
apparent  fermentation,  is  given  off  by  a  freshly  voided  acid  urine ;  but 
this  blue  color  will  disappear  when  the  paper  is  dried.  It  is  character- 
istic of  urines  which  owe  their  alkalinity  to  fixed  alkalies  that  only 
upon  the  immersion  of  red  litmus  paper  in  the  urine  will  the  paper 
become  blue,  and  that  this  color  is  permanent  even  upon  the  application 
of  heat. 

Whenever  the  reaction  of  the  urine  is  alkaline  from  free  ammonia,  it 
is  safe  to  assume  that  the  condition  is  the  result  of  the  decomposition  of 
the  urine  or  ammoniacal  fermentation.  To  decide  whether  this  has 
taken  place  within  or  outside  the  urinary  tract,  it  is  necessary  to  test 
the  urine  directly  after  it  has  been  voided.^ 

The  alkaline  fermentation  of  the  urine  brought  about  by  the  action 

NH. 

of  micro-organisms  is  characterized  by  the  change  of  urea,  ^'^  <C-jv^tt^' 

into  NH2  COOXH^  and  (NHJg  CO3,  with  the  taking  on  of  one  or  two 
molecules  of  water,  as  the  case  may  be.  These  latter  two  substances, 
in  consequence  of  their  instability,  easily  break  down  and  give  off. 
ammonia.  The  alkaline  reaction  due  to  fixed  alkalies  is  never  caused 
by  decomposition  of  the  urine,  but  by  other  conditions  already  men- 
tioned. 

The  urine  of  dogs  has  been  rendered  alkaline  (without  the  aid  of 
bacteria)  by  administering  an  excessive  amount  of  milk  of  lime.  The 
normal  acidity  of  the  urine  may  be  pathologically  increased  by  an  in- 
creased decomposition  of  the  body  proteids,  especially  in  fever.  The 
cause  of  the  acid  in  this  case  is  the  same  as  in  the  ingestion  of  food 
rich  in  proteid. 

It  is  not  yet  definitely  determined  whether  patients  with  the  so- 
called  uric  acid  diathesis  excrete  an  abnormally  acid  urine.  (See  541 
et  seq.  for  the  Quantitative  Estimation  of  the  Reaction  of  the  Urine ; 
Acidimetry ;  Alkalimetry). 

SEPARATION  OF  THE    URINES    OF  THE  TWO 
KIDNEYS. 

Modern  renal  surgery  frequently  demands  the  separate  examination  of  the 
urine  fi-om  each  kidney.  This  requirement  is  most  exactly  met  by  ureteral 
catheterization  by  means  of  the  cystoscope,  for  the  details  of  which  the  reader  is 
referred  to  the  text-books  of  cystoscopy. 

This  method  requires  special  technical  training,  and  may  be  replaced  to  a 
certain  extent  by  the  use  of  the  so-called  urinary  separators  which  have  recently 
been  devised.  All  these  instruments  depend  upon  a  similar  principle  :  the  blad- 
der is  emptied,  a  sagittal  septum  is  introduced  into  the  viscus,  and  the  separate 
urines  are  withdrawn  by  catheters  appropriately  attached  to  the  sagittal  septum. 

^  When  it  is  not  possible  to  examine  the  urine  perfectly  fresh,  the  addition  of  about 
one-third  its  volume  of  chloroform  water  (1 :  200),  or  of  a  few  pieces  of  coarsely  granu- 
lated camphor,  will  preserve  tlie  specimen. 


458 


URINAE  Y  EXAMINA TION. 


The  best  instrument  of  this  type  seems  to  be  that  of  Luys  (Fig.  168),  which 
Garre  ^  describes  as  follows  : 

' '  It  consists  of  two  metallic  grooves  which  may  be  united  to  form  a  catheter 
of  about  the  caliber  of  22  (French),  and  having  the  usual  curve.  Since  these  lat- 
eral metallic  grooves  embrace  a  third  flat 
piece  they  form  a  two-way  catheter,  each 
side  of  which  possesses  two  eyes  at  one  ex- 
tremity and  a  lateral  discharge  tube  at  the 
other.  The  middle  piece  is  enclosed  in  a 
condom  which  may  be  made  tense  by  a 
screw,  so  that  it  fills  the  concavity  of' the 
curve.  The  instrument  is  introduced  closed, 
the  urine  in  the  bladder  is  drawn,  the  sep- 
tum is  made  tense  by  turning  the  screw, 
and,  since  the  bladder  is  divided  sagittally 
into  halves,  the  urine  from  each  kidney  may 
be  obtained  separately.  Handy  accessory 
appliances  make  it  possible  to  attach  sep- 
arate vessels  to  receive  the  urines  from  the 
discharge  tubes.  The  instrument  may  be 
employed  in  the  female  with  extraordinary 
ease,  and  its  use  in  the  male  is  not  attended 
with  great  difficulty  or  much  annoyance  to 
the  patient.  In  male  subjects  with  enlarged 
prostates  a  space  may  be  left  between  the 
gland  and  the  catheter,  which  is  not  drained 
upon  the  introduction  of  the  instrument, 
and  this  mixed  urine  may  consequently  in- 
terfere with  the  accuracy  of  the  method. 
This  source  of  error  may  be  avoided  by  in- 
troducing the  finger  into  the  rectum  and 
pressing  the  base  of  the  bladder  against  the 
catheter.  When  the  screw  is  reversed  the 
tension  chain  and  the  condom  are  accom- 
modated between  the  grooved  halves,  and 
the  instrument  may  be  easily  withdrawn. 
The  apparatus  works  best  with  the  patient  in  a  sitting  or  semirecumbent  position." 
[We  have  found  Cathelin's  instrument  more  reliable.  The  sound  is,  how- 
ever, larger,  and  hence  more  difficult  to  insert  through  a  narrow  meatus. — Ed.] 

Opinions  differ  as  to  the  reliability  of  the  urinary  separation.  Practice  pos- 
sibly plays  a  large  role.  The  results  are  certain,  however,  when  one  discharge  tube 
furnishes  are  entirely  normal,  and  the  other  a  pathologic,  urine.  If,  on  the  con- 
trary, both  urines  are  abnormal,  the  possibility  of  an  incomplete  separation  must 
be  considered  and  cystoscopy  finally  employed. 


Fig.  168 — a,  The  composite  instrument 
ready  for  introduction  :  i  and  t,  discharge 
tubes  :  h,  screw  to  regulate  the  tension  of 
the  membrane  ;  6,  flat  middle  piece ;  c  and 
rf,  grooved  lateral  portions  ;  e,  tip  uniting 
the  parts  ;  g  /,  rubber  membrane,  tense. 
The  chain  is  not  visible  in  the  figure. 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE  URINE. 
EXAMINATION  FOR  PATHOLOGIC  CONSTITUENTS. 

ALBUMINURIA. 

The  clinical  expression  albuminuria  applies  merely  to  nrines  -wliich 
contain  albumin  or  globulin  (coagulable  proteids)  and  does  not  include 
nucleo-albumin,  proteoses,  nor  peptone.^ 

^  Tkerapeutische  Ilonatshefte,  1903,  No.  1. 

^  It  is  customary  to  designate  as  albumin  any  proteid-like  substance  which  appears 
in  the  urine  and  which  responds  to  the  ordinary  "  tests  for  albumin."  On  this  account 
the  term  albumin,  although  it  signifies  a  definite  class  of  proteids,  has  become  synono- 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE   URINE.   459 

Albuminuria  may  be  subdivided  under  two  heads  :  (1)  The  true  or 
renal  albuminuria,  in  which  the  albumin  is  excreted  by  the  kidneys 
themselves ;  and  (2)  false  or  accidental  albuminuria,  in  which  the  albu- 
min comes  from  the  admixture  of  some  albuminous  exudate,  blood,  or 
lymph  with  the  urine  in  its  course  through  the  urinary  tract.  To  dis- 
tinguish between  these  two  forms,  it  is  necessary  to  examine  the  urinary 
sediment  under  the  microscope  and  to  consider  carefully  the  entire 
clinical  picture. 

Renal  albuminuria  always  depends  upon  an  abnormal  permea- 
bility of  the  epithelium,  especially  of  the  glomeruli,  which  permits  the 
proteids  of  the  blood  to  escape  into  the  urine.  The  vessels  themselves 
cannot  be  responsible,  because  physiologically  they  permit  the  transu- 
dation of  albuminous  liquid  in  the  formation  of  lymph.  Whether  the 
passage  of  the  proteid  through  the  renal  epithelium  is  always  pathologic, 
or,  in  other  words,  whether  a  so-called  physiologic  albuminuria  can 
actually  exist,  has  created  considerable  discussion,  and  some  misunder- 
standing of  terms  has  complicated  the  question.  Albuminuria  is  usually 
considered  the  most  important  symptom  of  the  diffuse  kidney  disorders 
called  Bright's  disease.  Hence  the  term  "  physiologic  "  has  been  applied 
to  cases  of  transitory  albuminuria  which  are  associated  with  no  other 
symptoms,  and  whose  subsequent  development  proves  the  absence  of 
any  real  nephritis  or  other  disturbances.  Examples  of  this  form  are 
the  albuminuria  observed  in  apparently  healthy  individuals,  and  the  so- 
called  "  cyclic  albuminuria  "  found  at  certain  hours  of  the  day  (gener- 
ally after  rising),  especially  in  the  young.  As  a  matter  of  fact,  the 
term  "  physiologic  "  means  merely  that  this  type  of  albuminuria  is  not  at 
all  serious,  but  it  is  hardly  an  appropriate  term.  Just  because  a  biologic 
phenomenon  is  harmless,  it  is  not  necessarily  physiologic.  It  seems  to 
the  writer  that  we  are  quite  as  justified  in  designating  as  physiologic  a 
catarrhal  process  which  causes  an  individual  no  discomfort,  as  we  are  in 
assuming  such  an  excretion  of  albumin  to  be  physiologic.  It  is^  not 
physiologic,  but  rather  due  to  some  slight  affection  of  the  renal  epithe- 
lium which  causes  a  harmless  albuminuria  in  otherwise  healthy  people, 
unassociated  with  any  grave  anatomic  renal  change.^  This  conception 
is  of  considerable  importance  from  a  practical  standpoint,  because  the 
kidney  of  an  individual  with  physiologic  albuminuria  would  naturally 
be  regarded  as  rather  sensitive  or  even  predisposed  to  actual  disease,  and 
so  suggest  to  a  careful  physician  appropriate  prophylaxis.  Perhaps  it 
holds  the  same  relation  to  actual  nephritis  as  the  alimentary  glycosuria 
bears  to  actual  diabetes  mellitus. 

Definite  pathologic  forms  of  albuminuria  must  certainly  depend  upon 
some  affection  of  the  renal  epithelium,  which  is  most  pronounced  in 

mous  with  proteids,  and  the  word  is  so  employed  in  the  text.  As  is  well  known,  however, 
the  proteids  in  the  in-ine  may  consist  of  globulins,  proteoses,  etc.,  to  the  exclusion  ot 
albumins.  For  further  characterization  of  these  proteid  bodies  see  Cohnheim  ('  Chemie 
der  Eiweisskorper,"  Text-book  of  Physiologic  Chemistry)  and  Hammai-sten. 

^  According  to  recent  researches  the  minute  traces  of  proteid  found  quite  commonly 
in  the  urine  of  healthy  people  are  neither  albumin  nor  globulin,  but  nucleo-albumin, 
which  has  certain  reactions  in  common  with  the  former  (see  p.  468  el  seq.). 


460  URINARY  EXAMINATION. 

inflammatory  and  circulatory  disturbances  of  the  kidneys  (nephritis) 
and  in  amyloid  disease  of  the  kidneys.  But  the  renal  epithelium  also 
may  be  damaged  sufficiently  to  permit  the  transudation  of  albumin  in  : 
local  or  general  anemia,  cachexia,  venous  congestion,  transitory  renal 
ischemia,  temporary  occlusion  of  a  ureter,  prolonged  retention  of  the  urine 
in  diseases  of  the  bladder  or  of  the  spinal  cord,  the  circulatory  disturbances 
accompanying  attacks  of  epilepsy,  temporary  compression  of  the  thorax, 
and  prolonged  cold  baths.  To  the  same  category  the  so-called  febrile 
albuminuria  observed  in  various  fevers  belongs. 

Nephritic  albuminuria  varies  decidedly  with  the  type  of  the  disease. 
In  acute  nephritis  a  large  amount  of  albumin,  sometimes  2  per  cent,  or 
over  (though  generally  not  more  than  1  per  cent,),  is  excreted ;  in 
chronic  nephritis  the  amount  varies.  The  more  the  disease  approaches 
the  type  of  a  true  contracted  kidney,  despite  the  severity  of  the  disease, 
the  smaller  is  the  amount  of  albumin  excreted ;  and  in  an  extremely 
chronic  case  it  may  even  disappear  temporarily. 

The  same  variability  and  temporary  disappearance  may  characterize 
amyloid  disease. 

The  amount  of  proteid  in  passive  congestion  is  in  most  cases  not 
very  great.  There  are,  however,  exceptions,  in  which  the  amount  is 
large.  In  these  cases  the  amount  of  proteid  corresponds  closely  to  the 
diminution  in  the  volume  of  the  urine  resulting  from  the  congestion ; 
whereas  in  nephritis,  on  the  contrary,  the  degree  of  albuminuria  does 
not  correspond  in  any  well-defined  way  to  the  quantity  of  urine.  A 
large  amount  of  albumin  and  a  relatively  large  volume  of  urine  are 
hardly  ever  combined  in  passive  congestion  ;  but  such  a  combination  is 
not  uncommon  in  nephritis,  although  ordinarily  only  in  very  serious 
conditions  of  disease. 

Febrile  albuminuria  rarely  occurs  except  in  the  severe  infectious 
diseases,  where  the  quantity  of  albumin  may  become  so  considerable 
that  it  is  very  difficult,  perhaps  impossible,  to  make  a  differential  diag- 
nosis between  such  albuminuria  and  actual  nephritis. 

DETECTION  OF  PROTEIDS  AND  RELATED  SUBSTANCES  IN  THE  URINE. 

Recent  opinions  regarding  the  nature  of  the  proteids  and  their 
derivatives  have  altered  so  materially  that  the  reader  is  recommended 
to  study  the  annexed  table  to  comprehend  the  differences  and  mutual 
relationships  of  such  of  these  substances  as  may  occur  in  the  urine. 
(See  Table  facing  this  page.) 

Detection  of   the   Ordinary   Coagulable  Proteids  of   the  Urine    (Serom-albuminj 

Serum-globuHn ) . 

(The  albumin  test  in  the  usual  sense  of  the  word.) 

Heat  Test  for  Albumin. — This  test  depends  upon  the  principle 

that  in  weakly  acid  or  neutral  solutions  albumin  will  be  coagulated  at 

the  boiling-point.     A  test  tube  of  urine  is  heated  to  the  boiling-point, 

preferably  only  at  the   upper  portion.     If  a  precipitate   (cloudiness) 


n  of  the  Urine. ^ 


Water. 
Boiling, 

Alcohol 


5  to  10 
salt  s( 

Saturati 
with  ] 

Saturati 
with  '. 


Saturati' 
with  ( 


Dilute  a 
Dilute  s 

Concent 

Metapli 
Nitric  a 


Potassiu 
+  ace 


Conimor 


Tannic 
acid  i 

Trichlo] 

Phosphc 
in  mil 


or  by  alc( 


8.  Peptone  (Kuhne). 

End  product  of  the 
peptic  and  tryptic  di- 
gestimi  of  1,  li,  3,  and 
4  (appearance  in  the 
urine  tlin>\iL;h  newer 
expcriincntiilif)!!  lias 
become  doubtful). 


Soluble. 

Not  coagulated. 

Precipitated. 

Soluble. 

Not  precipitated. 

Not  precipitated. 

Not  precipitated. 

Not  precipitated. 

Not  precipitated. 

Not  precii^itated. 

Not  precipitated. 
Not  precipitated. 

Not  precipitated. 

Not  precipitated. 

Precipitated. 

Not  precipitated. 
Precipitated. 


Compound  Proteids. 

Extremely  complicated  c<)ml>inatioiis,  which  may  be  decomposed 
by  boiling  with  diluted  acids,  or  by  peptic  degeneration  into  a 
proteid  and  another  substance  (carbohydrate,  pigment,  nuclein) 


9.  Hemoglotoin 

(Blood-pigment) 
breaks  down  by  boil- 
ing with  diluted  acids 
into    hematin     and 
proteid. 


Soluble. 

Coa,gidat,ed.  and  de- 
compot^ed. 

Precijiitated       and 
coagulated. 

•Soluble. 


Not  precipitated. 
Not  precipitated. 


Decomposed. 
Decomposed. 

Decomposed. 

Decomposed. 
Decomposed. 

Decomposed. 

Decomposed. 

Decomposed. 

Decomposed. 
Decomposed. 


10.  Nucleoproteid 

breaks  down  by  pep- 
tic  digestion  into 
nuclein,  and  proteid 
contains  phosphorus. 


Insoluble. 
Coagulated. 


Precipitated  (pajlly 
changed). 


Precipitated. 


Partly  soluble,  part- 
ly swelling  into 
slimy  masses. 

Easily  soluble  in 
mineral  acid,  very 
difficultly  in 

acetic  acid. 


Soluble. 


Precipitated,    solu- 
ble in  excess. 


Precipitated. 


Incompletely     pre- 
cipitated. 

Precipitated. 


? 
Precipitated. 


11.  Mucin. 

Presence  in  the  urine 
through  newer  ex- 
perimentation has 
become  doubtful ; 
breaks  down  by  boil- 
ing with  diluted 
acids  into  reducing 
carbohydrate  and 
proteid. 


Insoluble. 

Precipitated. 

? 

? 
Not  precipitated. 


Soluble. 


Soluble  in  mineral 
acid,  not  in  acetic 
acid. 


Soluble. 

? 
? 


■n  this  synopsis  in  contrast  to  "precipitated,"  if  the  precijiitate,  produced  by  heating 


Characteristics  and  Reacti  ms  of  the  Proteids  Coining  Under  Consideration  in  the  Examination  of  the  Urine.' 


1.  Serum-albumin 
(Albumin,  proteids  in  tbc 


Boiling. 
Alcohol. 


Soluble. 

Cotiffiilnfed  (ill  we;ik  acid 


Soluble. 

Not  precipitated. 

Nnl    p,rr!p!fat.yl    (ihr 


i.l). 


Coucenlraled  inineml  acid. 


Metaplio-spliuric  acii 
Nitric  acid. 


Potassium       ferrocyanide 


cid  solution. 
I  Trichloracetic  iicid. 


AuL-urdiii-  lu  Ni 


Not  jirecipitated  ;  will  be 
changed    by  an    excess 

Not  precipitated,  and  by 
excess  gi-iulually  changed 
into  acid  albumiti. 


Precipitated,  and  by  excess 
gradually  changed  into 
acid  albumin. 


Precipitated. 

Preriiiitated. 

Precipitated. 
Precipitated. 


r  Paraglobuliu. 


Soluble. 

Incompletely  precipitated. 

Chmplckhj  prccipitaled. 


ulbui 

Not  precipitated  (in  alka- 
line solution  only  pre- 
cipitated). 13y  excess 
gradually  changed  into 
acid  albumin. 

Pi-ecipitated,  and  by  ex- 
cess gi-adually  changed 
into  acid  albumin. 


Precipitated. 

Precipitated. 

Precipitated. 
Precipitated, 


3.  Fibrinogen. 
is  a  clobiilin  which  tins  the 
peculiaril y  of  being  changed 
111  solutioua  containing  eiil- 
eium  by  fibrin  ferment 
(serum,  defibrinated  blood) 
into  fibrin  (coagulating 
"spontaneously"). 


Soluble. 

Completely  precipitated. 

Completclij  prccipihtteiL 

Complelcly  prccipUatal. 


Not  precipitated  {in  alka- 
line solution  only  pre- 
cipitated). By  excess 
gradually  changed  into 
acid  albumin. 

Precipitated,  and  by  ex- 
cess gmdualiy  changed 
into  acid  albumin. 


Precipitated. 

Precipitated. 

Precipitated. 
Precipitated. 


4.  Fibrin 
originates   from   I'l 
rinogenby  theactii 
of  fibrin  ferment 
soluliuu  of  calcin 


Primary  Albumoses. 


6.  Hetero-albumose.     6.  Frotalbumose 


Iimoluhlc. 
Coagulated. 

Insoluble. 

Insoluble. 


Greatly  swollen 
(especially  in  0.3 
per  cent.  HCl). 


Not  precipitated. 
Not  precipitated. 


Cloudy  upon  heat- 
ing. 

Precipitated. 

Precipitated. 
Precipitated. 


Not  precipitated. 
Not  precipitated. 


Precipitated,    solu- 
ble iijion  heating. 


Precipitated. 

Precipitated. 
Precipitated. 


7.  Deutero- 


Soluble. 

Not  precipitated. 

Not  precipitated. 


Not  precipitated, 
Nt.t  precipJtaleil. 


Precipitated. 

Not      precipitated 


Precipiiaicd,  hnl 
onlybyslromjcow 
cf.nlrution,  soluble 
upon  healiny- 


Precipitated. 
Precipitated. 


f  the  synopsis  refer  to  the  pure  substances,  and  the  reactions  may  be  modified  by  the  presence  of  other  substances  in  the  urine.  The  expression 
i^oluble  in  water  or  in  neutral  salt  solutions.  For  the  sike  of  distinction  fiie  most  important  reactions  are  printed  in  heavy  type  in  this  synopsis, 
u  ^eister,  deutero-albumose  orighiatiug  from  i)rotalbuuiose  will  not  be  completely  precipitated. 


peptic  and  tryptit-  di- 


Soluble. 

Not  com/ulali'd. 

Precipitated. 

Soluble. 

Not  precipitated. 

Nut  precipitated. 

Niil  prccipilalal. 

Not  inecipitated. 

Ncl  preoipilatcl. 


Not  precipitated. 
Not  precipitated. 


Not  precipitated. 

Precipitated. 

Not  precipitated. 
Precipitated. 


Compound  Proteids. 


Extremely  compliented  < 


9.  Hemoglobin 

(Blood- pigment) 

breaks  down  by  boil- 


Soluble. 

Not  precipitated. 

Not  precipitated. 


Decomposed. 
Decomjiosed. 


Decomposed. 

Decomposed. 

Decomposed. 
Decomposed. 


10.  Nucleoproteid 

hreiiksdowiiby  ni-p- 
tic  digestion  into 
iiuclein,  and  proteid 


Coayuhtcu 


Eaaily    .soluble 
mineral  acid,  v( 
difficultly 


i  may  be  decomposed 
•  degeneration  into  a 
te,  pigment,  nuclein), 


througli     newer   ex- 

pcrimL-ntiilioii  has 
become  doubtful; 
breaks  down  by  boil- 
ing witJi  diluted 
acids   intfi  reducing 

proteid. 


oagulated"  is  used  in  this  synopsis  in  contrast  to  "precipitated,"  if  the  precipitate,  produced  hy  heating 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE   URINE.   461 

appears,  it  will  consist  either  of  albumin  or  of  phosphates  and  carbon- 
ates, for  the  latter  are  also  precipitated  by  heat  (see  p.  557  et  seqX  A 
distinct  flaky  precipitate  would  probably  "^indicate  albumin ;  but  to  be 
certain  the  urine  should  be  acidified  drop  by  drop  (dilute  acetic  acid 
1  :  9).  If  the  precipitate  then  dissolves,  it  was  due  to  phosphates  and 
carbonates.  If  it  does  not  dissolve,  but,  on  the  contrary,  becomes 
more  flaky  and  heavier,  it  is  albumin.  The  heat  test  will  not  always 
cause  a  precipitate  in  an  albuminous  urine  which  is  alkaline  or  only  very 
faintly  acid.  This  is  the  reason  why  the  acid  is  added  drop  by  drop 
until  the  urine  becomes  distinctly  acid.  It  is  generally  advisable  to 
employ  a  dilute  solution  of  acetic  acid,  because,  although  an  alkaline 
urine  may  require  considerable  acid,  too  strong  acid  might  allow  a  mod- 
erate amount  of  albumin  to  escape  notice  by  being  rapidly  changed  to 
the  soluble  acid  albumin.  Again,  acidulating  the  urine  too  strongly 
before  boiling  may  entirely  prevent  the  precipitation  of  the  albumin. 
In  this  way  many  cases  of  mild  albuminuria  may  escape  detection.  If 
slight  in  amount,  albumin  often  does  not  precipitate  from  the  urine  until 
after  the  lapse  of  some  time.  This  is  true  in  other  tests  as  well  as  in 
the  heat  test. 

The  reason  it  is  advisable  to  heat  only  the  upper  portion  of  the 
urine  in  the  test  tube  is  because  in  this  way  we 'can  differentiate  a 
cloudiness  due  to  albumin  even  when  the  urine,  before  heating,  was  not 
perfectly  clear.  In  case  of  marked  turbidity,  however  (such  as  would 
be  caused  by  bacteria,  pus,  or  excess  of  phosphates),  the  urine  should  be 
filtered  before  an  exact  test  is  attempted.  If  filtration,  does  not  succeed 
in  clarifying  the  urine,  it  is  advisable  to  add  calcined  magnesia  and  then 
filter  again.  This  powder  will  clog  the  pores  of  the  filter  mechanically, 
and  assist  in  clarifying  a  cloudiness,  even  that  which  is  caused  by  bac- 
teria. Cloudiness  due  to  a  considerable  excess  of  urates  wall  not  com- 
plicate this  test,  because  heating  the  urine  dissolves  the  urates  and 
clarifies  the  urine  before  the  albumin  is  coagulated. 

Another  method  of  performing  the  heat  test  is  first  to  acidify  the  urine 
strongly  with  several  drops  of  dilute  acetic  acid,  and  then  add  one- 
sixth  of  its  volume  of  concentrated  salt  solution  (30  salt  to  100 
water).  If  much  albumin  is  present  a  precipitate  will  form  even  in  the 
cold  mixture  and  decidedly  increase  upon  heating.  The  advantage  of 
this  method  is  that  it  shows  the  presence  of  albumoses,  since  the  latter 
are  precipitated  in  the  cold  mixture  and  dissolved  by  heating.  If  both 
albumin  and  albumoses  are  present,  the  latter  will'  be  precipitated  by 
cooling  the  filtrate  from  the  boiled  specimen. 

The  nucleo-albumin  in  normal  urine  will  be  precipitated  by  either 
heat  test.  If  abundant  enough  to  produce  a  cloudiness  upon  boilins', 
it  may  be  mistaken  for  true  albumin.  This  confusion  may  readily  be 
avoided  by  adding  a  few  drops  of  concentrated  acetic  acid  to  a  cold 
specimen  of  urine.  If  this  acidulation  produces  a  cloudiness  of  th.e 
same  intensity  in  the  cold  as  in  the  boiled  urine,  the  ])recipitntion  in 
both  is  due  to  nucleo-albumin  ;  but  if  the  cloudiness  is  of  less  intensity, 


462  URINARY  EXAMINATION. 

the  precipitation  must  depend  upon  a  combination  of  nucleo-  and  true 
albumin. 

The  ordinary  heat  test  is  one  of  the  safest  and  most  accurate  methods 
of  determining  the  presence  of  coagulable  proteid.  (See  below  in 
regard  to  its  advantages.)  But  we  must  remember  that  not  only  nucleo- 
albumin  and  albumose,  but  also  resinous  acids,  may  be  precipitated  by 
acidifying  the  urine  too  strongly.  (See  below  for  the  Xitric  Acid  Test 
Kelative  to  the  Differentiation  Between  Besins  and  Proteids.) 

Tests  for  Albumin  in  the  Cold. — A  large  variety  of  chemical 
reagents  are  capable  of  precipitating  albumin  even  at  a  low  tempera- 
ture. Requiring  no  alcohol  lamp,  these  tests  are  of  distinct  advantage 
to  the  practitioner.     The  best  known  are  : 

The  Nitric  Acid  Test  (Heller's  Test). — One-half-inch  of  concentrated 
nitric  acid  is  placed  in  a  test  tube,  and  filtered  urine  is  allowed  to  flow 
down  the  sides  of  the  tube  and  stratify  itself  upon  the  acid.  Albumin, 
if  present,  causes  a  precipitate  at  the  line  of  junction  of  acid  and  urine 
and  forms  a  ring  or  zone  of  cloudiness.  If,  however,  there  is  only  a 
very  small  amount  of  albumin  present,  this  precipitate  may  not  separate 
until  after  the  lapse  of  several  minutes. 

Under  certain  conditions — e.  g.,  a  very  concentrated  urine — the  uric 
acid  or  urates  may  be  precipitated  by  this  test ;  but  if  the  zone  is  quite 
flocculent  it  will  probably  be  due  to  albimiin.  To  be  absolutely  sure  the 
specimen  should  be  gently  heated  (not  boiled),  when  the  ring,  if  due  to 
urates  or  uric  acid,  will  promptly  disappear.  Or,  before  testing,  the 
specimen  can  be  diluted  with  two  or  three  times  its  volume  of  water,  in 
which  case  nitric  acid  will  precipitate  only  albumin.  Moreover,  the 
uric  acid  ring  is  usually  broader,  less  sharply  defined  along  its  uj^per 
border,  and  often  plainly  situated  in  the  urine  itself  above  the  line  of 
junction  of  the  two  fluids. 

After  the  internal  administration  of  some  of  the  balsams  the  nitric 
acid  test  sometimes  brings  down  a  precipitate  of  resinous  acids,  which 
may  be  confused  with  that  of  albumin.  Such  a  precipitate,  however, 
will  be  to  some  extent  cleared  up  by  heat.  Or,  if  the  nitric  acid  and 
urine  are  mixed  and  the  liquid  then  sucked  up  from  the  precipitate 
with  a  pipet,  the  precipitate,  if  composed  of  resinous  acids,  will  dis- 
solve in  an  excess  of  alcohol.  According  to  Tappeiner,  it  is  sufficient 
to  add  two  volumes  of  alcohol  to  the  mixture  of  urine  and  nitric  acid 
without  first  separating  the  precipitate.^  Alexander  has  objected  that 
certain  proteids  precipitable  by  nitric  acid  will  under  certain  conditions 
be  dissolved  in  alcohol,  as  well  as  resinous  acids.  He  recommends  the 
solution  of  the  precipitate  by  the  addition  of  ether,  although  a  great 
excess  of  the  latter  will  be  necessary  to  prevent  the  formation  of  an 
emulsion.  A  precipitate  soluble  in  ether  is  due  only  to  resinous  acids. 
The  heat  test  also  permits  a  differentiation,  for  the  resinous  acids  are  not 
precipitable  by  heat  unless  the  urine  has  been  very  strongly  acidulated 
with  acetic  acid.  Alexander  performs  a  control  test  by  adding  to  the 
heated  urine  one-third  its  volume  of  nitric  acid ;  any  cloudiness  must 
1  Beutsch.  med.  Woch.,  1893,  Xo.  14,  p.  323. 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE  URINE.  463 

then  be  due  to  albumin,  since  the  resinous  acids  could  not  be  precipi- 
tated because  of  the  heat  and  the  considerable  excess  of  nitric  acid. 
Another  characteristic  of  the  resinous  acids  is  that  the  addition  of  a  few 
drops  of  hydrochloric  acid  produces  a  cloudiness  of  the  urine.  (See  p. 
503,  Balsams  of  Copaiba  and  Santahvood  Oil.) 

Albumoses  and  nucleo-albumin  are  also  precipitated  by  the  nitric 
acid  test ;  but  the  latter  is  dissolved  by  an  excess  of  acidity,  and  the 
former  by  heating. 

Under  certain  conditions  nitric  acid  precipitates  the  bile  acids,  and  in  very 
concentrated  urine  the  urea,  as  urea  nitrate.  To  prevent  this  and  the  other  sources 
of  error  mentioned  above,  Hammarsten  suggests  a  dilution  of  the  urine  to  a 
specific  gravity  of  1005  or  lower.  Heller's  test  then  precipitates  only  albumin, 
nucleo-albumin,  and  albumoses,  because,  unless  the  urine  is  concentrated,  neither 
uric  acid,  urea,  the  bile  acids,  nor  the  resinous  acids  can  be  precipitated.  Albu- 
mose  can  then  be  excluded  if  the  precipitate  persists  after  warming  ;  nucleo- 
albumin  can  be  excluded  if  the  precipitate  does  not  dissolve  in  an  excess  of  nitric 
acid,  or  if  the  urine  remains  clear  after  an  addition  of  an  excess  of  acetic  acid. 

Test  with  Acetic  Acid  and  Potassium  Ferrocyanid. — The  specimen  is 
strongly  acidified  with  acetic  acid,  and  a  solution  of  potassium  ferro- 
cyanid (1  :  10)  is  then  added  drop  by  drop;  the  slightest  amount  of 
albumin  will  cause  the  appearance  of  a  cloudiness  or  the  precipitation 
of  small  flocks.  This  reaction  is  one  of  the  most  trustworthy  of  all 
the  tests  for  proteid.  j^evertheless,  the  albumoses  and  nucleo-albumin 
will  also  be  precipitated  (the  former,  however,  only  when  present  in  con- 
siderable concentration).  In  the  preceding  paragraph  we  have  already 
detailed  the  method  of  differentiating  them  from  the  albumin. 

Metaphosphoric  Acid  Test. — If  a  small  particle  of  this  substance  (HPO,)  is 
dropped  into  albuminous  urine  the  proteid  will  be  precipitated.  The  test  is  of 
little  value,  because  it  applies  only  to  fairly  large  amounts  of  proteid,  1  per  cent, 
or  more.  The  same  precautions  as  before  must  be  observ^ed  in  order  to  distinguish 
urates,  uric  acid,  and  resinous  acids.  The  only  advantage  this  test  possesses  is 
that  the  metaphosphoric  acid  can  be  readily  transported  as  a  solid,  although  it  must 
be  kept  sealed  to  prevent  the  absorption  of  water  and  a  resulting  change  to  the 
ordinary  phosphoric  acid,  which  does  not  precipitate  proteid. 

Picric  Acid  Test. — Picric  acid,  either  in  the  solid  substance  or  in  solution,  may 
be  used  like  metaphosphoric  acid.  It  precipitates  albumoses,  peptone,  nucleo- 
albumin,  resinous  acids,  and  sometimes  uric  acid  and  urates. 

Since  with  these  cold  tests  so  many  precautions  are  necessary,  it  becomes  evi- 
dent that  the  practitioner  will  select  the  ordinary  heat  test  for  albumin  (p.  460  et 
seq.)  as  being  the  most  reliable  and  the  simplest. 

Appendix. —  To  Remove  Proteid  from  the  Urine. — This  is  often  necessary 
before  many  of  the  following  qualitative  and  quantitative  tests  can  be  performed. 
The  best  method  is  to  effect  an  insoluble  combination  with  it  and  some  metallic 
oxid.  Hofmeister  adds  10  c.c.  of  a  saturated  solution  of  sodium  acetate  to  half 
a  liter  of  urine,  and  into  this  mixture  stirs  a  solution  of  ferric  chlorid,  drop  hj 
drop,  until  the  color  becomes  blood  red.  Such  a  mixture,  which  is  strongly  acid, 
is  then  exactly  neutralized  with  sodium  or  potassium  hydroxid,  or  at  most  allowed 
to  remain  very  faintly  acid,  and  then  boiled,  cooled,  and  filtered.  The  filtrate 
should  be  free  from  proteid  and  iron.  (Test  with  potassium  ferrocyanid.)  The 
method  is  of  no  value  for  a  urine  containing  sugar,  because  the  oxid  of  iron  would 
be  kept  in  solution. 

It  is  usually  sufficient  to  boil  an  acid  urine  until  the  proteid  is  coagulated,  and 
then  to  remove  the  latter  by  filtration.     If  the  urine  is  alkaline  or  neutral  it 


464  URINARY  EXAMINATION. 

should  be  slightly  acidulated  with  dilute  acetic  acid.  "N^Tien  the  proteid  coagulates 
as  a  sort  of  cloudiness  rather  than  in  flocculi,it  is  advisable  to  add  a  little  more  acetic 
acid,  while  still  boiling,  until  large  flocks  form.  If  coagulation  by  boiling  does 
not  produce  coarse  flocks,  filtering  will  not  completely  remove  the  proteid.  If  the 
acid  reaction  is  too  faint,  or  if  too  much  acetic  acid  is  added,  the  proteid  may  be 
prevented  from  separating  in  large  flocks.  Unless  another  specimen  of  the  urine 
is  used,  the  mistake  of  adding  too  much  acid  may  be  corrected  by  carefully 
neutralizing  the  excess  of  acid  by  the  addition  of  dilute  sodium  hydroxid.  If  the 
amount  of  proteid  is  large,  it  is  a  good  plan  first  to  dilute  the  urine  with  water 
before  attempting  to  make  a  separation.  The  only  way  to  be  certain  that  the 
proteid  has  been  completely  removed  is  to  be  sure  that  the  addition  of  acetic  acid 
and  potassium  ferrocyanid  to  the  filtrate  does  not  produce  any  cloudiness.  If  any 
turbidity  still  persists  it  is  due  to  the  addition  of  too  much  or  too  little  acid,  and 
the  test  should  be  performed  again,  vaiying  the  acidity  slightly. 

Detection  of  Serum  or  Paraglobulin. 

Globulin  always  seems  to  accompaDy  serum-albumin  in  urine,  and 
not  to  be  present  without  it.  Any  diagnostic  significance  of  the  presence 
of  globulin  in  urine  has,  therefore,  not  yet  been  found.  To  demon- 
strate globulin  we  add  enough  ammonia  to  make  the  urine  neutral  or 
faintly  alkaline.  This  is  done  in  order  to  precipitate  the  phosphates, 
which,  in  the  subsequent  treatment  with  ammonium  sulphate,  would 
produce  a  turbidity.  Then  we  filter,  and  add  to  the  filtrate  an  equal 
volume  of  saturated  ammonium  sulphate  solution.  After  the  resulting 
precipitate  has  settled  well  (one  hour)  it  is  collected  upon  a  filter,  and 
then  washed  with  a  half-saturated  ammonium  sulphate  solution  until 
the  filtrate  is  proteid-free.  The  precipitate  contains  the  globulin,  and 
under  certain  conditions  albumose  as  well.  The  albumin  has  not  yet 
been  precipitated,  because  this  -requires  complete  saturation  with  the 
reagent.  (See  Table,  facing  p.  460.)  The  precipitate  is  next  dissolved  in 
a  little  water  and  the  filtrate  heated  over  a  water  bath.  This  will  coagu- 
late the  globulin,  fibrinogen,  and  albumose.  This  precipitate  is  filtered, 
washed  with  water,  and  then  digested  and  dissolved  in  a  1  per  cent, 
solution  of  soda  over  a  water  bath.  If  necessary  the  resulting  solution 
can  be  filtered  again,  and  then  carefully  neutralized  Avith  acetic  acid. 
If  any  globulin  or  fibrinogen  was  originally  present,  an  albuminate 
will  be  precipitated  which  will  not  be  dissolved  by  the  addition  of  a 
solution  of  sodium  chlorid.  If  the  deposit  consists  of  albumose,  acetic 
acid  either  gives  no  precipitate  whatever  or  the  precipitate  is  dissolved 
by  a  solution  of  sodium  chlorid.  Solutions  of  fibrinogen  differ  from 
those  containiug  globulins  in  that  the  latter  are  not  coagulated  by  the 
addition  of  fibrin  ferment  (fresh  blood-serum).  This  difference,  how- 
ever, is  of  no  practical  value  in  urinary  examinations,  as  will  be  observed 
in  the  subsequent  observations  upon  the  demonstration  of  fibrinogen  in 
the  urine. 

Detection  of  Fibrinogen. 

Fibrinogen  belongs  to  the  globulins,  and  is  precipitated  like  serum- 
globulin  (see  above).  The  test  for  it  is  practically  very  simple,  however, 
because  fibrinogen  will  coagulate  spontaneously  in  the  presence  of  lime 
salts  and  fibrin  ferment.    Now  when  fibrogen  is  preseut  in  the  urine,  these 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE   URINE.  465 

last  two  factors  necessary  for  coagulation  are  never  absent,  so  that  if  a 
coagulation  occurs  spontaneously  when  the  urine  is  allowed  to  stand,  the 
presence  of  fibrinogen  is  always  indicated.  This  phenomenon  is  usually 
associated  with  a  considerable  admixture  of  blood  in  the  urine.  The  coag- 
ulation then  resembles  an  ordinary  blood-clot.  Spontaneous  coagulation 
occurs  very  exceptionally  in  the  urine  without  an  admixture  of  blood. 
So  far  as  we  know  now  this  has  been  observed  only  in  tropic  chylu^'ia 
-and  in  very  rare  cases  of  nephritis. 

Detection  of  Fibrin* 

Fibrin  forms  in  the  urine  when  the  latter  contains  fibrinogen.  It 
occurs  in  the  form  of  small  clots,  which  are  easily  recognized  under  the 
microscope  by  their  shredded  structure,  and  are  oftentimes  tinged  with 
blood.  These  physical  peculiarities  and  the  fact  that  it  swells  in  dilute 
acetic  acid  will  suffice  for  its  recognition. 

Albumosuria  (Propeptonuria;  Peptonuria). 

The  terms  albumosuria,  propeptonuria,  and  peptonuria  should  be 
considered  synonymous  and  all  three  included  in  the  term  albumosuria 
(better  proteosuria),  because  the  term  peptonuria  was  applied  at  a  time 
when  peptones  and  albumoses  had  not  been  differentiated,  and  because 
so-called  "  true  peptone,""  which  has  since  been  distinguished  from  the 
albumoses  by  Kiihne,  has  not  been  absolutely  proved  to  occur  in  the 
urine.  (See  Table,  facing  p.  460).  Another  reason  why  albumosuria 
and  peptonuria  should  be  included  under  the  one  term  is  that  Kuhne's 
separation  of  true  peptone  from  the  albumoses  is  somewhat  artificial  and 
based  upon  one  single  reaction,  the  precipitation  of  the  albumoses  by 
ammonium  sulphate  and  the  non-precipitation  of  true  peptone.  More- 
over, even  this  reaction  does  not  permit  of  any  sharp  distinction  between 
them,  for  certain  of  the  albumoses  are  not  completely  precipitated. 

The  albumoses  have  been  found  in  the  urine  both  by  themselves  and 
combined  with  albumin  during  the  puerperiwm,  in  acute  yellow  atrophy  of 
the  liver,  in  phosphorus-poisoning,  in  ulceration  of  the  stomach  and  intes- 
tines (enterogenic  albumosuria),  in  most  febrile  conditions,  especially  in 
the  infectious  diseases,  particularly  the  suppurating  processes  (pyogenic 
albumosuria),  in  pneumonia  during  resolution,  in  scurvy,  in  nephritis, 
and  in  vndtiple  medullary  osteosarcoma. 

The  presence  of  the  albumoses  in  the  urine  is  of  clinical  importance 
only  when  the  urine  does  not  contain  albumin,  because  in  albuminuria 
the  albumoses  are  almost  always  to  be  found  in  the  urine  after  removal 
of  the  albumin.  It  then  appears  questionable  whether  they  existed  pre- 
formed or  were  formed  from  the  albumin  by  the  chemical  processes 
employed  for  its  removal. 

The  presence  of  albumoses  alone  in  the  uriue  is  of  only  limited 
diagnostic  value.  But  when  it  is  very  pronounced,  and  when  there  are 
no  other  reasons  for  albumosuria,  it  may  lead  to  the  recognition  of  deep- 
seated  suppuration.     This  symptom  must  therefore  be  considered  in  the 

30 


466  URINARY  EXAMINATION. 

diagnosis  of  perityphlitis,  in  the  differential  diagnosis  between  tubercular 
and  purulent  meningitis,  in  the  diagnosis  of  abscess  of  the  brain,  and  of 
empyema  of  the  pleura,  etc.  A  decided  albumosuria  is  most  suggestive 
of  multiple  myeloma  or  myelogenic  osteosarcoma  (Bence-Jones  Albumose). 

Detection  of  the  Primary  Albumoses  by  Employing-  the  Ordinary  Test 
for  Albumin.  Bence-Jones  Albumose. — Albumoses  may  sometimes  be  recog- 
nized in  the  urine  when  the  ordinary  nitric  acid  test  or  the  potassium  ferrocyanid 
and  acetic  acid  test  for  albumin  proteid  is  employed.  A  precipitate  is  formed  like 
that  of  true  proteid,  but  differing  from  it  by  disappearing  when  heated.  In  per- 
forming the  heat  test  for  coagulable  proteid,  a  slight  turbidity  appears  in  a  case  of 
this  sort  upon  gentle  heating,  or  even  before  heating,  if  the  sodium  chlorid  modi- 
fication of  this  test,  described  upon  p.  461,  is  used.  This  precipitate  dissolves 
again  when  the  boiling-point  is  reached.  If  abundant  the  primary,  and  more 
especially  the  so-called  Bence-Jones  albumose,^  may  be  detected  in  this  way. 
The  latter  belongs  to  the  primary  albumoses,  or,  at  any  rate,  is  closely  related  to 
them  (Kiihne).  A  urine  which  responds  positively  to  this  test  for  albumoses 
usually  reacts  to  the  biuret  test  (p.  467). 

Spath  states  that  the  following  is  a  characteristic  reaction,  particularly  for  the 
Bence-Jones  albumose  (which  is  related  to  hetero-albumose)  :  The  urine  should  be 
distinctly  acid  and  contain  a  sufiicient  quantity  of  sodium  chlorid  ;  it  may  therefore 
be  necessary  to  add  some  acetic  acid  and  a  concentrated  solution  of  sodium  chlorid. 
The  urine  is  then  heated  to  50°  C.  If  it  contains  Bence-Jones  albumose  it  becomes 
milky  ;  at  60°  C.  a  precipitate  is  thrown  out,  which  is  not  flocculent,  but  tenacious 
and  adJierent  to  the  side  of  the  test  tube,  and  which  subsequently  forms  a  granular 
mass  floating  upon  the  surface.  If  the  heating  be  continued,  the  cloudiness  and 
precipitate  completely  disappear  and  a  clear  solution  remains,  which  upon  cooling 
again  throws  down  this  proteid  substance.  When  examined  microscopically  the 
precipitate  consists  of  globules  without  crystalline  structure. 

Bence-Jones  albumose  is  of  especial  importance  in  the  diagnosis  of  myelogenic 
osteosarcoma  or  myeloma.  It  cannot,  however,  be  regarded  as  pathognomonic  of 
these  conditions,  since  Askanzy  '^  has  demonstrated  it  in  a  case  of  lymphatic  leu- 
kemia. This  author's  conclusions  as  to  the  value  of  the  reaction  are  as  follows  : 
Bence-Jones  albumosuria  always  indicates  a  lesion  of  the  bone-marrow,  and  usually 
multiple  myeloma,  but  in  exceptional  cases  it  may  exist  in  diffuse  lymphatic  changes, 
such  as  are  observed  in  lymphemia. 

The  above-mentioned  tests  are  not  adapted  to  demonstrate  the  presence  of 
deutero-albumoses,  to  which  most  albumoses  found  in  the  urine,  especially  those 
present  in  febrile  conditions,  belong.  Only  when  they  are  present  in  very  con- 
centrated amounts,  which  very  rarely  occurs,  can  they  be  precipitated  by  the 
method  above,  and  then  only  slowly  and  incompletely.  But  the  following  method 
of  testing  for  albumoses  in  general  is  also  adapted  to  deutero-albumoses  : 

Salkowski's  ^  Test  for  Briicke's  Peptone,  Albumoses,  or  Deutero-albu- 
moses.— This  is  a  modification  of  Hofmeister's  early  method.  Fifty  cubic  centi- 
meters of  urine  free  from  coagulable  proteid  are  required.  If  the  specimen  con- 
tains nucleo-albumin,  the  latter  may  be  precipitated  with  a  little  neutral  lead  ace- 
tate. A  thick  floccular  precipitate  appears  (with  which,  by  means  of  filtration,  the 
nucleo-albumin  is  removed).  "The  filtrate  is  then  placed  in  a  beaker  with  5  c.c. 
of  HCl,  precipitated  with  phosphotungstic  acid,  and  then  heated  over  a  wire  gauze. 
In  a  few  moments  the  precipitate  collects  in  a  resinous  mass  at  the  bottom  of  the 
glass.  The  supernatant  fluid  is  then  decanted  as  completely  as  possible,  and  the 
resinous  mass  is  washed  twice  with  distilled  water,  which,  if  done  carefully,  may 

^  Matthes,  Congr.  f.  inn.  Med.,  1896.  Here  Bence-Jones  albumose  is  differentiated 
from  the  other  albumoses,  Kosin,  Berlin.  kUn.  WocL,  1897,  No.  48,  p.  1044. 

2  D.  Arch.  J.  klin.  Med.,  vol.  Ixviii.,  parts  1  and  2,  p.  34. 

^  Centralbl.f.  d.  med.  Wissen.,  32, 113, 1894,  and  Prakticum  der  physiol.  Chemie,  2d  ed., 
1900. 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE    URINE.   467 

be  accomplislied  with  scarcely  any  loss.  We  now  add  to  the  precipitate  about 
8  CO.  of  water  and  0.5  c.c.  of  sodium  hydroxid  (of  about  1160  specific  gravity). 
The  precipitate  now  crumbles  and  easily  dissolves  when  the  beaker  is  gently 
shaken.  The  resulting  solution,  usually  of  a  deep-blue  color,  is  heated  again 
over  the  wire  gauze.  It  usually  becomes  turbid  and  dirty-grayish  yellow  ;  some- 
times it  turns  yellow  but  remains  clear.  If  the  discoloration  occurs  slowly,  it 
may  be  hastened  somewhat  by  the  addition  of  a  few  drops  of  sodium  hydrate. 
When  it  is  completed  the  liquid  is  poured  into  a  test  tube,  cooled,  and  the  biuret 
reaction  1  tried.  For  this  purpose  a  dilute  (1  to  2  per  cent.)  solution  of  copper 
sulphate  is  added  drop  by  drop  with  shaking.  If  peptone  is  present  the  liquid 
will  turn  a  decided  red,  and  this  color  will  be  intensified  if  the  liquid  is  now  fil- 
tered. The  whole  process  does  not  occupy  more  than  five  minutes.  Another 
great  advantage  of  the  method  lies  in  the  fact  that,  owing  to  the  small  amount 
of  urine  required,  nucleo-albumin  is  less  liable  to  affect  the  reaction." 

The  addition  of  a  few  drops  of  barium  chlorid  solution  has  seemed  to  the 
writer  distinctly  advantageous  when  the  solution  upon  which  the  biuret  reaction 
is  to  be  performed  is  already  colored.  After  filtering  off"  the  resulting  precipitate, 
the  solution  will  be  decolorized. 

Quite  recently  Salkowski  discovered  a  source  of  error  in  his  own  method 
which  decidedly  interfered  with  its  practicability.  ^  He  found  that  the  albumose 
reaction  might  be  simulated  if  the  urine  contained  much  urobilin,  for  with  the 
biuret  test  urobilin  gives  a  color  very  much  like  that  obtained  with  the  albumoses. 
To  make  the  value  of  a  positive  biuret  test  absolute,  Salkowski  therefore  considers 
that  the  solution  must  first  be  shown  to  furnish  no  spectroscopic  evidence  of  uro- 
bilin (p.  478).  If  the  urine  contains  much  urobilin  besides  albumoses,  we  should 
first  extract  with  amyl-alcohol  after  acidifying,  in  order  to  remove  the  urobilin  as 
completely  as  possible.  By  this  plan,  however,  some  loss  of  albumose  can  hardly 
be  prevented.  Employing  barium  chlorid,  as  suggested  above,  will  sometimes, 
but  not  always,  free  the  urine  from  urobilin. 

V.  Aldor' modified  Salkowski' s  test  in  order  to  eliminate  the  urobilin.  He 
separates  the  phosphotungstic  acid  precipitate  by  centrifugalization  instead  of  by 
heating  the  fluid,  then  washes  repeatedly  with  alcohol,  Avhich  takes  up  the  uro- 
bilin, and  centrifugalizes  again  until  it  becomes  absolutely,  colorless.  The  washed 
precipitate  is  then  suspended  in  water  and  dissolved  in  sodium  hydrate,  and  finally 
the  biuret  test  is  performed.  If  no  centrifuge  is  available,  the  precipitate  may  be 
washed  on  filter  jDaper  with  alcohol. 

Detection  of  Albumoses  According'  to  Schulte's*  Method. — The  urine 
is  first  filtered,  and  any  nucleo-albumin  which  may  be  present  is  precipitated  by 
dilute  acetic  acid  and  removed  by  filtration.  Then  the  tests  for  coagulable 
proteid  are  made — the  heat  test,  ferrocyanid  test,  and  Heller's  test.  Urine  con- 
taining coagulable  proteid  need  not  be  examined  further,  because  it  is  of  no 
clinical  interest  (see  p.  465).  If  this  is  absent,  20  to  30  c.c,  prepared  as  above, 
are  dropped  into  six  times  the  quantity  of  absolute  alcohol  and  then  allowed  to 
stand  for  twelve  to  twenty-four  hours.  The  solution  is  then  decanted  and  the 
precipitate  dissolved  in  a  slight  amount  of  warm  water.  After  refiltering  and 
testing  the  solution  again  for  precipitable  nucleo-albumin  with  very  much  diluted 
acetic  acid,  the  biuret  reaction  is  performed.  The  j^resence  of  urobilin  in  the 
urine  (see  Salkowski' s  method)  does  not,  as  a  rule,  give  rise  to  any  difficulty  in 
this  case,  because  when  precipitation  is  accomplished  the  urobilin  remains  in 
solution.  In  any  case  the  precipitate  may  be  washed  with  absolute  alcohol,  and 
so  completely  freed  from  urobilin. 

^  The  biuret  reaction  is  a  color  reaction  common  to  all  proteids  in  solution.  It  is, 
however,  especially  marked  with  albumoses  and  peptones.  It  is  performed  as  follows  : 
After  an  excess  of  sodium  or  potassium  hydroxid  has  been  added  to  the  solution  of  pro- 
teid, a  very  dilute  copper  sulpliate  solution  is  added.  It  will  produce  a  violet  color,  the 
shade  varying  according  to  the  kind  of  proteid  present ;  with  albumins  it  is  a  blue  violet, 
with  peptones  and  albumoses  it  is  a  red  violet. 

"^BerUn.  klin.  Woch.,  1897,  No.  17,  p.  353.  '^  Ibid.,  1899,  Nos.  35  and  36. 

*D.  ArcLf.  klin.  Med.,  1897. 


468  URINARY  EXAMINATION. 

Detection   of  Substances    Resembling    Mucin    (Now   Regarded   as   Nucleo-albumin, 
but   Formerly  Supposed   to   be   True  Mucin), 

Most  of  what  was  formerly  described  as  mucin  in  the  urine  is  now 
recognized  to  be  really  nucleo-albumin.  The  two  substances  resemble 
each  other  very  closely  in  their  physical  and  chemical  characteristics, 
but  mucin  is  a  glycoproteid  and  nucleo-albumin  a  phosphoproteid. 
Mucins  are  free  from  phosphorus,  and  when  decomposed  produce  proteid 
and  carbohydrate.  Xucleo-albumins,  on  the  contrary,  contain  phosphorus, 
and  when  decomposed  furnish  proteid  and  a  group  containing  phosphorus 
(nuclein).'  Despite  so  great  a  difference  in  their  composition,  the  two 
substances  are  difficult  to  distinguish.  The  only  simple  differentiating 
reaction  which  the  author  has  been  able  to  find  in  literature  is  the  pre- 
cipitation of  nucleo-albumin,  and  the  non-precipitation  of  true  mucin 
by  magnesium  sulphate.  This  statement  needs,  however,  to  be  corrobo- 
rated. 

Further  investigation  ^  will  have  to  determine  whether  nucleo-albu- 
min and  mucin  are  not  both  concerned  in  what  we  used  to  call  ofPhand 
the  mucus  of  the  urine.  For  the  time  being  it  is  justifiable  to  call  the 
mucin-like  substance  nucleo-albumin. 

Nucleo-albumin  occurs  in  urine  both  physiologically  and  pathologi- 
cally, partly  in  solution  and  partly  (the  larger  share)  undissolved.  The 
latter  constitutes  the  "  nubecula,"  a  slight  cloudiness  which  is  usually 
visible  only  after  the  urine  has  stood  for  some  time.  On  account  of  its 
lightness  it  remains  suspended  in  the  urine,  and  is  concentrated  as  a  sort 
of  cloud  in  the  center  of  the  vessel.  An  increased  amount  of  this 
undissolved  portion  of  nucleo-albumin  constitutes  what  has  always  been 
kno^vn  as  "  the  mucous  sediment."      It  is,  of  course,  pathologic. 

Nucleo-albumin  can  be  demonstrated  in  every  urine,  although  often 
not  in  sufficient  quantity  to  be  weighed.  It  possesses  certain  reactions  in 
common  with  serum-albumin  (see  Table,  facing  p.  460 — nucleo-albumin); 
hence  the  erroneous  opinion  that  the  presence  of  albumin  in  the  urine 
might  be  physiologic  (see  p.  459,  note).  The  amount  of  nucleo-albumin 
is  increased  in  all  affections  of  the  urinary  tract,  particularly  in  inflam- 
mation of  the  bladder  and  pyelitis,  in  nephritis,  and  in  several  other  dis- 
orders. An  abundant  mucous  sediment  occurs  only  in  inflammation  of 
the  urinary  organs,  very  likely  because  the  nucleo-albumin  is  mainly  a 
product  of  desquamation  of  the  mucous  membrane,  and  perhaps  of 
some  admixture  of  pus.  This  theory  agrees  with  the  observation  that 
these  mucous  sediments  always  contain  cellular  elements. 

Modern  chemical  investigations  are  now  concerned  almost  entirely 
with  that  portion  of  the  nucleo-albumin  which  is  held  in  solution  in  the 
urine.  The  salts  contained  in  the  urine  probably  hold  it  in  solution,  for 
it  seems  to  be  insoluble  in  water. 

To  demonstrate  the  soluble  nucleo-albumin,  an  excess  of  glacial  ace- 

^  [The  author  has  here  confused  the  two  terms  nucleoproteid  and  nucleo-albumin. 
The  former,  upon  decomposition,  splits  off  nucleins,  but  the  latter  does  not. — Ed.] 

*  Malfatti  believes  that  he  has  demonstrated  both  mucin  and  nucleo-albumin  in  nor- 
mal urine. 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE   URINE.   469 

tic  acid  is  added  to  the  urine.  If  the  urine  becomes  cloudy,  particularly 
if  it  has  been  previously  diluted,  nucleo-albumiu  is  present.  Dilution 
serves  two  purposes  :  it  diminishes  the  solvent  action  of  the  salts  and 
at  the  same  time  prevents  the  precipitation  of  urates  so  frequently 
noticed  in  concentrated  urines.  The  addition  of  an  excess  of  acetic 
acid  precludes  the  possibility  of  confounding  the  precipitate  with  the 
globulins ;  for,  although  acetic  acid  may  also  separate  the  latter  from 
their  comlDinations  with  the  alkalies,  they  will  be  immediately  dissolved 
again  by  the  least  excess  of  the  acid.  Both  uric  acid  and  the  resinous 
acids  are  precipitated  by  acetic  acid,  so  that  to  avoid  any  possibility  of 
confusing  either  of  them  with  nucleo-albumin,  it  is  advisable  to  make  a 
control  test  with  hydrochloric  acid.  This  acid  precipitates  both  these 
substances,  but  not  the  nucleo-albumin,  or,  at  least,  if  it  does,  the  least 
excess  of  HCl  will  promptly  redissolve  the  nucleo-albumin. 

The  general  proteid  tests  (heat  test,  p.  460  et  seq.)  and  cold  nitric 
acid  test  (p.  462)  demonstrate  nucleo-albumin.  Perhaps  this  is  one  of 
the  reasons  for  the  erroneous  supposition  that  serum-albumin  occurs  con- 
stantly physiologically  in  the  urine.  The  distinction  is  simple  enough, 
however,  because  an  excess  of  the  nitric  acid  dissolves  the  nucleo-albu- 
min (on  shaking  the  test  tube),  and  because  nucleo-albumin  is  precipi- 
tated by  acetic  acid,  while  serum-albumin  is  not. 

Nucleo-albumin  differs  from  serum-globulin  in  that  an  acetic  acid 
precipitate  of  the  former  will  not  be  dissolved  upon  the  addition  of  an 
excess  of  the  acid. 

The  actual  character  of  the  substance  known  as  nucleo-albumin  has 
been  recently  questioned  again,  since  Morner  ^  regards  it  as  a  combina- 
tion of  serum-albumin  with  chondroitin-sulphuric,  nucleic,  or  taurocholic 
acid,  while  Rostoski  ^  concludes  that  it  is  a  globulin.  It  probably  consists 
of  a  number  of  substances,  in  which  case  the  designation  used  at  the 
head  of  this  section,  "  substances  resembling  mucin,"  is  to  be  preferred. 

Detection  of  Hemoglobin  (Blood  Coloring  Matter)  and  its  Nearest  Derivatives: 
Hematuria  i  Hemoglobinuria. 

Blood  Coloring  matter  as  it  appears  in  the  urine  may  arise  from  the 
admixture  of  blood  in  the  kidneys  or  in  the  urinary  passages,  or  from 
the  transudation  of  dissolved  hemoglobin  from  within  the  vessels.  In 
the  first  case  we  speak  of  hematuria  ;  in  the  second,  of  hemoglobinuria. 
Hematuria  is  found  in  all  kinds  of  inflammation  of  the  kidneys  or  of 
the  urinary  tract,  in  new  growths  which  involve  any  portion  of  the 
organs,  and  after  some  injuries. 

Hemoglobinuria  is  symptomatic  of  certain  poisonings  (potassium 
chlorate,  truffles,  hydrogen  sulphid  or  arsenid,  pyrogallic  acid,  etc.). 
It  was  formerly  observed  after  transfusion  of  the  blood  of  another 
species.  It  also  occurs  after  burns,  in  severe  infectious  diseases  (rare), 
and  finally  as  an  independent  affection  in  the  form  of  the  so-called 
'periodic  hemoglobinuria.     Hemoglobin  can  often  be  recognized  in  the 

1  Skandin.  Arch.  f.  Physik,  vol.  vi.,  p.  332,  1895. 

^  Sitzungsbericht  der  physik-med.  Gesellsch.  zu  Wiirzburg,  1902. 


470  URINARY  EXAMINATION. 

urine  by  its  characteristic  color  (see  p.  453).  In  hematuria  the  blood- 
corpuscles  always  make  the  urine  turbid,  whereas  in  hemoglohinuria  the 
urine  may  be  perfectly  clear.  The  urine  may,  however,  be  turbid  in 
hemoglobinuria,  because  it  may  contain  casts  (see  p.  571)  and  granular 
masses  of  hemoglobin  (see  p.  561),  and  because,  too,  hemoglobinuria  is 
usually  combined  secondarily  with  nephritic  processes  (casts,  renal  cells, 
red  and  white  corpuscles).  Xevertheless,  in  such  cases,  if  the  urine  is 
allowed  to  settle,  the  clear  supernatant  fluid  will  still  exhibit  a  bloody 
color.  Of  course,  we  must  remember  that  after  a  hematuria  urine  has 
stood  for  some  time  many  of  the  blood-corpuscles  will  dissolve.  Hence, 
we  need  as  fresh  a  specimen  as  possible  to  distinguish  between  hematuria 
and  hemoglobinuria. 

The  presence  of  red  corpuscles  can  be  demonstrated  under  the  micro- 
scope. (Compare  Organized  Admixtures  and  Sediments  of  Urine.) 
Hemoglobin  itself,  whether  dissolved  or  still  contained  in  the  red  cor- 
puscles, can  be  shown  to  be  present  in  the  urine  by  the  following  means  : 

Cliemical  Detection  of  Hemoglobin. — The  different  deriva- 
tives of  hemoglobin  which  are  found  in  the  urine  react  alike  to  the 
chemical  tests.      (Compare  Spectroscopic  Test,  p.  471). 

Heat  Test.^-^J.n  performing  the  heat  test  for  coagulable  proteid  (p. 
460  et  seq.),  if  hemoglobin  is  present  a  brownish  coagulum  will  result. 
This  test  is  not  very  delicate.  In  contradistinction  to  the  proteid  pre- 
cipitate, the  coagulum  tends  to  float  upon  the  surface  of  the  fluid. 
Shaking  with  alcohol  and  sulphuric  acid  will  bleach  the  color. 

Heller's  Blood-test. — To  a  test  tube  half-full  of  urine,  5  drops  of 
potassium  or  sodium  hydroxid  are  added  and  the  mixture  heated.  If 
hemoglobin  is  present  a  brownish-red  or  blood-red  flocky  precipitate 
appears.  It  consists  of  the  phosphates  and  carbonates  of  the  earthy 
alkalies,  which  have  carried  down  with  them  the  hematin  that  has  been 
formed  from  the  hemoglobin  in  the  reaction.  In  alkaline  urines  the 
above  method  often  produces  no  precipitate,  because  the  phosphates  and 
carbonates  have  already  completely  separated  out  spontaneously.  The 
necessary  quantity  of  phosphates  and  carbonates  may  be  supplied  by 
adding  to  the  specimen  about  the  same  volume  of  a  normal  urine. 
With  this  test  the  coloring  matters  which  appear  in  the  urine  after  the 
use  of  chrysarobin,  senna,  rheum,  or  rhamnus  may  react  very  much 
like  hemoglobin,  and  so  may  lead  to  confusion.  But  in  the  latter  case 
the  red  color  which  arises  in  the  fluid  portion  of  the  specimen  upon  the 
addition  of  an  alkali  after  cooling,  and  the  decoloration  upon  the  addi- 
tion of  acetic  acid,  are  characteristic  (see  p.  503). 

Teichmann's  Hemin  Test. — After  filtration,  the  precipitate  from  the 
heat  or  Heller's  test  or,  better  still,  the  precipitate  produced  by  a  solu- 
tion of  tannic  acid  is  washed  and  dried  in  the  air.  Any  hemoglobin 
present  will  be  contained  in  this  dried  precipitate,  which  we  employ  for 
Teichmann's  delicate  test.  A  small  bit  of  the  dry  material  is  placed 
upon  a  glass  slide  with  a  particle  of  sodium  chlorid,  a  drop  of  glacial 
acetic  acid  is  added,  the  mixture  is  laid  upon  a  cover-slip,  and  the  whole 
is  heated  to  the  steam ing-point  for  about  one  minute.     A  little  acetic 


PLATE  5. 


Teiehmann's  Hemin  Crystals. 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE   URINE.   471 

acid  is  added  from  time  to  time  to  make  up  for  evaporation.  If  the 
fluid  turns  brown,  it  is  warmed  gently  and  then  allowed  to  evaporate. 
Teichmann's  characteristic  hemin  crystals  (Plate  5)  are  then  evident 
on  microscopic  examination.  Chemically,  they  consist  of  the  hydro- 
chlorid  of  hematin.  The  test  frequently  fails  because  excessive  heat  is 
employed  and  the  mixture  evaporated  too  quickly,  so  that,  of  course, 
the  characteristic  crystals  are  not  formed  so  readily.  Very  beautiful 
crystals  are  sometimes  obtained  when  the  test  is  performed  in  the  cold. 

Schonbein-Alinen's  Turpentine- Guaiac  Test — This  is  one  of  the  most 
delicate  of  the  blood-tests.  A  layer  consisting  of  a  mixture  of  equal 
parts  of  tincture  of  guaiac  ^  and  oil  of  turpentine  is  carefully  stratified 
upon  the  top  of  the  urine.  If  hemoglobin  is  present  a  cloudy  ring 
gradually  forms  at  the  junction  of  the  two  layers,  little  by  little  becom- 
ing an  intense  blue.  This  test  will  sometimes  give  a  positive  result 
when  the  spectroscopic  test  fails.  The  oil  of  turpentine  employed  must  be 
ozonized — i.  e.,  must  be  old.  It  may  be  well  to  test  the  reagent  first  with 
a  well-diluted  blood-solution.  Before  performing  the  test  we  should  see 
that  the  urine  is  acid  (adding  acetic  acid  to  an  alkaline  urine,  if  necessary). 

Pus  in  the  urine  may  turn  the  reagent  blue,  but  it  is  claimed  that  this 
blue  color  appears  quite  as  well  without  the  oil  of  turpentine  (Tap- 
peiner).  The  same  modification  which  we  mentioned  upon  p.  447 
(shaking  with  ether)  for  examining  the  gastric  juice  may  be  employed 
with  the  urine  to  avoid  the  above  confusion. 

Spectroscopic  Detection  of  Hemoglobin. — In  employing 
the  spectroscopic  test,  it  does  not  make  any  difference  whether  the  hemo- 
globin is  still  contained  in  the  blood-corpuscles  or  whether  it  is  in  solu- 
tion in  the  urine.  In  the  urine  hemoglobin  usually  occurs  in  three 
modifications — in  the  form  of  oxyhemoglobin,  reduced  hemoglobin,  or 
raethemoglobin.  The  spectra  of  these  substances  differ  ;  they  are  repre- 
sented in  Fig.  167. 

These  various  derivatives  of  hemoglobin  may  occur  in  the  urine 
simultaneously  and  so  produce  a  mixed  spectrum.  With  a  recent  and 
profuse  hemorrhage  into  the  urinary  passages  we  find  chiefly  oxyhemo- 
globin. With  hemoglobinuria  and  with  true  nephritic  hemorrhages,  on 
the  other  hand,  we  find  principally  methemoglobin.  The  latter,  how- 
ever, maybe  altered  to  reduced  hemoglobin,  and  eventually  to  oxyhemo- 
globin by  the  bacterial  decomposition  in  the  urine. 

For  clinical  purposes  the  spectroscopic  test  can  be  performed  by  look- 
ing at  a  layer  of  urine  1—2  c.c.  thick,  by  transmitted  bright  daylight,  sun- 
light, or  lamplight,  through  a  small  hand  spectroscope  (see  Fig.  166).  If 
the  urine  is  very  dark  or  cloudy,  it  must  first  be  diluted  with  water. 

DETECTION    OF    HEMATOPORPHYRIN. 
Hematoporphyrin  occurs  in  the  urine  principally  after  the  protracted  admin- 
istration of  sulphonal,  trional,  and  tetronal,  but  in  rare  cases  it  occurs  under 
pathologic   conditions   about   which    little    is   known.  ^     Traces   occur   also   in 
normal  urine. 

^  Alcoholic  solution  of  resina  guaiac,  1 :  5. 

^  Of.  Schulte,  Aus  der  Quinckeschen  Klinik,  D.  Arch,  f.klin.  Med.,  1897,  vol.  Iviii., 
parts  4  and  5. 


472  URINARY  EXAMINATION. 

It  is  considered  to  be  a  red  pigment  derived  from  hematin  and  free  from 
iron.  Nencki  and  Sieber  consider  that  it  is  isomeric  with  the  biliary  pigment 
bilirubin. 

It  is  demonstrated  by  Salkowski  ^  as  follows:  30  to  50  c.c.  of  urine  are  com- 
pletely precipitated  by  an  alkaline  barium  chlorid  solution  (a  mixture  of  equal 
parts  of  a  cold  saturated  solution  of  barium  hydrate  and  a  10  per  cent,  solution, 
of  barium  chlorid).  The  precipitate  is  washed  with  water  and  then  with  abso- 
lute alcohol,  and  the  hematoporphyrin  extracted  by  treating  it  with  alcohol 
acidulated  with  hydrochloric  acid. 

The  extraction  is  best  performed  by  repeatedly  pouring  a  warm  mixture  of 
10  c.c.  of  alcohol  and  6  to  8  drops  of  hydrochloric  acid  upon  the  precipitate  in, 
the  filter.  The  resulting  red- violet  gives  the  two  bands  of  acid  hematoporphyrin 
(compare  Fig.  167,  No.  6,  p.  448).  Supersaturation  with  ammonia  turns  the  solu- 
tion yellowish,  and  the  four  bands  belonging  to  hematoporphyrin  in  alkaline 
solution  appear  in  the  spectroscope. 

DETECTION  OF  BILIARY  PIGMENTS. 

The  most  important  biliary  pigments  are  bilirubin  and  biliverdin. 
The  latter  is  derived  from  the  former  by  oxidation  in  the  spontaneous 
decomposition  of  bile  by  putrefaction.  These  two  pigments  (and 
more  especially  bilirubin)  always  appear  in  the  nrine  whenever  biliary 
pigment  gets  into  the  blood — e.  g.,  in  jaundice  (p.  42  et  seq.). 

Icteric  urine  can  usually  be  recognized  by  its  color,  which  varies 
from  a  dark  yellowish  red  or  brown  to  a  greenish  black.  A  yellowish 
foam  and  yellowish  stains  of  the  urine  upon  clothes  are  particularly 
characteristic.     The  sediment  also  is  usually  stained  yellow. 

The  following  methods  are  employed  to  demonstrate  the  presence  of 
biliary  pigments  : 

Gmelin's  Test. — Filtered  urine  is  allowed  to  slowly  trickle  down 
the  side  of  a  test  tube  and  stratify  itself  upon  a  layer  of  nitric  acid.  If 
biliary  pigment  is  present,  color  changes  occur  at  the  line  of  junction 
of  the  two  fluids — from  greenish  blue  through  violet  red  to  yellow.  The 
individual  layers  of  urine  pass  through  this  play  of  colors  with  varying 
rapidity  according  to  their  distance  from  the  nitric  acid,  so  that  we 
usually  see  several  of  the  colors  superimposed.  Sometimes  the  green 
ring  is  the  only  one  we  can  see  plainly,  but  this  is  usually  enough.  A 
red-violet  ^  alone,  however,  may  he  produced  by  skatol  or  indol  coloring- 
matters  (p.  477).  Gmelin's  reaction  depends  upon  the  various  steps  in 
the  oxidation  of  bilirubin  ;  hence,  the  nitric  acid  should  contain  some 
nitrous  acid.  Crude  yellow  nitric  acid  fulfils  this  qualification,  or  the 
pure  nitric  acid  may  be  employed  if  it  is  first  heated  with  some  organic 
substance — e.  g.,  some  bits  of  wood.  Both  bilirubin  and  biliverdin 
react  to  Gmelin's  test ;  only  with  biliverdin  the  reaction  is  abbreviated, 
as  it  were,  because  the  biliverdin  is  already  the  partially  oxidized  green 
product,  to  which  bilirubin  must  be  changed  as  the  first  step  in  the 
process  of  oxidation. 

Rosenbach's  Modification  of  Gmelin's  Test. — Icteric  urine  is  filtered  after 
having  been  acidulated  with  hydrochloric  acid,  and  nitric  acid  is  then  dropped 

^  Zeits.  f.  phys.  Chemie,  vol.  xv.,  1891.  Cf.  also  Hammai-sten,  Skand.  Arch.  f.  PhusioL, 
1891,  vol.   i'ii. 

^  Compare  below  with  regard  to  the  possibility  of  confusion  with  indican. 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE   URINE.  473 

upon  the  paper.  The  play  of  colors  which  surrounds  the  drops  of  nitric  acid  will 
demonstrate  even  very  slight  traces  of  bile  pigment.  ^ 

If  this  modified  test  is  doubtful,  the  bile  pigment  may  be  first  extracted  with 
chloroform.  About  2  c.c.  of  the  latter  and  3  drops  of  hydrochloric  acid^  are 
added  to  a  test  tube  almost  filled  with  urine.  The  two  liquids  are  then  intimately 
mixed,  but  without  violent  shaking.  The  chloroform  takes  up  the  bile  pigment 
and  becomes  yellow  ;  but  the  solvent  will  not  settle  readily  if  the  mixture  is  shaken 
vigorously.  The  chloroform  is  now  separated  from  the  supernatant  urine  and  an 
equal  volume  of  water  and  a  few  drops  of  sodium  hydrate  are  added,  and  then 
mixed  by  repeatedly  inverting  the  tube.  The  jiigment  will  then  be  dissolved  by 
the  water,  because  the  salt  combination  of  the  pigment  is  insoluble  in  chloroform. 
Gmelin's  test  can  now  be  employed  with  this  concentrated  solution  of  bile  pig- 
ment. It  will  also  succeed,  though  not  so  well,  if  tried  on  the  chloroform  extract. 
The  least  trace  of  an  aqueous  solution  of  potassium  iodid  or  a  drop  of  diluted 
ferric  chlorid  solution  will  gradually  turn  the  chloroform  extract  green.  The 
bile  pigment  may  also  be  demonstrated  as  microscopic  crystals  by  evaporating 
the  chloroform  extract  in  a  watch  glass  (compare  Fig.  211,  d). 

Eecently,  Jolles  has  described  a  procedure  which  he  claims  increases  the  deli- 
cacy of  Gmelin's  reaction.  It  is  as  follows:  Fifty  cubic  centimeters  of  urine  are 
shaken  in  a  separatory  fiinnel  with  5  c.c.  each  of  a  10  per  cent,  barium  chlorid 
solution  and  chloroform.  Part  of  the  bile  pigment  will  be  extracted  by  the  chloro- 
form and  part  precipitated  by  the  barium  chlorid.  The  precipitate  and  the 
chloroform  are  separated  from  the'  urine  and  the  chloroform  evaporated  upon  a 
water  bath.  A  little  yellow  nitric  acid  is  now  added  to  the  residue,  and  Gmelin's 
characteristic  play  of  colors  appears  immediately. 

In  Gmelin's  test,  nitric  acid  may,  of  course,  bring  out  an  indican  reaction 
(p.  477).  The  blue  of  the  indigo  mixed  with  the  yellow  of  the  urine  pigment 
will  produce  a  green  tint,  and  so  may  simulate  Gmelin's  reaction.  But  the  indigo 
ring  always  has  a  blackish  shade  and  consists  of  a  fine  precipitate.  In  a  doubtfiil 
case  the  question  may  be  settled  by  first  isolating  the  bile  pigment  by  chloroform 
extraction  (see  above)  and  then  performing  Gmelin's  test.  This  method  is  also 
necessary  before  we  can  be  sure  that  both  indican  and  bile  pigment  are  present. 
(See  also  the  following  test  of  Salkowski.) 

The  presence  of  proteid  in  the  urine,  as  a  rule,  does  not  interfere  with  Gmelin's 
test  unless  the  amount  of  bile  pigment  is  very  small.  In  such  an  event  it  is  better 
to  first  extract  the  bile  pigment  with  chloroform.  The  test  cannot  be  well  performed 
with  urine  from  which  the  proteid  has  been  removed,  because  the  precipitated  albu- 
min will  carry  a  small  amount  of  bile  pigment  with  it. 

Salkowski's  Test. — The  urine  is  rendered  alkaline  by  the  addition  of  a  few 
drops  of  a  sodium  carbonate  solution  ;  a  solution  of  calcium  chlorid  (1 :  10)  is  then 
added  drop  by  drop  until  the  solution  over  the  precipitate  shows  after  thorough 
mixing  the  normal  color  of  the  urine.  The  precipitate  is  then  filtered,  well 
washed,  placed  in  a  test  tube  with  alcohol,  and  then  dissolved  by  adding  hydro- 
chloric acid  and  shaking.  If  the  clear  solution  contains  bile  pigment,  boiling  will 
turn  it  green  ;  if  not,  the  fluid  will  not  change  color.  The  green  solution  will 
change  to  blue,  violet,  and  red.  This  test  is  often  successful  when  Gmelin's  test 
gives  no  reaction,  and  Salkowski  recommends  it  particularly  in  those  cases  where 
the  indican  in  the  urine  interferes  with  Gmelin's  test. 

Trousseau's  Test. — A  few  drops  of  tincture  of  iodin  are  added  to  the  urine. 
If  bile  pigment  is  present  the  specimen  will  turn  a  beautiftil  emerald  green.  If 
the  tincture  of  iodin  is  diluted  ten  times  with  alcohol,  and  the  dilution  is  then 
stratified  upon  the  urine,  a  green  ring  will  appear  at  the  line  of  junction  of  the  two 
fluids.     This  is  more  delicate  than  Gmelin's  test. 

'  This  test  is  to  be  i-ecomniended.  Caution  must  be  observed,  however,  that  a  posi- 
tive test  is  not  due  to  the  filter  paper  itself,  since  impure  paper  may  give  a  similar  reaction. 

^  The  object  of  acidity  is  to  free  the  bile  pigment  (the  latter  reacts  chemically  as  an 
acid)  from  the  alkaline  combination  in  which  it  occurs  in  the  urine.  In  this  way  the 
extraction  is  rendered  more  complete,  because  free  bile  pigment  is  insoluble  in  water  but 
readily  soluble  in  chloroform,  while  the  reverse  is  true  of  the  salt  of  the  bile  pigment. 


474  UBINARY  EXAMINATION. 

Hammarsten's  Test.^ — A  mixture  of  19  parts  of  25  per  cent.  HCl  and  1 
part  of  25  per  cent.  HNO3  i^  allowed  to  stand  at  room  temperature  for  from  several 
hours  to  a  day  until  it  has  turned  slightly  yellowish.  One  part  of  this  acid  mix- 
ture is  added  to  5  parts  of  95  per  cent,  alcohol.  A  few  drops  of  urine  are  added 
to  a  few  cubic  centimeters  of  this  acidulated  alcohol.  If  the  urine  contains  bile 
pigment,  a  characteristic  green  color  appears  almost  immediately  even  at  room 
temperature.  The  author  considers  the  test  sensitive,  but  not  more  delicate  than 
Salkowski's. 

Stockvis'  Test  for  Cholecyanin  {bilicyanin). — 5  to  10  c.c.  of  a  20  per 
cent,  solution  of  zinc  acetate  are  added  to  20  to  30  c.c.  urine.  Sodium  carbonate 
solution  is  added  to  slightly  diminish  the  marked  acidity.  The  abundant  pre- 
cipitate will  contain  all  the  bile  pigments ;  it  is  washed  on  a  filter  and  then 
dissolved  in  a  little  ammonia.  This  transforms  the  bile  pigment  to  cholecyanin. 
A  neutral  solution  of  the  latter  is  blue  green,  and  exhibits  red  fluorescence  and  a 
characteristic  spectrum  with  three  absorption  bands.  One  of  these  bands  is  in 
red,  sharply  outlined  and  dark,  between  C  and  D,  nearer  to  C  ;  a  second,  less 
sharp,  in  yellow,  covering  D  ;  and  the  third,  a  very  faint  one,  in  green,  between 
D  and  E. 

Haycraft  claims  that  in  urine  which  contains  bile  pigment  powdered  sulphur 
will  immediately  or  almost  immediately  sink  to  the  bottom.  This  peculiarity  is 
even  more  characteristic  of  urine  which  contains  biliary  acids.  The  test  is  not  very 
accurate,  since  after  a  certain  time  some  of  the  powdered  sulphur  will  sink  in 
normal  urine.  It  is  probable  that  the  temperature  of  the  urine  has  something 
to  do  wath  the  result  of  the  experiment,  but  it  has  not  been  determined  to  what 
extent. 

Microscopic  Detection  of  Bile  Pigments. — The  urine  must  contain  a  suffi- 
cient amount  of  bile  pigment.  It  is  acidified  with  hydrochloric  acid  and  allowed 
to  stand  for  some  time  in  the  cold,  after  which  bilirubin  will  be  precipitated  as 
bundles  of  microscopic  needles  colored  intensely  brown.  (Fig.  211,  d.)  These 
little  bunches  of  needles  are  often  observed  when  icteric  urine  is  evaporated  to  test 
for  the  presence  of  leucin  or  tyrosin  (p.  498).  The  bilirubin  needles  are,  however, 
much  browner  than  tyrosin  needles. 

Method  for  Removing  Bile  Pigment  from  the  Urine  in  Order  to  Perform  Other 
Tests. — The  color  of  bile  pigment  may  be  removed  very  easily  either  by  extracting 
the  acidified  urine  with  chloroform  or  boiling  the  specimen  with  some  anircial 
charcoal.  This  is  necessary  before  testing  for  salicyluric  acid  with  ferric  chlorid, 
because  this  reagent,  like  the  tincture  of  iodin,  is  apt  to  produce  a  green  discolor- 
ation in  icteric  urine,  which  hides  the  violet  color  of  the  iron  salicylurate.  The 
urine  must  not  be  boiled  too  long  with  the  charcoal,  as  the  latter  is  apt  to  com- 
bine with  the  salicyluric  acid.  It  is  always  advisable  to  make  a  control  test,  in 
order  to  be  sure  that  the  process  of  decolorizing  has  not  destroyed  the  substance 
we  are  trying  to  detect. 

DETECTION  OF    BILE    ACIDS. 

The  bile  acids  occur  iu  the  urine  chiefly  in  cases  of  obstructive 
(retention)  jaundice.  These  acids  should  be  isolated  before  we  attempt 
to  test  for  them. 

Hoppe-Seyler  *  gives  the  following  directions  :  Lead  acetate  and  a  little  ammonia 
are  added  to  the  urine.  The  resulting  precipitate  is  washed  with  water,  then 
boiled  with  alcohol,  and  filtered  while  hot.  The  lead  salts  of  the  bile  acids  dis- 
solve in  hot  alcohol.  A  few  drops  of  soda  solution  are  added  to  this  solution, 
which  is  then  evaporated  over  a  water  bath  till  diy,  and  the  residue  boiled  out 
with  absolute  alcohol,  when  the  sodium  salts  of  the  bile  acids  dissolve.  The 
filtered   alcoholic   extract   is   evaporated  to  a  small   volume,    then   precipitated, 

1  Shind.  Arch.  f.  Physiol,  vol.  ix.,  p.  313 ;  ref.  in  Centralbl.  f.  Physiol.,  vol.  xiii.,  p.  644. 
^  Handbuch  der  Physiol,  u.  path.-chemischen  Analyse,  1893,  p.  378. 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE   URINE.   475 

and  allowed  to  stand  with  an  excess  of  ether  in  a  closed  bottle.  In  this  way  the 
sodium  salts  of  the  bile  acid  scan  often  be  obtained  as  crystals.  But  it  is  not  neces- 
sary to  wait  for  them,  as  the  resinous  precipitate  may  be  dissolved  immediately  in 
a  little  water,  and  Pettenkofer' s  test  applied  as  follows  : 

Pettenkofer'S  Test. — To  the  solution  of  the  bile  salts  we  add 
two-thirds  of  its  volume  of  concentrated  sulphuric  acid  very  slowly, 
so  that  the  mixture  does  not  become  heated  above  60°  C  Then  we 
add  3  to  5  drops  of  a  solution  of  1  part  of  cane  sugar  in  4  to  5  parts 
of  water,  and  shake,  whereupon  the  liquid  turns  a  beautiful  violet 
color. 

Strassburg '  has  at  times  succeeded  in  demonstrating  the  presence  of  bile  acids 
in  the  urine  directly  by  adding  a  small  amount  of  cane  sugar  and  then  filtering. 
To  the  dried  filtrate  is  added  a  drop  of  pure  concentrated  sulphuric  acid.  If  bile 
acids,  are  contained  in  the  urine  a  beautiful  violet  spot  appears  within  a  quarter  of 
a  minute  in  the  particular  place  at  which  the  drop  was  added.  This  spot  soon 
turns  to  a  dark  purplish  red,  which  is  particularly  plain  by  transmitted  light. 

V.  Udransky  considers  a  direct  detection  sometimes  possible.  He  dilutes  1 
drop  of  urine  with  1  c.  c.  of  water  and  1  drop  of  furfiirol  water  (obtained  by  shak- 
ing 1  drop  of  fiirfurol  thoroughly  in  one-half  test  tube  of  water),  and  then  adds 
1  c.c.  of  concentrated  sulphuric  acid. 

Haycraft  claims  that  his  method  (see  p.  474)  for  determining  the  presence  of 
biliary  acids  is  perfectly  trustworthy.  But,  as  a  matter  of  fact,  in  positive  cases 
the  test  does  not  discriminate  between  biliary  acids  and  biliary  coloring  matter, 
even  when  the  latter  occurs  in  very  slight  traces.  (See  p.  474  in  regard  to  the 
significance  of  biliary  acids  in  icteric  urine.) 

DETECTION  OF  INDICAN  AND    INDIGO. 

Indican,  or  indoxyl  sulphuric  acid,  in  the  urine  is  the  product  of  the 
putrefaction  of  proteids,  and  is  a  derivative  of  indoxyl,  which  in  turn 
is  an  oxidation  product  of  indol.  This  decomposition  occurs  in  the 
intestine  normally,  but  is  more  pronounced  in  digestive  disturbances 
with  diminished  peristalsis  (intestinal  obstruction).  Indican  may  also 
be  found  under  some  circumstances  in  various  other  parts  of  the  body, 
from  suppurative  processes. 

An  increased  amount  of  indican  in  the  urine  is  of  some  diagnostic 
importance  in  helping  to  locate  the  seat  of  an  intestinal  obstruction. 
Experience  has  shown  that  an  obstruction  in  the  small  intestine  is  quickly 
followed  by  a  marked  increase  in  the  amount  of  indican  in  the  urine,  as 
contrasted  with  an  obstruction  in  the  large  bowel,  where  there  is  very 
rarely  any  such  increase,  unless  perhaps  in  the  later  stages.  This  is 
probably  because  the  trypsin  of  the  pancreatic  juice  favors  decomposi- 
tion and  the  formation  of  indican.  Both  factors  aid  each  other  in  the 
decomposition  of  the  proteids.  In  deep-seated  obstruction  in  the 
large  intestine  the  stagnation  of  the  contents,  which  favors  decomposi- 
tion, occurs  primarily  where  trypsin  is  no  longer  active.  (The  latter, 
as  is  well  known,  is  destroyed  or  reabsorbed  in  the  course  of  the  intes- 
tine.) In  obstruction  in  the  small  intestine  the  stagnation  takes  place 
where  the  trypsin  favors  the  decomposition.     A  further  explanation  is 

'  Areh.f.  d.  ges.  Physiol.,  vol.  iv.,  p.  461. 


476  URINARY  EXAMINATION. 

that  the  greater  portion  of  the  proteids  which  furnish  the  indican  have 
been  already  absorbed  in  the  large  intestine. 

If  the  duct  of  the  pancreas  is  occluded,  the  amount  of  indican  in 
the  urine  will  be  diminished.  However,  as  the  indican  in  the  urine 
is  normally  quite  small  in  amount,  or  even  absent  altogether,  a  dimi- 
nution can  be  clinically  significant  of  an  occlusion  of  the  pancreatic 
duct  only  under  conditions  which  would  ordinarily  favor  the  production 
of  a  large  amount  of  indican — e.  g.,  jaundice  and  a  meat  diet. 

In  peritoneal  aifections,  particularly  in  perityphlitis,  any  increase  in 
the  amount  of  indican  suggests  an  increase  of  trouble  ;  any  diminution, 
an  improvement  in  the  condition. 

We  can  frequently  demonstrate  indican  in  normal  urine  by  one  of 
the  following  methods.  They  depend  upon  the  fact  that  oxidizing 
agents  transform  indican  into  indigo.  The  reaction  must  be  very 
striking  to  enable  any  safe  diagnostic  conclusions  (as  to  increased  intes- 
tinal decomposition  or  any  other  process  of  decomposition  in  the  interior 
of  the  body,  or  as  to  the  location  of  an  obstruction). 

Jaflfe's  Indican  Test. — One-quarter  of  a  test  tube  of  urine  is 
mixed  with  an  equal  volume  of  concentrated  hydrochloric  acid,  and  a  drop 
of  a  half-saturated  solution  of  commercial  chlorid  of  lime  (chlorinated 
lime)  is  added.  If  no  reaction  takes  place  immediately,  more  of  the 
chlorid  of  lime  solution  is  added,  drop  by  drop,  without  shaking.  If  the 
urine  contains  considerable  quantities  of  indican,  a  blue-black  ring  of  pre- 
cipitated indigo  will  appear  in  the  upper  part  of  the  tube,  at  the  lower 
zone  of  action  of  the  chlorid  of  lime  solution.  This  ring  will  become 
more  intensely  colored  upon  standing.  If  a  very  large  amount  of 
indican  is  present,  the  entire  fluid  will  turn  black.  We  must  be  very 
careful  not  to  add  too  much  of  the  chlorid  of  lime  solution,  since  in 
that  case  the  indigo  formed  by  the  oxidation  of  the  indican  will  become 
further  oxidized  to  yellow  isatin.  Proteid,  if  present,  should  be  first 
removed  by  boiling  and  filtration.  The  indigo  formed  in  this  way  will 
dissolve  in  a  few  cubic  centimeters  of  chloroform  by  gentle  agitation, 
coloring  the  latter  blue.  If  only  a  small  amount  of  indican  is  present, 
there  is  considerable  danger  of  adding  too  much  chlorid  of  lime.  Hence, 
the  test  has  been  modified  at  the  Bern  Clinic  in  the  following  way  : 
First  a  few  cubic  centimeters  of  hydrochloric  acid  are  poured  into  a 
test  tube  and  a  drop  of  the  chlorid  of  lime  solution  is  added.  The 
mixture  is  well  shaken,  and  then  the  urine  is  carefully  stratified  upon 
it,  either  by  letting  the  urine  flow  down  the  side  of  the  tube  or,  better 
still,  by  letting  it  fall  upon  the  surface  of  the  hydrochloric  acid,  drop 
by  drop,  through  a  filter.  The  indican  reaction  will  then  be  shown  very 
beautifully  at  the  line  of  junction  of  the  two  fluids. 

Obermayer's  Test. — Obermayer^  claims  that  he  can  avoid  the  danger  of 
excessive  oxidation,  which  is  a  defect  in  Jaffe's  test,  by  the  use  of  ferric  chlorid 
as  an  oxidizing  agent  instead  of  chlorid  of  lime.  He  adds  to  the  urine  a  small 
amount  of  a  20  per  cent,  solution  of  sugar  of  lead,  in  order  to  precipitate  those 
substances  which  prevent  the  shaking  out  of  the  indigo  by  the  chloroform.    After 

1  Wien.  klin.  Wock,  1890,  No.  9. 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE   URINE.   477 

removing  the  precipitate  by  filtration,  he  adds  an  equal  volume  of  fuming  con- 
centrated hydrochloric  acid  which  contains  4  gm.  of  ferric  chlorid  to  the  liter. 
The  mixture  is  then  shaken.  The  reaction  will  take  place,  he  claims,  within  a 
few  moments,  and  the  indigo  may  then  be  extracted  with  chloroform.  Ober- 
mayer  believes  that  this  process  is  adapted  for  an  accurate  colorimetric  determi- 
nation of  the  amount  of  indican  present. 

Amann's  Test. — J.  Amann '  recommends  sodium  pyrosulphate  (Na2S20,)  as 
an  oxydizing  reagent.  He  claims  that  this  reagent  also  will  not  cause  any  loss 
of  indigo  by  excessive  oxidation.  The  test  is  performed  as  follows  :  To  20  c.c. 
of  urine  are  added  a  few  drops  of  pure  suljjhuric  acid,  5  c.c.  of  chlorform,  and 
then  5  c.c.  of  a  10  per  cent,  solution  of  sodium  pyrosulphate.  They  are  mixed 
gently  for  several  minutes  (too  much  shaking  may  produce  an  emulsion).  The 
chloroform  is  then  allowed  to  settle  and  will  be  colored  blue  by  the  indigo.  The 
method  can  be  utilized  for  an  exact  colorimetric  determination. 

Other  oxidizing  reagents  often  produce  a  more  or  less  distinct  indican 
reaction — e.  g.,  nitric  acid  in  the  test  for  bile  pigments.  (See  p.  473). 
In  the  employment  of  nitric  acid  for  the  detection  of  indican  there  is 
great  danger  of  decolorizing  the  indigo.  It  will  be  recalled  that  the 
decolorization  of  indigo  is  one  of  the  reactions  of  nitric  acid,  which  is 
therefore  not  a  reliable  agent  for  the  detection  of  indican. 

As  already  mentioned,  indican  is  sometimes  oxidized  spontaneously 
to  indigo  in  the  urine  before  or  after  being  voided.  Urine  which  con- 
tains indigo  presents  a  black,  green,  or  bluish  tint.  All  that  is  neces- 
sary to  prove  that  the  color  is  due  to  indican  is  to  shake  the  urine  with 
chloroform  and  then  allow  the  latter  to  settle,  when  it  will  be  seen  to 
have  turned  blue.  The  needle-shaped  or  thin  plate-like  crystals  of 
indigo  may  sometimes  be  detected  microscopically  in  the  urine  sedi- 
ment, or  even  in  the  residue  of  the  dried  chloroform  extract. 

DETECTION  OF  MELANIN  (PHYMATORRHUSIN)  AND  MELANOGEN. 

A  peculiar  brownish-black  coloring  matter,  the  so-called  melanin  (phyma- 
torrhusin),  sometimes  appears,  partly  as  such,  partly  as  a  colorless  chromogen, 
in  the  urine  of  patients  suffering  with  melanotic  neoplasms.  Urine  which  con- 
tains melanin  is  blackish.  Oxidizing  agents,  such  as  nitric  acid  or  ferric  chlorid, 
will  turn  it  still  darker  when  exposed  to  the  air.  Urine  which  contains  colorless 
melanogen  exhibits  a  dark  color  only  after  the  melanogen  has  been  changed  by 
these  agents  into  melanin.  The  addition  of  bromin  water,  and  sulphuric  acid  or 
chlorin  water  also  produces  a  dark  color.  An  excess  of  bromin  or  chlorin 
water  will  cause  a  decolorization  and  throw  down  a  dense  dirty-yellow  precipi- 
tate. Boiling  with  fuming  nitric  acid  will,  under  certain  circumstances,  decol- 
orize melanotic  urine.  Melanin  may  be  confounded  with  indigo,  and  melanogen 
with  indican  (see  p.  475  et  seq.).  The  solubility  of  indigo  in  chloroform,  and 
the  resulting  blue  color,  will  serve  to  differentiate  them. 

ROSENBACH'S    REACTION    (Red  Indol  and  Skatol  Pigments). 

Several  years  ago  Rosenbach  described  the  following  reaction.  Con- 
centrated nitric  acid  is  added  drop  by  drop  to  a  test  tube  of  urine  while 
it  is  being  continually  boiled.  The  urine  gradually  assumes  a  Burgundy 
red  color,  while  the  foam  produced  by  shaking  turns  a  bluish  red.  A 
reddish  or  brownish-red  color  without  the  foam  becoming  violet  red  is 
not  distinctive,  as  it  may  be  due  to  the  urobilin  in  the  urine.  Contin- 
*  Revue,  med.  de  la  Suisse  Rom.,  1897,  No.  6,  p. 449. 


478  UBINARY  EXAMINATION. 

ued  addition  of  nitric  acid  will  turn  the  red  color  rather  rapidly  to  a 
yellowish  red  or  yellow  with  a  yellow  foam.  The  addition  of  a  solution 
of  soda  or  ammonia  drop  by  drop  will  cause  a  bluish-red  precipitate, 
which  dissolves  in  an  excess  with  the  formation  of  a  reddish-brown 
color.  In  these  cases  the  urine  is  sometimes  already  of  a  reddish  shade, 
or  sometimes  a  slight  reddish  tinge  occurs  upon  the  addition  of  nitric 
acid  while  the  specimen  is  still  cold.  The  reaction  seems  to  depend 
principally — although  perhaps  not  exclusively — upon  the  formation  of 
indigo-red  (indirubin,  indigo-purpurin),  an  oxidation  product  of  indoxyl 
or  indican  (see  p.  475).  It  may,  too,  perhaps  depend  upon  the  forma- 
tion of  skatol  pigments  by  means  of  the  oxidizing  influence  of  nitric 
acid.  Indigo  is  often  produced  in  this  way — hence  the  violet  shades  of 
the  reaction.  The  test  has  a  diagnostic  importance  similar  to  that  of 
the  indican  reaction. 

UROROSEIN  (Urrhodin). 

A  red  color  is  not  infrequently  noticed  in  the  urine,  appearing  soon  after  the 
addition  of  mineral  acids,  especially  hydrochloric  acid.  It  occurs  both  in  health 
and  in  many  conditions  of  disease.  Nencki  and  Sieber  recognized  it  as  due  to  a 
pigment  which  they  called  urorosein,  the  chromogen  of  which  is  contained  in  the 
urine.  It  is  probably  identical  with  the  pigment  described  by  Heller  as  urrhodin, 
evidently  differs  from  indigo-red,  and  may  possibly  be  a  derivative  of  skatol.  In 
contrast  to  Rosenbach's  reaction  (indigo-red,  p.  477),  the  red  color  disappears  upon 
the  addition  of  alkaline  carbonates  to  the  urine.  This  pigment,  unlike  tadigo-red, 
is  insoluble  in  chloroform  and  ether. 

UROERYTHRIN. 

This  pigment  occurs  in  normal  urine,  particularly  after  the  ingestion  of  large 
quantities  of  food  and  alcohol,  and  after  profuse  perspiration  ;  it  is  also  found  in 
pathologic  urines  in  digestive  disturbances,  in  gout,  and  in  febrile  conditions. 
This  is  the  pigment  which  is  responsible  for  the  beautiful  rose  tint  in  many  of  the 
uratic  sediments.  It  was  formerly  regarded  as  identical  with  urorosein,  but  is  now 
known  to  be  a  different  substance.  Urines  containing  large  quantities  of  this  pig- 
ment are  of  a  decided  orange  color.  When  concentrated  sulphuric  acid  is  added 
to  the  pigment,  a  carmin-red  color  is  produced;  alkalies  (not  ammonia)  change  the 
color  of  the  pigment  first  to  a  purplish  blue  and  then  to  a  green.  These  reactions 
obtain  only  with  pure  solutions  of  the  pigment,  however,  and  such  solutions  are 
difficult  to  obtain. 

DETECTION    AND    OCCURRENCE    OF   UROBILIN. 

Urobilin  is  in  all  probability  a  derivative  of  bilirubin.  Modern 
investigations  have,  however,  cast  doubt  upon  the  old  assumption  that 
it  was  identical  with  hydrobilirubin.  Urobilin  occurs  in  small  amounts 
even  in  normal  urine,  but,  according  to  Saillet,  not  until  the  urobilinogen 
has  been  acted  upon  by  light.  The  normal  yellow  color  of  the  urine  is 
not  due  to  urobilin,  but  to  urochrome. 

Pathologically,  urobilin  is  excreted  in  increased  amounts  in  some 
forms  of  icterus  (urobilin  icterus,  see  p.  44),  and  in  all  diseases  asso- 
ciated with  destruction  of  red  blood-corpuscles,  such  as  fever,  scurvy, 
internal  hemorrhage,  and  pernicious  anemia. 

The  demonstration  of  such  an  increase  is  sometimes  of  diagnostic 
importance  in  proving  the  occurrence  of  internal  hemorrhage — e.  g., 
cerebral  hemorrhage,  hemorrhagic  infarction,  retro-uterine  hematocele, 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE   URINE.   479 

and  hemorrhage  in  ectopic  gestation.  The  blood-pigment  of  the  trans- 
uded blood  is  first  transformed  into  bilirubin  or  hematoidin,  and  is  then 
excreted  as  urobilin.  But  if  fever  complicates  any  of  the  above  con- 
ditions, an  increase  in  the  excretion  of  urobilin  will  be  of  no  diagnostic 
importance,  for  fever  alone  is  a  frequent  source  of  urobilinuria. 
Unfortunately,  the  amount  of  urobilin  in  the  urine  is  of  slight  value  in 
the  diagnosis  of  brain  hemorrhage,  however  desirable  it  would  be  to 
possess  a  reliable  criterion  to  differentiate  cerebral  softening  from  hem- 
orrhage. On  the  one  hand,  most  cerebral  hemorrhages  are  much  too 
slight  to  produce  any  marked  increase  in  the  amount  of  urobilin  in  the 
urine.  Large  cerebral  hemorrhages,  on  the  other  hand,  usually  result 
fatally  before  the  necessary  changes  of  the  blood-pigment  have  taken 
place.  Even  in  favorable  cases  an  excess  of  urobilin  does  not  appear 
in  the  urine  for  some  time  after  the  hemorrhage,  when  the  differential 
diagnosis  between  hemorrhage  and  softening  is  of  no  particular  thera- 
peutic value.  Further,  fever  so  frequently  occurs  in  the  acute  focal 
lesions  of  the  brain  as  to  decidedly  influence  the  amount  of  urobilin  in 
the  urine. 

Urine  which  contains  a  very  large  amount  of  urobilin  is  often  very 
dark.  This  is  not  invariably  the  case,  because  urobilin  does  not  possess 
very  intense  coloring  properties.  Usually,  other  pigments  which  may 
be  increased  in  quantity  along  with  it  are  principally  responsible  for  the 
dark  color.  In  fact,  a  very  dark  urine  may  contain  very  little,  and  a 
light  urine  a  large  amount  of,  urobilin. 

The  most  accurate  method  for  the  demonstration  of  the  presence 
of  urobilin  is  by  means  of  the  spectroscope,  after  first  acidifying  the 
urine  with  a  little  hydrochloric  acid  to  make  the  spectrum  more  dis- 
tinct. Acid  urobilin  solutions  when  very  concentrated  or  in  thick  layers 
absorb  the  entire  blue  end  of  the  spectrum  as  far  as  the  middle  of 
green.  On  the  other  hand,  a  thin  layer  or  a  less  concentrated  solution 
shows  an  absorption  band  between  green  and  blue  (Fig.  167).  In  con- 
trast to  urobilin,  the  biliary  pigments  proper  absorb  the  spectrum 
diffusely.  A  simple  chemical  method  for  demonstrating  the  presence 
of  urobilin  is  as  follows  :  The  urine  is  rendered  strongly  alkaline  with 
ammonia,  filtered,  and  a  few  drops  of  a  10  per  cent,  alcoholic  or  aqueous 
solution  of  zinc  chlorid  are  added.  A  beautiful  green  fluorescence  occurs 
if  urobilin  is  present. 

To  demonstrate  chemically  a  very  small  quantity  of  urobilin  in  the 
urine,  it  must  be  first  extracted  by  gently  shaking  a  specimen  of  urine 
acidulated  with  a  few  drops  of  hydrochloric  acid  with  one-third  its 
volume  of  amyl  alcohol.  When  the  alcohol  has  extracted  the  urobilin, 
it  will  be  colored  brown.  If  the  layers  are  not  distinct  and  the  amyl 
alcohol  portion  remains  cloudy,  like  an  emulsion,  the  separation  and  the 
clarifying  may  be  aided  by  the  addition  of  a  few  drops  of  ethyl  alcohol. 
Several  drops  of  an  alcoholic  ammonium  chlorid  solution  (spiritus 
Dzondii)  and  some  1  per  cent,  alcoholic  solution  of  zinc  chlorid  are 
then  added  to  the  amyl  alcohol  layer,  and  the  resulting  fluorescence 
shows  the  presence  of  urobilin. 


480  URINARY  EXAMINATION. 

Whether  the  urobilin  as  characterized  by  the  above-mentioned  tests  is  a  spe- 
cific substance,  or  whether  there  exist  several  urobilins,  has  been  recently  much 
discussed.  ^  A  final  verdict  is  not  yet  possible.  In  any  case  a  differentiation  (sug- 
gested by  JoUes)  of  physiologic  and  pathologic  urobilins  has  not  been  sufficiently 
worked  out  to  be  of  any  clinical  value. 

QUALITATIVE  DEMONSTRATION  OF  GRAPE  SUGAR  (GLUCOSE ;  DEXTROSE). 
Preparation    of    the    Urine    for    the    Qualitative   Test  for    Sugar. 

If  the  urine  contains  proteid,  this  must  be  removed  before  proceeding 
with  the  tests  for  sugar  (see  p.  463).  If  it  contains  hydrogen  sulphid 
(hydrothionuria,  see  p.  455),  this  compound  may  be  removed  by  shak- 
ing the  urine  with  white  lead,  and  fihering. 

Almost  all  of  the  qualitative  tests  for  sugar  are  most  successful  when 
the  acid  urine  is  precijoitated  with  lead  acetate.  About  5  c.c.  of  a  solu- 
tion of  lead  acetate  are  added  to  50  c.c.  of  urine  ;  the  mixture  is  filtered, 
and  the  excess  of  lead  removed  from  the  filtrate  by  the  addition  of  sev- 
eral cubic  centimeters  of  a  saturated  solution  of  sodium  phosphate,  this 
solution  being  added  until  precipitation  no  longer  occurs.  The  decolor- 
ized filtrate  is  then  employed  for  the  tests,  and  is  better  adapted  for  this 
purpose  than  the  original  urine,  since  various  substances  which  might 
have  interfered  with  the  reactions  have  been  removed.  The  original 
urine  must  be  distinctly  acid,  and  also  remain  acid  after  the  addition  of 
the  sodium  phosphate,  since  sugar  is  precipitated  from  an  alkaline  urine 
by  the  addition  of  lead.  The  acid  reaction  should  be  finally  insured  by 
the  addition  of  several  drops  of  acetic  acid.  All  concentrated  urines 
should  be  diluted  with  two  or  three  volumes  of  water,  in  order  to  min- 
imize the  effect  of  certain  substances  which  interfere  with  the  reactions. 

An  appropriate  preparation  of  the  urine  for  the  qualitative  sugar 
tests  is  also  the  treatment  with  mercuric  nitrate,  as  recommended  upon 
p.  516  for  the  polarimetric  examination. 

Very  small  amounts  of  dextrose  probably  occur  in  every  normal 
urine.  We  have  no  simple  reaction  to  prove  this  absolutely,  but  we  do 
know  that  normal  urine  reduces  less  after  than  before  fermentation  by 
yeast.  Pathologic  amounts  of  sugar  can,  on  the  contrary,  be  demon- 
strated by  very  simple  methods.  We  must,  in  the  first  place,  discrimi- 
nate between  a  permanent  or  persistent  dextrose  excretion  {diabetes  mel- 
litus)  and  one  of  the  transient  type  {glycosuria).  No  sharply  defined 
distinction  can  as  yet  be  drawn  between  these  two.  Glycosuria  accom- 
panies various  disorders,  particularly  cerebral  and  digestive  affections, 
certain  forms  of  poisoning  (morphin,  carbon  monoxid,  chloral  hydrate, 
oil  of  turpentine  (in  the  two  latter  cases  the  presence  of  glycuronic  acid 
is  responsible  for  the  condition),  corrosive  sublimate,  arnyl  nitrate,  nitro- 
benzol,  curare,  phloridzin,  etc.),  and  prolonged  hunger.  It  sometimes 
happens  that  otherwise  perfectly  healthy  people  temporarily  excrete  dex- 
trose in  the  urine  after  too  abundant  ingestion  of  sugar  or  of  other  car- 
bohydrates {alimentary  or  physiologic  glycosuna). 

1  Of.  Jolles,  Centralbl.f.  inn.  Med.,  1895,  and  Pfilger's  Arch.,  vol.  Ixi.,  pp.  623-637; 
and  Archibald  S.  Garrod  and  F.  Gowland,  Hopkins  Jour,  of  Physiol.,  vol.  xx.,  pp.  112-114. 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE   URINE.   481 

It  is,  however,  quite  essential  to  distinguish  cases  of  alimentary  glycosuria 
due  merely  to  excessive  ingestion  of  sugar  from  those  attributable  to  undue  con- 
sumption of  starches.  The  latter  presumably  indicate  some  grave  disorder, 
because  the  tolerance  for  starches  is  much  greater  than  for  sugar,  probably  for 
the  reason  that  the  absorption  of  starch  takes  place  much  more  slowly.  Hence, 
when  abundant  starch  ingestion  gives  rise  to  sugar  excretion,  we  may  best  consider 
the  case  as  related  to  diabetes  mellitus,  and  reserve  the  term  '•  physiologic  or 
alimentary  glycosuria"  for  cases  where  the  starches  can  be  freely  ingested  without 
exciting  sugar  excretion,  but  where  excessive  ingestion  of  sugar  occasions  a 
glycosuria.  As  a  matter  of  fact,  excessive  ingestion  of  sugar  may  overstep  the 
tolerance  of  perfectly  healthy  individuals. 

Urine  containing  much  dextrose  is  peculiar  in  presenting  a  light  or 
pale  color  combined  with  a  high  specific  gravity.  In  true  diabetes  the 
amount  of  urine  is  usually,  although  not  always,  increased.  Hence  a 
pale  urine,  excreted  in  excess  of  the  normal  daily  quantity,  and  with  a 
specific  gravity  of  1030  or  more,  allows  of  the  most  decided  suspicion 
of  diabetes  mellitus.  Urine  containing  dextrose  ferments  spontaneously 
after  standing  for  some  time.  This  characteristic  alcoholic  fermentation 
may  be  recognized  either  from  the  development  of  carbonic  acid  bub- 
bles or  from  the  microscopic  demonstration  of  yeast  in  the  sediment. 
Therefore  sugar  tests  must  always  be  performed  with  a  fresh  specimen. 

To  detect  a  small  quantity  of  dextrose  in  a  doubtful  case  we  natu- 
rally select  for  examination  a  specimen  voided  during  the  day  and  a 
short  time  after  eating,  because  the  quantity  of  sugar  is  apt  to  be  then 
at  a  maximum.  If  the  meal  was  rich  in  starch  or  sugar  we  are  still 
more  liable  to  obtain  a  positive  result.  Of  course,  we  must  remember 
that  apparently  perfectly  healthy  people  may  excrete  sugar  after  too 
abundant  consumption  of  these  two  foods.  If  an  excessive  ingestion 
of  starch  alone  produces  glycosuria  in  such  people  they  may  be  consid- 
ered as  straddling  the  border  line  between  health  and  diabetes  mellitus. 

If  it  be  desired  to  preserve  the  urine  for  some  time  before  making 
the  qualitative  test  for  sugar,  it  has  been  recommended  to  add  1  per 
cent,  of  cupric  sulphate,  in  order  to  prevent  fermentation.  Trommer's 
test  may  then  be  employed. 

Dextrose  may  be  detected  in  the  urine  by  the  following  chemical 
tests : 

Moore-Hellef's    Test. 

A  few  cubic  centimeters  of  potassium  or  sodium  hydrate  are  added 
to  about  three  times  this  volume  of  urine  in  a  test  tube  and  then  boiled. 
If  considerable  sugar  is  present  the  mixture  will  turn  a  dark  brown  as 
a  result  of  the  oxidation  of  the  dextrose.  The  chemical  reaction  upon 
which  this  test  is  based  has  not  yet  been  definitely  ascertained.  The 
reaction  is  absolutely  characteristic  of  sugar  only  when  the  color 
becomes  dark  brown  or,  at  least,  yellowish  brown,  or  with  a  diluted 
urine  an  intense  clear  yellow.  The  test  is  rather  delicate,  a  characteris- 
tic reaction  being  obtained  even  with  a  considerably  diluted  diabetic 
urine.  Unless  the  result  is  absolutely  certain,  it  is  a  good  plan  to  com- 
pare the  reaction  with  that  obtained  from  a  normal  urine,  and  in  doubt- 
ful cases  even  with  that  from  a  diluted  urine.     If   the  mixture  of 

31 


482  URINARY  EXAMINATION. 

diabetic  urine  and  potassium  hydrate  is  allowed  to  cool,  and  is  then 
cautiously  acidulated  with  sulphuric  acid,  an  odor  of  burnt  sugar  should 
be  developed. 

Reduction  Tests. 

Trommer's,  or  the  Copper  Test. — One-third  the  volume  of 
potassium  or  sodium  hydrate  is  added  to  the  urine  in  a  test  tube,  and 
then  drop  by  drop  a  solution  of  cupric  sulphate  (1  :  10),  the  mixture 
being'  shaken  constantly  until  a  slight  excess  of  the  precipitated  cupric 
hydroxid  remains  undissolved.  If  sugar  is  present  we  can  add  a  good 
deal  more  of  the  cupric  sulphate  solution  without  producing  a  precipi- 
tate, and  the  mixture  will  turn  a  beautiful  blue  color.  This  depends 
upon  the  fact  that  in  the  presence  of  dextrose  the  formation  of  an  easily 
soluble  double  combination  takes  place,  which  holds  much  more  cupric 
hydroxid  in  solution.  The  blue  color  does  not,  however,  positively 
prove  the  presence  of  sugar,  because  it  also  occurs  if  the  urine  contains 
glycerin  or  tartrates,  or  if  ammoniacal  decomposition  has  set  in.  Urine 
Avhich  contains  proteid  also  holds  some  cupric  hydroxid  in  solution,  but 
here  a  violet  color  is  produced.  If  we  heat  this  dark-blue  solution  just 
to  boiling  in  the  presence  of  sugar,  cuprous  hydroxid  (Cu2(OH)2)  and 
cuprous  oxid  (Cu^O)  separate  in  greenish-yellow  clouds,  which  grad- 
ually turn  brick  red  and  finally  diffuse  throughout  the  fluid.  This  is 
due  to  the  fact  that  dextrose  has  the  power  in  alkaline  solution  to  reduce 
cupric  hydroxid  to  cuprous  hydroxid  and  cuprous  oxid.  These  separate 
out  as  a  yellow  to  brick-red  precipitate  ^  and  the  liquid  becomes  decolor- 
ized. If  a  large  amount  of  sugar  is  present,  metallic  copper  (Cu)  may 
even  separate  out  upon  the  side  of  the  test  tube  in  the  form  of  a  brown- 
ish-red coating. 

A  positive  and  typical  copper  reaction  certainly  permits  no  doubt  in 
regard  to  the  presence  of  sugar  in  the  urine,  for  no  other  substances 
occur  in  the  urine  which  can  furnish  in  every  detail  a  corresponding 
reaction.  At  most,  in  some  individual  instances,  it  is  only  necessary  to 
distinguish  whether  it  is  dextrose  or  some  other  reducing  carbohydrate 
that  is  present,  and,  from  the  much  greater  frequency  of  dextrose,  it  is 
generally  safe  to  attribute  a  positive  copper  test  to  it.  In  regard  to  the 
differentiation  between  the  individual  carbohydrates  and  the  recognition 
of  the  copper-reducing  combined  glycuronates  which  appear  more  or 
less  abundantly  after  the  ingestion  of  certain  drugs  (camphor,  morphin, 
phenol,  derivatives  such  as  paracresol,  salicyl,  salol,  thallin,  chryso- 
phanic  acid,  saccharin,  santonin)  and  sometimes,  under  both  physiologic 
and  pathologic  conditions,  abundant  skatol  and  indol  formation,  compare 
p.  477  et  seq. 

If  the  copper  reduction  is  less  typical,  a  reasonable  doubt  may  arise 
as  to  whether  the  urine  contains  dextrose  or  not,  because  normal  urine, 
in  virtue  of  the  presence  of  uric  acid,  kreatin,  kreatinin,  and  combined 
glycuronic   acid,  does  reduce  copper  to  a  certain  extent.     In  order  to 

'  Cuprous  hydi'oxid  is  yellow ;  the  oxid  is  brick  red.  The  more  alkaline  the  solu- 
tion, the  more  pronounced  the  brick-red  color,  the  oxid  taking  the  place  of  the  yellow 
cuprous  hydroxid. 


QUALITATIVE  CHEMICAL   EXAMINATION  OF  THE   UEINE.    483 

diiferentiate  a  reaction  due  to  dextrose  from  a  similar  one  occasioned  by 
one  of  the  above  constituents  of  the  urine,  the  following  distinction 
should  be  noted  :  If  the  reduction  is  due  to  dextrose,  the  blue  solution 
must  not  only  be  decidedly  decolorized,  but  there  must  also  be  formed  a 
distinct  granular  precipitate  of  cuprous  oxid  and  cuprous  hydroxid. 
On  the  contrary,  the  reduction  by  normal  urine  is  never  associated  with 
the  immediate  formation  of  a  yellow  or  brick-red  precipitate,  but  there 
is  produced  merely  a  dirty-yellowish  fluid,  because  kreatinin,  ammonium 
salts,  and  other  substances  keep  in  solution  the  small  amount  of  cuprous 
oxid  which  is  formed.  It  does  often  happen,  however,  that  after  allow- 
ing the  test  to  stand  for  some  time  in  the  cold,  normal  urine  will  bring 
down  a  yellowish-red  precipitate.  Such  a  late  separation  is  not  sug- 
gestive of  dextrose.  The  above  distinction  in  regard  to  the  rapidity  of 
reduction  is  in  reality  a  quantitative  test.  Urine  containing  dextrose 
keeps  a  much  larger  amount  of  cuprous  hydroxid  in  solution,  but  is  also 
able  to  still  further  reduce  this  soluble  excess  to  the  red  suboxid,  which 
cannot  remain  in  solution.  It  is  evident  that  the  above  is  the  real  dif- 
ference between  urine  containing  sugar  and  one  free  from  it,  since,  if  the 
urine  contains  less  than  0.2  per  cent,  of  sugar,  the  reduction  occurs  just 
as  in  normal  urine  without  precipitation,  for  the  moderate  amount  of 
cuprous  oxid  will  remain  in  solution.  Heating  urine  which  contains 
such  slight  amounts  of  sugar  simply  turns  it  yellow,  but  without  any 
turbidity.  Yet  even  in  these  cases  we  must  acknowledge  (and  this  is  of 
some  diagnostic  importance)  that  the  yellow  color  is  very  much  more 
intense,  clearer,  and  in  a  measure  more  translucent  than  with  normal 
urine,  very  likely  because  the  fluid  contains  a  considerable  amount  of 
suboxid,  despite  the  fact  that  it  remains  clear.  In  such  instances  where 
Trommer's  test  produces  a  clear-yellow  color,  a  granular  precipitate  of 
the  red  suboxid  usually  appears  a  short  time  after  cooling.  By  paying 
attention  to  these  facts,  an  expert  can  frequently  make  use  of  such 
atypical  reactions  in  recognizing  a  doubtful  case  of  diabetes  mellitus 
which  has  been  influenced  by  the  diet.  Moreover,  the  reducing  action 
of  the  normal  urinary  constituents  may  be  prevented  if  we  perform 
Trommer's  test  at  a  temperature  of  60°  to  70°  C.  This  is  a  more  cer- 
tain method  in  doubtful  cases,  because  at  this  temperature  the  normal 
constituents  do  not  reduce  to  any  noticeable  degree.  This  temperature 
is  easily  obtained  by  first  boiling  the  urine,  then  adding  one-third  its 
volume  of  cold  potassium  hydrate,  and  then  the  cupric  sulphate  solu- 
tion. 

To  make  Trommer's  test  as  delicate  as  possible,  the  first  essential  is  to  have 
as  much  cupric  oxid  as  possible  in  solution,  so  that  the  abundantly  reduced 
cuprous  oxid  may  be  precipitated.  This  end  is  accomplished,  as  already  men- 
tioned, by  continuing  to  add  cupric  sulphate  until  a  small  amount  remains  undis- 
solved. On  the  other  hand,  too  much  should  not  be  added,  because  an  excess  of 
unreduced  cupric  hydroxid,  when  heated  with  potassium  hydroxid,  will  become 
blackened  from  the  formation  of  cupric  oxid,  and  so  very  likely  hide  the  reaction. 

The  delicacy  of  the  test  may  sometimes  be  further  increased  l>y  diluting  the 
urine  containing  sugar  two  to  five  times.  This  dilution  will  diminish  the  power 
of  the  urine  to  dissolve  the  suboxid  and  will  cause  a  granular  precipitate  to  form 


484  URINARY  EXAMINATION. 

where  tlie  undiluted  urine  gave  no  reaction.  If  the  urine  is  free  from  dex- 
trose, this  dikition  will  not  produce  any  change,  because  the  slight  trace  of  cuprous 
oxid  which  is  formed  will  remain  in  solution  in  spite  of  the  dilution. 

Another  method  of  improving  the  delicacy  of  Trommer's  test  is  to  shake  the 
urine  first  with  finely  powdered  animal  charcoal,  and  finally  filter.  The  animal 
charcoal  evidently  retains  certain  substances  which  dissolve  the  suboxid  and  pre- 
vents its  precipitation. 

Seegen' s  modification  of  Trommer' s  test  can  be  recommended  for  the  detection 
of  very  small  quantities  of  sugar.  It  depends  upon  the  fact  that  animal  charcoal 
will  absorb  dextrose  while  in  solution,  and  that  the  latter  can  be  w^ashed  out  of 
the  charcoal  again.  Seegen  makes  a  thin  paste  with  purified  animal  charcoal  and 
the  urine  to  be  examined.  A  few  minutes  later  this  paste  is  poured  upon  a  filter. 
After  the  urine  has  filtered  through  he  washes  the  charcoal  remaining  upon  the 
filter  paper  with  as  much  water  as  he  employed  urine,  and  then  repeats  the  process. 
The  filtrate  of  each  washing  is  kept  separate,  and  Trommer's  test  is  performed 
with  each  of  these  filtrates.  The  substances  which  cause  the  solution  of  the 
cuprous  oxid  will  be  retained  in  the  carbon  much  longer  than  will  the  dextrose. 
Frequently  the  test  succeeds  best  with  the  second  or  third  wash  water,  as  the 
first  may  contain  too  many  of  the  substances  which  dissolve  the  suboxid.  This 
method  is  very  much  more  sensitive  for  urine  which  contains  only  a  slight 
amount  of  sugar,  than  Trommer's  test  upon  the  urine  itself.  Seegen  claims 
that  a  positive  reaction  is  absolute  proof  of  the  presence  of  sugar,  because  the 
second  or  third  wash  water  from  a  normal  urine  will  no  longer  reduce. 

The  copper  test  may  also  be  performed  Avith  the  so-called  Fehling's  solidio7i, 
such  as  is  primarily  used  for  quantitative  determinations  (see  p.  507).  This 
should  be  freshly  prepared  each  time  before  use  ;  it  consists  of  equal  parts  of 
solutions  I.  and  II.  The  test  should  be  performed  as  follows  :  About  5  c.c.  of 
urine  are  first  boiled  in  a  test  tube,  and  allowed  to  cool  for  about  twenty  seconds  ; 
then  about  1  c.c.  of  Fehling's  solution  is  added.  If  sugar  is  present  the  reac- 
tion appears  immediately.  The  reason  we  allow  the  specimen  to  cool  off"  to 
about  60°  or  70°  C.  is  because  at  that  temperature  normal  urine  will  no  longer 
reduce.  If  an  insufficient  amount  of  cojjper  is  added,  the  cu23rous  hydroxid 
which  is  formed  will  not  become  preciiaitated,  but  will  remain  dissolved  in  a  yel- 
low solution.  In  such  an  event  the  test  must  be  repeated  with  an  increased 
quantity  of  Fehling's  solution.  Fehling's  solution  possesses  no  particular  advan- 
tage for  the  qualitative  test  ;  on  the  contrary,  the  selection  of  exactly  the  amount 
of  copper  solution  to  procure  a  maximum  precipitation  of  cuprous  oxid  is  much 
more  difficult  with  this  than  it  is  with  Trommer' s  test,  where  the  least  excess  of 
copper  is  easily  recognized  by  the  appearance  of  undissolved  cupric  hydroxid. 

Proteid  in  the  urine  does  not  interfere  with  the  reduction  of  the 
copper,  but  it  does  hinder  the  precipitation  of  the  red  suboxid.  For 
this  reason  the  proteid  should  be  removed  from  the  urine  before  per- 
forming the  test  (see  p.  643).  It  is  equally  important  to  perform  all 
copper  tests  with  fresh  urine,  because  the  ammonium  carbonate  and  the 
free  ammonia  formed  in  alkaline  fermentation  will  also  prevent  the 
precipitation  of  red  cuprous  oxid. 

Provided  they  are  properly  performed  and  the  above  precautions 
are  observed,  the  copper  tests  are  still  the  most  practical  and  safest 
methods  for  the  qualitative  detection  of  sugar.  Only  a  large  amount 
of  the  other  carbohydrates  or  of  the  salts  of  glycuronic  acid  can  lead 
to  confusion.  (See  p.  490  et  seq.  in  regard  to  the  appearance  of  the  lat- 
ter, and  its  differentiation.)  It  should  be  remarked  that  after  success- 
ful treatment  of  diabetes  has  caused  the  dextrose  to  disappear  from  the 
urine,  we  often  find  large  quantities  of  combined  glycuronates  present. 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE   URINE.  485 

The  latter,  however,  can  be  easily  distinguished  from  dextrose  by  the 
very  tardy  appearance  of  the  copper  reduction.  In  doubtful  cases  the 
tests  yet  to  be  described  may  serve  as  controls,  particularly  Almeu- 
Nylander's,  the  fermentation  test,  and  Rubner's  test. 

{b)  Almen-Nylander's  Test  (Modified  Bottger's  Test). — The  original 
Bottger  test  depended  upon  the  reduction  of  bismuth  subnitrate,  N03Bi(OH2), 
by  the  dextrose  in  alkaline  solution.  But  the  test  was  not  reliable  until  modi- 
fied by  Almen-Nylander.  The  reagent  employed  is  prepared  as  follows:  Four 
gram  of  Rochelle  salt  (potassium  sodium  tartrate,  tartarus  natronatus)  are 
dissolved  in  100  c.c.  of  10  per  cent,  sodium  hydroxid  (specific  gravity  at  19° 
C.  =  1.115)  with  gentle  heat,  and  then  as  much  bismuth  subnitrate  is  added 
as  will  dissolve  (about  2  gm.).  After  cooling  we  filter  off'  wdth  glass-wool  any 
undissolved  bismuth  subnitrate  which  remains.  If  kept  in  a  dark  bottle,  the  re- 
a,gent  can  be  preserved  for  years.  To  the  urine  is  added  about  one-tenth  its  volume 
of  the  reagent,  and  the  mixture  boiled  for  a  few  minutes.  In  order  to  prevent 
the  urine  from  boiling  over  and  burning  the  fingers,  a  small  coil  of  platinum 
wire  may  be  dropped  into  the  fluid,  or  the  test  tube  may  be  held  to  one  side  of 
the  flame,  so  that  violent  ebullition  shall  not  occur.  If  dextrose  is  present  the 
fluid  darkens  and  a  black  precipitate  of  suboxid  of  bismuth  separates.  If  the 
solution  turns  dark  only  upon  cooling,  the  test  is  not  positive.  A  white  precipi- 
tate of  i^hosphate  will  be  all  that  is  formed  upon  boiling  with  urine  free  from 
sugar.  If  a  very  small  trace  of  sugar  is  present,  the  precipitate  of  the  phosphates 
may  be  seen  to  be  grayish  after  it  has  settled.  Nylander's  test  is  delicate  enough 
to  indicate  \  per  cent,  of  sugar. 

Before  attempting  Nylander's  test  we  must  first  remove  any  proteid  from  the 
urine,  because  an  albuminous  urine  will  produce  a  precipitate  of  sulphid  of 
bismuth.  With  small  quantities  of  proteid  the  latter  precipitate  may  be  easily 
differentiated  from  the  oxid  of  bismuth  by  its  reddish-brown  color.  But  if  the 
proteid  contents  of  the  urine  are  large,  a  brownish-black  precipitate  will  appear, 
which  can  very  readily  be  confounded  with  the  dextrose  reaction.  If  the  urine 
is  ammoniacal,  the  ajipearance  of  the  reaction  may  be  interfered  with. 

With  the  above-mentioned  reservations,  Nylander's  is  one  of  the  most  reliable 
of  the  sugar  tests.  It  is  always  negative  with  normal  urine,  and  so  is  particu- 
larly well  adajited  to  decide  a  case  where  Trommer's  test  is  doubtful.  Consider- 
able quantities  of  combined  glycuronic  acids  or  pentose  will  also  plainly  reduce 
Nylander's  solution,  and  in  doubtful  cases  these  two  substances  must  be  excluded 
(according  to  p.  492)  before  we  can  assume  that  the  urine  contains  sugar.  The 
reduction  of  Nylander's  reagent,  which  occurs  after  the  ingestion  of  senna,  of 
rhubarb,  of  eucalyjitol,  of  kairin,  of  quinin,  and  of  oil  of  turpentine,  probably 
■depends  upon  the  presence  of  combined  glycuronates. 

Manifold  Significance  of  the  Reduction  Tests. 

The  following  table  arranged  by  G.  Bruckner^  indicates  the  number  of 
substances  occurring  in  the  urine  which  may  effect  reduction  in  the  tests  of 
Nylander  and  Trommer,  and  the  necessity  of  employing  other  methods  of  ex- 
amination before  concluding  that  such  a  reduction  is  positive  evidence  of  the 
presence  of  dextrose : 

/.  Normal  urinary  constituents  which,  according  to  their  presence  in  larger 
or  smaller  amounts,  may  j^roduce  a  varying  degree  of  reduction  or  change  of 
<;olor  of  the  earthy  phosphates  (in  Nylander's  test). 

^Aerztliche  Rundschau,  1899,  Nos.  42-44. 


486 


URINARY  EXAMINATION. 


Almen- Ny lander^ s  Test. 

Uro-erythrin. 

Urinary  pigments  (urobilin  in  par- 
ticular) when  present  in  greatly 
increased  amounts  cause  a  brown- 
ish discoloration  of  the  phosphatic 
deposit. 

Indican. 


Trommer'  s  Test. 

Traces  of  carbohydrates  as  dex- 
trose, isomaltose,  pentoses, 
animal  gum,  glycuronic  acid 
compounds. 

Pyrocatechin. 

Bile  pigment. 

Urinary  pigment. 

Uric  acid. 

Indican. 

Kreatinin. 

Urobilin. 

Urobilinogen. 

Concentrated  urines  are  particularly  apt  to  effect  reduction,  and  the  same  is. 
true  of  urines  containing  a  moderate  or  large  quantity  of  formed  elements, 
(leukocytes,  erythrocytes,  epithelial  cells). 

//.   Products  of  abnormal  metabolism  which  effect  reduction : 


Trommer' s  Test. 
Homogentisic  acid. 
Uroleucinic  acid. 


Almen-Nylander' s  Test. 

Hexoses  (dextrose,  levulose,  iso- 
maltose, lactose  [in  puerperal 
women]),  pentoses,  glycogen,  in- 
creased quantities  of  glycuronic 
acid  compounds. 

Blood-pigment. 

Increased  quantities  of  hemato- 
porphyrin. 

Uroleucinic  acid  (weak). 

Homogentisic  acid  (weak). 

///.  Reducing  substances  added  to  the  urine  as  preservatives,  which  conse- 
quently make  the  reduction  tests  for  sugar  impossible  : 


Tromm^er'  s  Test. 
Formaldehyd. 
Chloroform. 


Alm'en-Nylander' s  Test. 


IV.  Drugs  or  the  derivatives  obtained  from  them  as  the  result  of  metabolic 
change : 


Trammer's  Test. 
Acetphenetidin. 
Antifebrin. 
Arbutin. 
Benzoic  acid. 
Benzosol. 
Copaiba  balsam. 
Chloral. 
Glycuronic  acid  compounds  of 

drugs  (see  p.  492). 
MoriDhin. 
Phenacetin. 
Saccharin. 
Salicylic  acid. 
Salol. 
Sulfonal. 
Turpentine. 
Thallin. 
Urethan. 


Almen-Nylander' s  Test. 
Antijiyrin. 
Arbutin. 
Benzoic  acid. 
Benzosol. 

Quinin  (large  doses). 
Chloral. 
Eucalyptol. 
Glycuronic    acid    compounds    of 

drugs  (see  p.  492). 
Indican. 
Kairin. 
Rheum  (also  frangula  and  cascara 

sagrada). 
Salol. 
Senna. 
Sulfonal. 
Turpentine. 
Trional. 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE   URINE.   487 

Phenylhydrazin  Test  (Fischer-v.  Jaksch). 

Two  drops  of  a  concentrated  solution  of  lead  acetate  are  added  to  about 
10  c.c.  of  urine,  and  the  preciijitate  filtered  off;  the  filtrate  is  acidified  with  a 
drop  of  acetic  acid  ;  phenylhydrazin  hydrochlorid  the  size  of  a  pea,  and  a  piece 
of  sodium  acetate  the  size  of  a  bean,  are  added.  The  mixture  is  heated  for 
about  a  half-hour  over  a  water  bath  and  then  allowed  to  cool. 

If  dextrose  is  jjresent,  a  yellow  precipitate  separates  out  upon  cooling.  This 
consists  of  characteristic  microscopic  aggregates  of  needle-like  crystals  of  phenyl- 
glucosazone  (Fig.  169).  If  the  precipitate  is  not  crystalline  or  of  a  yellow  color, 
or  if  the  crystals  are  not  of  the  form  represented  in  the  accompanying  jilate,  we 
must  not  consider  that  the  test  is  positive.  The  test  is  very  delicate  and  even 
sufficient  to  indicate  the  presence  of  0.01  percent,  of  sugar  in  the  urine.  As 
a  matter  of  fact,  it  is  almost  too  delicate  for  clinical  purposes,  as  under  certain 
conditions  the  normal  amount  of  sugar  in  a  urine  may  give  a  positive  reaction. 
Besides,  there  is  a  source  of  error  in  the  test,  since  certain  other  substances  that 
are  normally  found  in  urine  may  produce  a  similar  reaction.      By  the  determina- 


FiG.  169.— Crystals  of  phenylglucosazone  (phenylhydrazin  test  for  grape  sugar)  (after  v.  Jakseh). 

tion  of  the  melting-point  of  the  osazone  which  is  formed,  a  definite  identifica- 
tion may  be  obtained,  but  this  is  too  difficult  for  ordinary  clinical  methods.  This 
is  also  the  best  method  of  distinguishing  the  osazones  of  other  carbohydrates 
which,  though  rarely,  may  be  found  in  this  test  from  the  osazones  of  dextrose. 
Before  performing  the  phenylhydrazin  test,  it  is  advisable  to  first  remove  the  pro- 
teid  from  the  urine. 

The  phenylhydrazin  test  has  been  simplified  by  Gipollina^  under  Salkowski's 
direction.  Five  di'ops  of  pure  phenylhydrazin  (the  base),  ^  c.c.  of  glacial  acetic 
acid,  and  4  c.c.  of  urine  are  mixed  together  in  a  test  tube.  The  mixture  is  heated 
over  a  small  flame  for  about  a  minute,  being  carefully  and  constantly  shaken  so  as  to 
prevent  bumping.  Four  or  5  drops  of  sodium  hydroxid  of  a  specific  gravity  of 
about  1160  are  next  added,  but  the  fluid  must  still  remain  acid  ;  this  mixture  is 
heated  a  moment  more  and  then  cooled.  With  this  method  of  procedure,  espe- 
cially in  the  case  of  a  urine  of  low  specific  gravity,  the  characteristic  roset  crys- 
tals appear  immediately  or,  at  least,  within  twenty  minutes.  In  doubtful  cases  it 
is  necessary  to  allow  the  test  that  amount  of  time.  Thorn-apple  crystals  are  not 
at  all  characteristic,  but  yellow  balls  which  are  gradually  transformed  into  sheaths 
of  needles. 


^  Deutsch.  med.  WocL,  1901,  No.  21,  p.  334.     The  other  modifications  of  the  test 
(Neumann,  Kowarski)  are  also  mentioned  and  criticized  here. 


488  URINARY  EXAMINATION. 

Rubner's  Test.^ 

Ten  cubic  centimeters  of  a  concentrated  solution  of  neutral  lead  acetate  (1 
part  of  lead  acetate  to  10  j^arts  of  distilled  water)  are  added  to  10  c.c.  of  urine. 
The  mixture  is  filtered,  and  ammonia  carefully  added  to  the  filtrate  drop  by  drop 
until  a  cheesy  precipitate  remains.  The  mixture  is  then  heated  over  a  water 
bath  to  80°  C.  During  the  heating,  if  dextrose  is  present  the  precipitate  will 
become  a  beautifiil  rose  or  salmon  red.  The  chemistry  of  this  reaction  is  not 
positively  known.  The  test  is  reliable,  very  delicate,  and  therefore  particularly 
appropriate  when  Trommer's  test  seems  doubtful.  If  the  j^recipitate  is  heated  too 
much  the  color  becomes  brown,  like  cafe  au  lait,  and  is  no  longer  characteristic. 
]\[ilk  sugar  gives  a  yellow-red  to  brown  color.  The  writer  does  not  know  how  the 
pentoses  and  glycuronates  react  to  this  test. 

Fermentation  Test. 

Several  of  the  above  tests  for  dextrose  are  sometimes  uncertain 
unless  the  reaction  is  very  characteristic;  and  often  even  when  the  result 
is  positive. 

Trommer's  and  Nylander's  tests  merely  indicate  the  presence  of  a 
reducing  substance,  and  do  not  prove  that  this  substance  is  really  dex- 
trose. If  the  reduction  tests  result  positively  again  and  again  with  the 
same  patient,  and  if,  furthermore,  the  patient  presents  clinical  appear- 
ances of  diabetes  mellitus  (specific  gravity,  quantity  of  urine,  and  general 
appearance),  the  probability  of  dextrose  being  present  in  the  urine  be- 
comes for  all  practical  purposes  a  certainty.  But  Avhere  the  reducing 
substance  appears  temporarily,  and  when  there  are  no  further  data  for 
diagnosing  diabetes  mellitus,  we  need  a  more  definite  proof  that  the 
reducing  substance  in  question  is  some  carbohydrate.  Either  Rubner's 
test,  the  phenylhydrazin  test,  or  the  fermentation  test  will  answer  this 
purpose.  The  last  mentioned  is  one  of  the  surest  and  most  convincing 
of  all  sugar  tests,  and  should  be  resorted  to  in  all  doubtful  cases.  It 
depends  upon  the  fact  that  the  addition  of  yeast  to  any  urine  which 
contains  fermentable  sugar  produces  a  decomposition  or  fermentation — 
i.  e.,  the  carbohydrates  are  transformed  into  alcohol  and  carbon  dioxid 
gas.  Proof  of  the  fermentation  is  obtained  by  demonstrating  the  pres- 
ence of  the  carbon  dioxid.  (Concerning  the  conclusions  as  to  the  type 
of  carbohydrate,  see  p.  490  et  seq.) 

The  fermentation  test  is  performed  as  follows  :  A  test  tube  is  filled 
to  the  brim  with  the  urine,  a  piece  of  ordinary  compressed  yeast  the  size  of 
a  pea  is  dropped  in,  and  the  tube  is  then  gently  shaken  until  the  yeast  is 
finally  divided,  without  allowing  any  air  to  enter.  The  tube  is  closed 
with  a  perforated  cork  which  carries  a  V-shaped  piece  of  glass  tubing 
(Fig.  170,  6).  The  test  tube  is  then  inverted,  placed  in  a  beaker,  and 
left  in  some  moderately  warm  place  (best  25°  to  30°C.).  If  the  urine 
contains  dextrose,  carbonic  dioxid  will  be  formed  from  it  by  fermenta- 
tion inside  of  a  few  hours.  The  gas  will  accumulate  at  the  upper 
end  of  the  tube  by  expelling  the  urine  through  the  V-shaped  tube. 
Schrotter's  gas  tubes  or  fermentation  tubes  ^  are  still  more  con- 
venient (Fig.  170,  a). 

1  Zeits.f.  Biol,  vol.  xx.,  p.  397. 

^  Einhorn's  tubes  are  very  serviceable  ;  in  this  connection  see  p.  515. 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE   URINE.  489 

It  is  a  good  plan  to  prepare  two  other  similar  tubes,  the  one  filled 
with  normal  urine  and  yeast,  and  the  other  with  normal  urine,  yeast, 
and  a  knife-point  of  saccharose  or  dextrose.  These  will  serve  to  con- 
trol any  error  which  might  arise,  and  to  prove  that  the  yeast  is  active. 
The  fermentation  test  is  performed  with  all  the  necessary  precaution, 
provided  it  is  delicate  enough  to  show  yL  to  -^^  of  1  per  cent,  of  sugar 
in  the  urine. 

The  first  of  the  two  control  tests  is  absolutely  necessary.  The  author  has 
repeatedly  observed  that  compressed  yeast  often  develops  gas  in  perfectly  normal 
urine.  This  is  due  partly  to  the  so-called  "  self- fermentation "  of  the  yeast, 
which  bears  some  relation  to  the  amount  of  contained  glycogen,  and  partly  to  a 
presumed  bacterial  contamination,  which  very  quickly  produces  an  ammoniacal 
fermentation  of  the  urine  and  a  consequent  development  of  carbonic  acid  (from 
the  ammonium  carbonate  derived  from  the  urea).  In  this  fermentation,  how- 
ever, the  gas  is  not  formed  so  quickly  as  in  the  fermentation  of  sugar',  and  it 


Fig.  170.— Apparatus  for  the  quantitative  test  for  sugar  :  a,  Schrotter's  fermentation  tube ; 
b,  improvised  apparatus. 


should  consequently  be  required  not  only  that  the  formation  of  gas  be  consider- 
able, but  that  it  occur  within  a  few  hours  and  be  unaccompanied  by  the  signs 
of .  ammoniacal  fermentation.  This  ammoniacal  fermentation  may  always  be 
suppressed  by  adding  enough  tartaric  acid  to  make  the  urine  decidedly  acid  in 
reaction. 

Another  precaution  is  to  avoid  shaking  the  urine  too  much  when  mixing  it 
with  the  yeast,  for  in  that  case  the  liquid  may  absorb  a  considerable  qiuintity  of 
air,  which  afterward,  upon  standing,  accumulates  over  the  urine  and  ntay  lead 
to  error. 

Test   by   Evaporation   and   Carbonization, 

The  author  believes  that  a  very  simple  and  rather  sensitive  test  for 
sugar  is  to  evaporate  a  drop  of  urine  in  a  porcelain  dish  and  then  heat 
it  a  little  more  over  a  gentle  flame.  If  any  considerable  quantity  of 
sugar  is  present  the  residue  will  be  colored  a  pure  yellow  brow^n,  even 
when  the  urine  is  much  diluted  ;  an  odor  of  caramel  can  be  appreciated 
before  it  is  reduced  entirely  to  ash,  and  if  touched  with  a  moistened 


490  UEINAEY  EXAMINATION. 

finger  the  residue  will  feel  excessively  sticky.     Urine  free  from  sugar 
will  exhibit  only  a  dirty-grayish-brown  residue. 

OCCURRENCE  AND  DETECTION  OF  OTHER  FORMS  OF  CARBOHYDRATES 
AND  DIFFERENTIATION  OF  DEXTROSE  FROM  THEM.  (Levalose;  Maltose; 
Isomaltose;    Lactose;    Pentoses). 

Strictly  speaking,  the  fermentation  test  only  proves  the  presence  of  a  ferment- 
able sugar  in  the  urine  ;  or,  in  other  words,  it  merely  demonstrates  the  presence 
of  some  carbohydrate.  Now,  besides  dextrose,  other  types  of  fermentable  sugars 
do  occur  in  the  urine  ;  for  instance,  levulose  and  maltose.  Thus  far  these  have 
nearly  always  been  observed  in  urine  which  also  contains  dextrose,  and  they 
therefore  do'  not  materially  influence  the  value  of  the  fermentation  test  in  the 
recognition  of  diabetes  mellitus  and  of  glycosuria.  In  addition  to  maltose, 
isomaltose  (which  is  incapable  of  fermentation)  has  also  been  found  in  urine  con- 
taining dextrose  (see  below).  The  lactose  which  is  sometimes  found  in  the  urine 
of  nursing  women  and  of  individuals  fed  upon  large  and  exclusive  milk  diet,  and 
after  the  ingestion  of  large  quantities  of  lactose  (at  least  100  gm.),  does  not  fer- 
ment with  yeast,  although  it  reacts  to  Trommer'  s  test.  Other  important  points 
of  differentiation  between  the  various  carbohydrates  which  occur  in  the  urine  are 
the  varying  polarimetric  properties  of  their  solutions,  especially  as  compared  with 
their  reducing  power,  and,  further,  the  more  or  less  characteristic  osazones  which 
are  formed  in  the  phenylhydrazin  test  (p.  487  et  seq.),  and  more  especially  the 
melting-point  of  the  osazones.  More  accurate  particulars  upon  this  point  will  be 
found  in  text-books  of  chemistry.  Maltose  and  isomaltose  can  be  surely  recognized 
only  by  the  demonstration  of  their  osazones.  Maltose  and  isomaltose  are  dextro- 
rotatory and  reduce  an  alkaline  solution  of  copper.  Maltose  is  fermented  by 
yeast ;  isomaltose  is  not.  If  the  polariscopic  determination  indicates  a  smaller 
amount  of  sugar  than  that  shown  by  the  titration  method,  we  are  justified  in 
assuming  the  simultaneous  presence  of  levulose  and  dextrose.  The  levorotatory 
power  of  levulose  is  destroyed  by  yeast  fermentation;  while  the  similar  rotation 
of  oxybutyric  acid  and  comlDined  glycuronic  acid  remains  unchanged  (see  p.  493). 
For  the  demonstration  of  le^Tilose,'Seliwanow's  reaction  may  also  be  employed. 
To  apply  this  test,  the  suspected  urine  should  be  mixed  with  an  equal  volume  of 
fuming  hydrochloric  acid  and  a  small  quantity  of  a  solution  of  resorcin  (0. 5  re- 
sorcin°  30  water,  30  strong  hydrochloric  acid).  The  mixture  is  then  cautiously 
heated,  and  if  an  eosin  or  Bordeaux  color  appears  the  presence  of  levulose  may 
be  assumed. 

If  the  urine  contain  dextrose,  levulose,  and  oxybutyric  acid  (see  p.  497),  the 
recognition  of  each  becomes  still  more  difficult.  The  polarimetric  and  titration 
methods  do  not  give  the  same  results  ;  the  solution  remains  levorotatory  after  fer- 
mentation, but  the  degree  of  this  left-handed  rotation  is  not  sufficiently  large  to 
explain  the  discrepancy  in  the  results  obtained  by  the  polarimetric  and  titration 
methods  of  examination  of  the  original  urine. 

Still  another  complication  may  be  presented  by  the  not  infrequent  occurrence 
of  combined  glycuronic  acid  in  diabetic  urine  (see  p.  492),  since  this  substance  is 
also  levorotatorv. 

Detection  of  the  Pentoses.— Pentoses  are  carbohydrates,  each  molecule  of 
which  contains  5  atoms  of  carbon,  or  some  multiple  of  five.  They  have  been 
found  repeatedly  in  diabetic  urine,  but  frequently  also  in  urine  without  dextrose,  i 

Urine  which  contains  pentoses  possesses  the  power  of  reducing  copper,'^  but 
such  urine  is  either  almost  or  quite  inactive  optically.  They  do  not  ferment  with 
yeast. 

1  Salkowskiand  Jastrowitz,  Centralbl.  f.  d.  med.  WissenscL,  1892,  vol.  xix. ;  Salkowski, 
ibid.,  vol.  xxxii.,  or  Berlin.  Uin.  Woch.,  1895,  No.  17;  compare  the  collected  account  of 
Pentosuria  by  G.  Bendix,  Stuttgart,  1903. 

2  The  reduction  ordinarily  occurs  only  after  prolonged  heatmg,  and  then  quite  sud- 
denly throughout  the  entire  solution. 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE   URINE.  491 

Tollen's  reaction  is  commonly  employed  for  the  detection  of  pentoses.  Salkowski 
describes  it  as  follows  :  A  little  phloroglucin  is  heated  in  5  to  6  c.c.  of  fuming 
hydrochloric  acid,  care  being  taken  to  leave  a  slight  excess  undissolved  ;  the  solu- 
tion is  divided  into  approximately  equal  parts.  To  one  portion  |  c.c.  of  the  urine 
to  be  examined  is  added ;  to  the  other  portion  ^  c.c.  of  normal  urine.  Both 
specimens  are  then  warmed  over  a  water  bath.  If  the  urine  contams  pentose  an 
intense  red  zone  will  appear  at  the  top  in  a  few  moments  and  gradually  spread 
downward  through  the  fluid.  The  control  urine  will  not  show  any  marked  change 
of  color  The  tubes  should  be  removed  from  the  water  bath  as  soon  as  the  color 
has  developed  distinctly,  because  if  they  are  heated  too  long  the  clearness  of  the 
reaction  is  interfered  with.  The  red  coloring  matter  which  appears  m  the  reac- 
tion can  be  extracted  with  amyl  alcohol,  and  will  then  show  spectroscopically  an 
absorption  band  between  the  Frauenhofer  lines  D  and  E— i.  e.,  between  yellow 

and  green.  .       . 

Even  normal  urine  will  sometimes  furnish  a  doubtful  coloration  m  this  phloro- 
glucin reaction.  In  such  an  event  Salkowski  recommends  the  orcin  test  employed 
by  Eeichel.i  The  urine  is  heated  for  twenty  to  thirty  seconds  with  an  equal 
volume  of  concentrated  hydrochloric  acid  and  a  few  particles  of  orcin.  If  the 
urine  contains  pentoses  a  dark-green  color  appears ;  this  is  due  to  the  lormatioa 
of  furfurol  as  the  result  of  the  boiling  of  urine  containing  pentose  with  HCl. 
The  only  other  substance  which  gives  the  same  reaction  is  glycuromc  acid.  This 
occurs  however,  in  the  urine  only  in  combinations  which  cannot  be  split  up  with 
such  a  brief  boiling  with  HCl.  Practically,  therefore,  we  need  not  consider  gly- 
curonic  acid  when  performing  this  test. 

A  dark-green  precipitate  gradually  forms  in  the  dark-green  solution.  This 
precipitate  may  be  dissolved  in  amyl  alcohol,  producing  a  beautiful  dark  bluish- 
green  color.  The  spectroscopic  examination  of  this  solution  shows  a  character- 
istic absorption  band  between  C  and  D— i.  e. ,  between  red  and  yellow. 

The  urinary  pentoses  may  be  further  identified  by  the  preparation  of  their 
osazones,  which  is  accomplished  by  Salkowski  as  follows  :  In  a  beaker  ^  of  about 
400  c.c.  capacity  are  placed  5  gm.'  of  phenylhydrazin,  the  same  quantity  of  50 
per  cent,  acetic  acid,  and  200  c.c.  of  urine.  The  mixture  is  well  shaken,  gently 
heated  upon  a  piece  of  wire  gauze,  and  then  in  a  boiling  water  bath.  The  fluid 
is  then  filtered  while  hot,  and  cooled  by  placing  the  vessel  in  cold  water  ;  the 
crystals  of  pentosazone  are  then  collected  upon  a  filter,  and  purified  by  repeated 
recrystallizations  with  hot  water.  The  final  pure  product  is  a  golden-yellow 
powder,  and,  if  pentoses  were  present  in  the  urine,  should  have  a  melting-point 
of  156°    to  160°  C.  (166°-168°  C,  according  to  Spath). 

Bial'^  has  recently  recommended  the  following  procedure  for  the  practical 
demonstration  of  pentoses  in  the  physician' s  office.  He  believes  it  to  be  sufficiently 
accurate  to  differentiate  confusing"  cases  of  pentosuria  from  those  of  glycosuria. 
His  reagent  consists  of  500  c.c.  of  30  per  cent,  hydrochloric  acid,  1  gm.  of  orcin, 
and  25  drops  of  the  official  liquor  ferri  sesquichlorati  (German  Pharmacopeia). 
Four  to  5.  c.c.  of  this  reagent  are  boiled  in  a.  test  tube,  and,  after  removal  from 
the  flame,  several  drops  or,  at  most,  1  c.c.  of  urine  are  added.  A  green  color 
should  appear  at  once  or  almost  immediately.  If  the  test  is  carried  out  in  this 
manner,  Bial  states  that  the  small  amount  of  heat  employed  is  not  sufficient  to 
cause  any  reaction  between  the  reagent  and  the  most  unstable  glycuronates.  More- 
over, Bial  recommends  the  procedure,  not  for  the  differentiation  of  pentoses  and 
combined  glycuronates,  but  for  the  differentiation  of  pentosuria  from  glycosuria.  It 
should,  however,  be  remembered  that  both  pentose  and  dextrose  may  occur  together 
in  diabetic  urine. 

To  demonstrate  pentose  in  diabetic  urine,  the  dextrose  must  be  first  removed 
by  fermentation  with  yeast. 

Pentosuria  is  observed  temporarily,  as  so-called  alimentary  pentosuria,  after 
the  ingestion  of  large  quantities  of  vegetables  which  are  rich  in  pentoses,  such  as 

1  Cf.  Blumenthal,  Zells.  f.  kiin.  Med.,  vol.  xxxvii. ;  Bial,  ihid.,  vol.  xxxix. 

2  Deutsch.  med.  Wock,  1903,  No.  27. 


492  URINARY  EXAMINATION. 

cherries,  plums,  huckleberries,  and  other  fruits.  In  other  cases,  on  the  contrary, 
the  elimination  of  pentose  is  chronic  and  indeioendent  of  the  quantity  and  nature 
of  the  pentoses  in  the  ingested  food.  In  these  cases  there  is  a  specific  pentose 
which  is  recognized  by  Neuberg  as'  optically  inactive  arabinose.  The  amount 
of  pentose  in  the  urine  may  vary  between  0.1  and  1  per  cent.,  so  that  the 
daily  quantity  excreted  can  never  exceed  20  gm.  A  theorj^  for  this  actual  pen- 
tosuria is  still  quite  impossible.  But  jDentosuria  certainly  bears  no  relation  to  dia- 
betes mellitus.  Bial  ^  has  also  described  pentosuria  as  a  common  anomaly. 
Pentosuria  does  not  usually  give  rise  to  characteristic  clinical  phenomena  ;  and 
the  demonstration  of  pentose  in  the  urine  is  clinically  important  only  because  the 
patient  is  thus  guarded  from  an  erroneous  diagnosis  of  diabetes  mellitus.  This  is 
all  the  more  important  since  it  has  repeatedly  been  observed  that  jjatients  with 
pentosuria  are  injured  by  the  diabetic  diet  containing  no  carbohydrates,  and  that 
such  a  diet  does  not  influence  the  amount  of  excreted  pentose  in  the  slightest 
degree. 

DETECTION    OF    GLYCURONIC    ACID. 

Glycuronic  acid  is  formed  in  the  body,  probably  even  under  physiologic  con- 
ditions, by  the  oxidation  of  dextrose,  fi-om  which  it  differs  but  little  in  its  elemen- 
tary composition.  It  appears  in  the  urine  when  an  opportunity  is  furnished  for 
it  to  become  combined  in  the  organism  with  other  bodies,  and  so  to  escajDe  com- 
plete oxidation.  There  ai'e  a  great  many  substances  which  may  combine  with  gly- 
curonic acid.  Among  them  are  chloral  hydrate,  morphin,  camphor,  oil  of  turpen- 
tine, salicylic  acid,  saccharin,  santonin,  thallin,  chrysophanic  acid,  menthol,  most 
of  the  phenols  and  phenol  derivatives — i.  e. ,  indol,  skatol,  naphthol,  etc.  Fliickiger  2 
has  proved  that,  aside  from  the  uric  acid  and  kreatinin  contained,  the  reducing 
power  of  normal  urine  depends  upon  the  presence  of  the  paired  combinations  of 
glycuronic  acid,  especially  the  phenol,  parakresol,  indol,  and  skatol  glycuronates. 
P.  Mayer  "*  has  more  recently  confirmed  these  observations,  and  in  addition  has 
shown  that  the  excretion  of  the  combined  glycuronates  has  a  bearing  upon  diabetic 
mellitus  and  upon  alimentary  glycosuria.  He  claims  that  after  excessive  ingestion 
of  carbohydrates,  and  especially  of  dextrose,  large  quantities  of  the  glycuronic 
acid  salts  are  sometimes  excreted  in  human  urine  before  sugar  appears.  In  these 
cases  it  seems  as  if  the  organism  were  able  to  oxidize  the  ingested  sugar  up  to  the 
stage  of  glycuronic  acid,  but  no  further.  This  hypothesis  of  the  origin  of  gly- 
curonic acid  mil  explain  the  frequently  coincident  occurrence  of  combined  glycu- 
ronates and  dextrose  in  the  urine  which  has  been  observed  both  in  alimentary 
glycosuria  and  in  diabetes  mellitus.  Here  a  part  of  the  dextrose  which  is  not 
utilized  has  been  oxidized  only  to  glycuronic  acid.  Glycuronic  acid  is  capable  of 
reducing  but  not  of  fermenting.  This  explains  the  peculiarity  which  has  been 
observed  in  the  urine  of  a  diabetic  patient  upon  a  successful  diet — i.  e.,  it  still 
reduces  but  does  not  ferment.  Even  the  reduction  is  peculiar  in  that,  unlike  the 
dextrose  reduction,  it  occurs  verj^  slowly  (see  below).  Many  discrepancies  between 
the  quantitative  estimations  of  the  amount  of  sugar  by  the  polarization,  by  the 
fermentation,  and  by  the  copper  tests  can  thus  be  explained  by  the  simultaneous 
presence  of  dextrose  and  some  combined  glycuronates.  The  latter,  unlike  the 
sugar,  rotate  to  the  left,  but  like  it,  reduce.  Glycuronic  acid  has  never  been 
found  in  the  urine  except  in  combination.  P.  Mayer  claims  that  these  combina- 
tions can  be  split  up  by  boiling  for  one  to  five  minutes  with  1  per  cent.  HjSO^, 
and  that  the  peculiarities  of  the  combined  and  of  the  artificially  separated  glycu- 
ronic acid  can  be  examined  in  the  urine.  The  duration  of  the  boiling  must  be 
determined  in  the  case  of  each  combined  glycuronate  by  demonstrating  that  the 
urine  has  changed  its  character  in  the  maximum  manner  expected.  No  definite 
time  can  be  given  for  all  cases. 

The  following  are  the  reactions  usually  employed  to  detect  the  combined  gly- 
curonates in  the  urine  : 

'  Berlin,  klin.  Woch.,  1904,  No.  21.  ^  Zeits.f.  Physiol.  Chemie.,  No.  9, 1885. 

3  Berlin,  klin.  Woch.,  1899,  p.  617  el  seq.,  and  Deuisch.  med.  Woch.,  1901,  Nos.  16 
and  17. 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE   URINE.   493 

1.  The  urine  reduces  an  alkaline  solution  of  copper.  Since  the  combined  glycu- 
ronates  reduce  but  slowly,  this  reduction  occurs  only  after  prolonged  heating.  It 
will,  on  the  contrary,  take  place  ■  immediately  if  we  boil  the  urine  beforehand,  by 
the  method  mentioned  above,  Avith  1  per  cent.  H^SO^,  in  order  to  cause  the  clear- 
age  of  the  glycuronate  combinations. 

2.  The  free  acid  but  not  the  combined  glycuronates  will  enter  into  combina- 
tion with  phenylhydrazin.  Hence  the  phenylhydrazin  test,  employed  for  demon- 
strating the  presence  of  sugar  (p.  487  et  seq. ),  will  give  a  negative  result  if  we 
employ  the  ordinary  urine  containing  the  combined  glycuronates ;  but,  on  the 
contrary,  it  will  famish  a  positive  result  if  we  precede  the  test  by  first  boiling  the 
urine  with  1  per  cent.  H^SO^. 

3.  Glycuronic  acid  does  not  ferment,  but  it  does  reduce  alkaline  copper  solu- 
tions ;  therefore  a  urine  containing  glycuronates,  in  spite  of  its  reducing  power, 
does  not  ferment.  If  sugar  is  also  present,  fermentation  will  produce  an  incom- 
plete loss  of  the  power  of  reduction. 

4.  The  free  glycuronic  acid  is  dextrorotatory,  while  the  combined  glycuronates 
rotate  to  the  left.  With  urine  containing  salts  of  glycuronic  this  levogyrate  power 
will  be  changed  to  dextrorotation  after  boiling  with  HjSO^  (see  above).  Again, 
if  there  is  also  dextrose  in  the  urine,  the  dextrorotatory  power  will  be  increased 
after  boiling. 

5.  Tollen's  reaction  (see  p.  491  et  seq.)  is  positive  with  urine  containing 
glycuronic  acid  as  with  urine  containing  pentoses,  but  not  if  dextrose  is  present 
alone.       See  Pentoses. ) 

6.  Urine  containing  glycuronates  reacts  to  the  orcin  test  only  after  clearage 
of  the  combination  has  occurred  by  boiling  with  1  per  cent.  HgSO^.  This  is  in 
contrast  to  urine  containing  pentoses  (p.  490). 

DETECTION  OF  ACETONE  (CH3-CO-CH3). 

Traces  of  acetone  occur  in  every  normal  urine.  The  amount  will 
be  increased  in  fever,  with  starvation,  with  a  purely  meat  diet,  in  dia- 
betes mellitus,  in  certain  forms  of  digestive  disturbances,  and  in  some 
cases  of  carcinoma.  According  to  Hirschfeld,  a  considerable  amount 
of  acetone  may  be  found  in  non-diabetic  urine  if  proteid  substances  are 
decomposed  in  the  body  without  the  simultaneous  oxidation  of  carbo- 
hydrates. In  diabetes,  however,  other  causes  are  also  brought  to  bear. 
Urine  which  contains  a  good  deal  of  acetone  always  has  a  peculiar  fruity 
odor,  an  odor  which  may  be  detected  even  in  the  breath  of  such  a  patient. 
No  especial  symptomatology  can  be  determined  for  decided  aceton- 
uria  or  acetonemia.  Decided  acetonuria  in  diabetes,  despite  a  mixed 
diet,  suggests  a  grave  prognosis,  although  there  are  numerous  excep- 
tions to  this  rule.  In  other  conditions  the  presence  of  acetone  in  the 
urine  is  as  yet  of  no  diagnostic  value.  In  diabetes,  acetonuria  will  be 
favored  by  a  purely  meat  diet,  and  can  frequently  be  diminished  or  sup- 
pressed by  administering  carbohydrates. 

The  test  for  acetone  can  first  be  tried  with  the  urine  itself.  If  the 
result  is  negative,  the  urine  should  be  distilled.  Acetone  is  very  vola- 
tile, so  that  the  distillate  will  be  much  richer  in  acetone  than  the  urine, 
and  smaller  quantities  can  thus  be  detected. 

Distillation  can  be  performed  without  any  complicated  apparatus  in 
the  following  way  :  About  50  c.c.  of  urine  acidified  with  a  little  phos- 
phoric acid  (sufficient  for  a  marked  Congo  reaction,  to  prevent  foaming) 
are  poured  into  a  fractionation  flask  (Fig.  171)  and   heated  to  gentle 


494 


URINARY  EXAMINATION. 


boiling,  preferably  over  a  water  bath  or  over  a  wire  gauze.  A  test  tube  is 
then  slipped  over  the  projecting  arm  for  a  receiver  and  fastened  with  a 
piece  of  string  or  wire.  The  upper,  open,  end  of  the  flask  is  closed 
with  a  cork.  The  distillate  will  now  collect  in  the  test  tube  without 
any  special  cooling  apparatus.  Within  a  few  minutes  several  cubic  cen- 
timeters will  have  distilled  over,  and  the  acetone  test  can  then  be  per- 
formed upon  the  distillate. 

Hoppe-Seyler  claims  that  if  diacetic  acid  is  also  present  the  distillation  will 
produce  acetone  artificially,  so  that  in  such  an  event  another  method  must  be 
selected.     Instead  of  being  distilled,  the  urine  is  rendered  slightly  alkaline  and 

then  extracted  with  pure  ether,  the 
ether  shaken  with  water,  and  the  test 
performed  upon  the  aqueous  solution. 
To  demonstrate  the  presence  of 
acetone,  one  of  the  following  tests  is 
usually  employed  : 

Gunning's  Iodoform  Test. 

— A  little  tincture  of  iodin  or  Lu- 
gol's  solution  '  is  added  to  the  dis- 
tillate, and  then  enough  ammonia 
to  produce  an  intense  black  pre- 
cipitate of  nitrogen  iodid.  This 
precipitate  will  gradually  disappear 
upon  standing,  and  when  acetone  is 
present  a  yellowish  sediment  con- 
sisting of  iodoform  will  take  its 
place.  It  can  be  recognized  by 
its  odor,  or  microscopically,  as  it 
consists  of  hexagonal  plates  or 
small  stars  (compare  Fig.  172); 
occasionally  the  precipitate  is  amor- 
phous. We  must  be  careful  not 
to  confound  with  the  iodoform 
crystals  the  stellate  crystalline  ag- 
gregations of  triple  phosphate  which 
are  often  produced  along  with  them,  especially  where  the  urine  itself, 
instead  of  the  distillate,  is  employed.  (This  is  also  possible  with 
Lieben's  test,  see  below.)  (See  Fig.  190.)  If  the  urine  contains 
but  a  small  amount  of  acetone,  it  may  be  necessary  to  M-ait  twenty- 
four  hours  before  the  iodoform  crystals  can  be  demonstrated.  If  the 
crystals  are  not  distinctly  formed  they  may  be  recrystallized  for  more 
certain  recognition,  first  dissolving  them  in  ether  and  then  allowing  this 
to  evaporate  slowly.  Gunning's  test  has  a  great  advantage  over  Lieben's 
(see  below),  because  with  it  no  other  known  substance,  and  especially 
neither  alcohol  nor  aldehyd,  will  produce  iodoform.  On  the  other  hand, 
it  is  somewhat  less  delicate  than  Lieben's.  But  even  so,  it  is  extremely 
delicate,  and  often  readily  permits  the  detection  of  acetone  in  diabetic 

^Composition  of  Lugol's  solution:  1.2  gm.  iodin,  1.8  gm.  potassium  iodid,  30  parts 
of  water. 


Fig.  171.— Fractionation  flask. 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE   URINE.   495 

urine  without  distillation.  The  author  recommends  Gunning's  test  lirst 
of  all  for  clinical  use,  and  particularly  when  it  is  desirable  to  demonstrate 
acetone  in  the  urine  directly  without  distillation. 

I/ieben's  Iodoform  Test. — Some  potassium  hydrate  and  Lugol's 
solution  are  added  to  the  urine,  or  better  to  its  distillate.  If  acetone  is 
present  a  yellowish  precipitate  will  be  formed,  and  will  be  recognized, 
as  in  Gunning's  test  (see  above),  by  its  odor  and  by  the  shape  of  the 
crystals.  If  only  a  very  small  amount  of  acetone  is  present,  the  iodo- 
form precipitation  may  be  delayed  some  hours,  even  up  to  twenty-four. 
This  test  is  extremely  delicate,  but  it  is  less  distinctive  than  Gunning's, 
because  with  it  other  substances  besides  acetone  may  give  rise  to  iodo- 
form (alcohol,  for  example) ;  Gunning's  test  is  therefore  preferable. 

I^egal'S  Test. — Three  drops  of  a  freshly  prepared  concentrated 
solution  of  sodium  nitroprussid  (1  :  10)  are  added  to  the  urine  itself, 
or  better  to  its  distillate,  and  the  mixture  made  strongly  alkaline  with  a 
few  drops  of  sodium  or  potassium  hydroxid.     The  red  color  which 


Fig.  172.— Iodoform  crystals  from  the  precipitate  in  Gunning's  test  (after  a  microphotograph). 

arises  gradually  changes  to  yellow.  This  color  reaction  depends  upon 
the  presence  of  kreatinin,  and  will  be  seen  in  every  urine.  But  if  any 
considerable  amount  of  acetone  is  contained  in  the  urine  the  addition  of 
acetic  acid  will  discharge  the  yellow  color,  and  the  solution  will  become 
purple  red  or  violet.  This  test  may  lead  to  the  erroneous  supposition 
of  the  presence  of  acetone  if  the  urine  contains  parakresol  (v.  Jaksch). 
It  is  the  one  which  is  usually  recommended  for  the  direct  examination 
of  urine  without  distillation  ;  but,  according  to  the  author's  experience, 
it  is  not  in  that  case  very  delicate,  and  he  does  not  recommend  it.  If 
the  distillate  is  used,  however,  the  test  is  a  useful  one,  and  has  recently 
been  recommended  by  Studer. 

DETECTION  OF   DIACETIC  ACID  (CH3.COCH2.COOH). 

Diacetic  acid  does  not  occur  in  the  urine  of  healthy  individuals  upon 
an  ordinary  diet  except,  perhaps,  in  very  small  quantities.  It  has  been 
observed  pathologically,  usually  in  combination  with  ammonia,  in  severe 


496  URINARY  EXAMINATION. 

forms  of  diabetes,  in  fever,  in  dyspeptic  conditions  and  their  concomitant 
auto-intoxications,  in  gastric  carcinoma,  and  in  alcoholism.  Since  acetone 
is  derived  from  diacetic  acid,  the  conditions  requisite  for  diaceturia  are 
identical  with  those  for  acetonuria,  and,  as  a  matter  of  fact,  the  two 
substances  are  almost  always  associated  in  the  urine.  If  little  diacetic 
acid  is  formed,  it  is  all  transformed  into  acetone  ;  if  much  is  formed,  then 
both  substances  will  be  found  in  the  urine.  It  frequently  happens  that 
the  mother  substance  of  diacetic  acid,  /3-oxy butyric  acid,  is  also  present. 
Diaceturia,  like  acetonuria,  also  bears  some  relation  to  the  metabolism 
of  the  carbohydrates,  since  in  the  diaceturia  of  non-diabetic  individuals 
the  proteids  are  decomposed  without  the  simultaneous  oxidation  of  the 
carbohydrates,  and  it  may  frequently  be  suppressed  by  the  administra- 
tion of  carbohydrates.  Diacetic  acid  is  excreted  in  the  urine  of  indi- 
viduals upon  a  pure  meat  diet  and  in  cases  of  starvation.  The  excre- 
tion of  a  large  amount  of  diacetic  acid  by  a  diabetic  upon  a  mixed  diet, 
like  the  excretion  of  acetone  under  the  same  circumstances,  is  an  indica- 
tion of  a  severe  form  of  the  disease.  Such  diaceturia  is  favored  by  a 
rigid  meat  diet,  and  may  frequently  be  diminished  by  the  ingestion  of 
carbohydrates.  It  would  be  just  as  erroneous  to  assume  that  diaceturia 
has  a  definite  symptomatology  as  it  would  be  to  state  that  acetonuria  is 
a  distinct  clinical  entity.  It  should  also  be  noted  that  the  appearance 
of  diacetic  acid  in  the  urine  is  usually  accompanied  by  an  increased 
elimination  of  ammonia,  as  is  also  the  excretion  of  /?-oxybutyric  acid. 
The  presence  of  diacetic  acid  can  be  demonstrated  as  follows  : 
Gerhardt's  Diabetic  Ferric  Chlorid  Reaction. — One  or  two 
drops  of  a  ferric  chlorid  solution  are  added  to  the  urine.  If  diacetic 
acid  is  present  a  Bordeaux-red  color  appears,  which  is  most  distinct 
after  filtering  oif  the  precipitate  of  ferric  phosphate.  If  an  insufficient 
quantity  of  the  ferric  chlorid  solution  has  been  added,  an  extra  amount 
must  be  employed  after  the  phosphate  precipitate  has  been  removed  by 
filtration.  Sulphocyanids,  sodium  acetate,  salicylic  acid,  antipyrin, 
thallin,  kairin,  and  other  aromatic  substances  may  produce  a  similar  red 
color.  For  this  reason  the  presence  of  diacetic  acid  should  be  assumed 
only  after  positive  results  have  been  obtained  by  the  two  following  con- 
trol tests  : 

1 .  If  boiled  urine  is  employed  for  the  test,  the  red  color  should  be 
very  much  fainter,  because  boiling  gradually  transforms  diacetic  acid 
into  acetone.  2.  The  urine  is  acidified  with  sulphuric  acid  and  then 
shaken  with  ether.  Diacetic  acid,  if  present,  will  be  taken  up  by  the 
ether,  and,  if  the  latter  is  shaken  with  a  diluted  solution  of  ferric 
chlorid,  the  aqueous  layer  will  turn  red.  The  coloring  will  disappear 
spontaneously  in  twenty-four  to  forty-eight  hours.  The  sulphuric  acid 
merely  serves  to  free  the  diacetic  acid  from  its  salts,  so  that  it  may  be 
taken  up  by  the  ether.  Sulphocyanid  salts  react  similarly  in  this  con- 
trol test,  because  sulphocyanic  acid  also  dissolves  in  the  ether.  In 
that  case,  however,  the  red  color  does  not  disappear  spontaneously.  The 
color  produced  by  sodium  acetate,  salicylic  acid,  antipyrin,  thallin,  and 
kairin  also  remains  permanent  for  days. 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE   URINE.  497 

DETECTION   OF  ^-OXYBUTYRIC  ACID. 

Thus  far  /J-oxybutyric  acid  has  been  found  in  diabetes  mellitus,  scarlet  fever, 
measles,  scurvy,  and  in  the  insane  who  refuse  food  and  drink.  It  is  probably  a 
preliminary  stage  in  the  formation  of  diacetic  acid. 

In  diabetes  mellitus  a  considerable  amount  of  /3-oxybutyric  acid  in  the  urine 
suggests  the  onset  of  acid  intoxication  or  "acidosis"  (coma  diabeticum). 

/3-oxybutyric  acid  appears  to  be  present  in  the  urine  only  when  diacetic  acid  is 
there  also  (see  above). 

Unfortunately,  the  process  for  demonstrating  /3-oxybutyric  acid  is  very  com- 
plicated. The  acid  must  first  be  isolated,  and  then  a  well-characterized  salt  of 
oxybutyric  acid  is  formed.'  This  acid  is  levogyrate,  while  dextrose  is  dextrogyrate. 
In  some  cases  of  diabetes  mellitus  we  may  therefore  suspect  the  presence  of  /3-oxy- 
butyric acid  if  the  amount  of  dextrose,  as  determined  by  titration,  is  distinctly 
larger  than  that  obtained  by  the  polariscope.  Proteid  must,  of  course,  be  absent, 
as  that,  as  well  as  /3-oxybutyric  acid,  is  levogyrate.    Levulose  may  lead  to  confusion. 

E.  KiUz  first  removes  "the  proteid  fi-om  the  diabetic  urine,  removes  the  sugar 
by  fermentation  (which  will  also  dispose  of  the  levulose),  then  decolorizes  by 
precipitating  with  lead  acetate  and  ammonia,  and  finally  examines  with  the 
polariscope.  If  after  this  process  the  urine  still  exhibits  a  tendency  to  left-handed 
rotation,  /3-oxybutvric  acid  is  in  all  probability  present.  To  be  certain  we  must 
exclude  the  presence  of  combined  glycuronates.  The  latter  condition  must  also 
be  ftilfilled,  if  we  are  to  assume  the'  presence  of  /3-oxybutyric  acid  from  the  left- 
handed  rotation  of  the  ethereal  extract  obtained  from  the  fermented  urine  which 
has  been  strongly  acidulated  with  phosphoric  acid. 

An  almost  positive  proof  for  the  presence  of  /3-oxybutyric  acid  in  cases  of  dia- 
l)etes  mellitus  is  the  detection  of  acidosis,  or  of  a  considerable  increase  in  the 
quantity  of  ammonia  excreted  in  the  urine  (see  p.  538). 

DETECTION    OF  ALKAPTON   (HYDROCHINON  ACETATE  OR  HOMOGENTISIC 

ACID). 

The  substance  which  has  been  named  alkapton  lends  to  the  urine  the  peculiar 
property  of  becoming  extremely  dark  after  standing  for  some  time.  The  urine 
turns  a  dark  to  brownish-black  color  from  oxidation,  especially  if  it  is  alkaline  in 
reaction.  Urine  stains  upon  the  clothes  are  dark-red  to  brownish.  Urine  con- 
taining alkapton  .reacts  positively  to  Trommer's  test,  but  it  can  be  distinguished 
from  urine  containing  sugar  by  its  negative  reaction  to  Nylander's  test  and  by  its 
inability  to  ferment,  and  by  the  greenish  tinge  produced  by  the  addition  of  a 
•dilute  solution  of  ferric  chlorid.  This  color  will  disappear  promptly,  but  can  be 
brought  out  again  by  the  fresh  addition  of  the  reagent. 

The  chemical  nature  of  alkapton  was  for  a  long  time  unknown.  Baumann 
and  Wolkow'  s  ^  investigations  have,  however,  definitely  placed  the  substance  as  a 
derivative  of  hydroquinon,  and  regard  it  as  the  acetate  of  hydrochinon  or  homo- 
^entisic  acid.  Only  in  one  case  were  they  able  to  demonstrate  with  it  a  related 
acid — lactate  of  hydrochinon  or  uroleucinic  acid.  Alkaptonuria  is  for  the  most 
part  unassociated  with  any  discomfort,  and  has  generally  been  demonstrated  as  a 
rare  circumstance  occurring  in  an  apparently  healthy  individual.  In  Stange's 
case  it  was  associated  with  dysuria.  Its  etiology  is  still  quite  unknown.  The 
amount  of  homogentisic  acid  excreted  seems  to  depend  upon  the  amount  of 
proteid  ingested.  E.  Meyer,  (vol.  Ixx.,  Deutsch.  Arch.  f.  Min.  Med.)  mentions 
the  latest  work  upon  the  subject  of  this  puzzling  anomaly,  and  quotes  the  older 
literature  as  well. 

DETECTION    OF   LEUCIN   AND    TYROSIN. 

Any  appreciable  quantity  of  leucin  and  tyrosin  in  the  urine  is  always 
pathologic.     They  are  nearly  always  in  solution.     Their  presence  is 

^  For  a  detailed  desci-iption  see  Minkowski,  Arch.  f.  exp.  Path.,  vols,  xviii.  and  xxi., 
1884,  and  Kiilz,  ibid.,  or  Kiilz,  Zeits.f.  Biol.,  vols.  xx.  and  xxiii. 
^  Zeits.f.  physiol.  Chemie,  vol.  xv. 

32 


498 


URINARY  EXAMINATION. 


very  characteristic  of  acute  yellow  atrophy  of  the  liver  and  phosphorus- 
poisoning,  and  is  found  more  rarely  in  typhus,  variola,  pernicious 
anemia,  and  leukemia. 

In  order  to  detect  them,  the  urine  is  first  evaporated  to  about  one- 
tenth  its  volume  and  a  little  alcohol  then  added.  The  characteristic 
crystals  of  the  two  substances  can  then  be  recognized  microscopically. 
Tyrosin  crystallizes  in  the  shape  of  needles  ;  leucin,  in  nodules  (Fig.  173). 
The  latter  can  be  differentiated  from  the  crystals  of  ammonium  urate 
(see  Fig.  189)  by  their  much  sharper  line  of  contour,  their  less  refractive 
power,  and  their  absence  of  prickles.  Leucin  and  tyrosin  are  precipitated, 
as  a  rule,  in  icteric  urine  (acute  yellow  atrophy  of  the  liver  and  phos- 


FiG.  173.— Crystals  of  leucin  (a)  and  tyrosin  (b)  (after  Ultzmann  and  Hofmann). 


phorus-poisoning).  Hence  we  must  not  confound  the  tyrosin  needles 
with  bilirubin  needles,  which  are  sometimes  precipitated  (Fig.  216) 
by  the  concentration  of  the  urine.  The  latter  can  usually  be  recog- 
nized by  their  intense  brownish-red  color. 

Unless  the  crystals  of  leucin  and  tyrosin  are  very  characteristic,  it  is  always 
much  safer  to  perform  the  following  test  (taken  in  part  verbally  from  Huppert) : 
The  urine  is  precipitated  with  basic  lead  acetate  (liq.  plumbi  subacetatis).  The 
filtrate  is  freed  from  the  excess  of  lead  with  hydrogen  sulphid,  then  evaporated 
as  much  as  possible,  the  residue  extracted  with  a  small  amount  of  absolute  alcohol 
(to  remove  the  urea),  then  the  undissolved  residue  extracted  with  slightly  ammo- 
niacal  alcohol.  The  extract  is  evaporated  to  a  small  volume  and  left  to  itself  until 
leucin  and  t^-rosin  crystallize  out.  Leucin  and  tyrosin  may  now  be  separated  by 
crystallization  from  water.  That  substance  crystallizes  first  which  saturates  the 
solution  first  according  to  the  amount  and  degree  of  solubility.  By  recrystallizing 
from  the  ammoniacal  alcohol,  both  substances  may  be  obtained  fairly  pure.  The 
two  substances  may  be  separated  by  recrystallization  in  a  little  alcohol,  in  which 
leucin  is  more  soluble  than  tyrosin. 

The  pure  tyrosin  which  is  thus  formed  must  react  to  Pirki' s  test.  This  is 
performed  by  boiling  the  dry  tyrosin  in  a  dry  test  tube  with  a  few  drops  of  sul- 
phuric acid  in  a  water  bath  for  one-half  hour.  The  resulting  reddish  solution  of 
tyrosin  sulphuric  acid  is  allowed  to  cool,  and  then  poured  into  several  times  as 
much  water,  the  test  tube  rinsed  with  water,  and  the  solution  neutralized  with 
barium  carbonate.  The  mixture  is  then  filtered  and  boiled  down  to  a  few  cubic 
centimeters;  when  cool,  some  dilute  neutral  ferric  chlorid  is  carefully  added.  A 
beautiful  violet  color  results,  quite  like  that  of  iron  salicylate  (p.  502).  Besides 
this  (according  to  Hofl5nann)  a  hot  aqueous  solution  of  tyrosin,  to  which  has  been 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE   URINE.  499 

added  potassium  nitrate  and  mercuric  nitrate,  should  produce  a  beautiful  dark 
color  and  an  abundant  red  precipitate  so  long  as  it  is  kept  hot. 

Leucin,  on  the  other  hand,  when  gently  heated,  is  characterized  by  subliming 
without  melting,  and  at  the  same  time  emitting  an  odor  of  amylamin.  It  can 
also  be  identified  by  Sherer's  test.  This  is  performed  by  evaporating  leucin  with 
nitric  acid  on  a  piece  of  platinum  foil  ;  sodium  hydrate  is  added  to  the  cold  residue 
and  then  warmed.  When  the  resulting  solution  is  concentrated,  it  contracts  to  an 
oily  drop,  which  rolls  around  and  does  not  adhere  to  the  platinum.  Salkowski 
also  tries  the  following  reaction  :  A  sample  of  the  substance,  not  too  small,  is 
dissolved  in  water,  then  decolorized,  if  necessary,  with  bone  charcoal ;  the  filtrate 
is  made  alkaline  with  NaOH,  and  1  to  2  drops  of  copper  sulphate  solution  (1  :  10) 
added.  The  cupric  hydroxid,  which  is  first  precipitated,  dissolves,  and  a  blue 
solution  results  from  the  formation  of  leucin-copper,  which  is  not  reduced  on 
heating.  Leucin  crj^stals  dissolve  in  solutions  of  caustic  potash  and  are  insoluble 
in  ether.  This  serves  to  differentiate  them  from  fat,  with  which  they  might  be 
confused. 

DIAZO-REACTION. 

Ehrlich  ^  tried  to  discover  unknown  constituents  of  the  urine  by 
employing  the  diazo-compounds,  which  produce  colored  combinations 
with  a  large  number  of  aromatic  substances.  The  nature  of  the  body 
which  is  found  in  certain  pathologic  urines,  and  which  gives  the  so-called 
diazo-reaction,  is  still  unknown.  Spath  claims  that  the  reaction  should 
be  ascribed  to  oxyproteic  (uroproteic)  acid,  a  recently  discovered  ^  normal 
urinary  constituent,  in  case  the  urine  contain  an  increased  quantity  of 
this  substance.     The  author  cannot  confirm  this  statement. 

The  test  is  performed  as  follows  :  Two  stock  solutions  are  employed. 
(1)  A  0.5  per  cent,  solution  of  sodium  nitrate.  (2)  A  solution  of  5  gm.  of 
sulphanilic  acid  in  50  c.c.  of  hydrochloric  acid  and  1000  c.c.  of  distilled 
water.  Fifty  cubic  centimeters  of  the  latter,  freshly  mixed  for  each  test 
with  1  c.c.  of  the  former  solution,  make  up  the  reagent.  It  maybe  prepared 
approximately  in  a  test  tube,  in  the  absence  of  a  measuring  glass,  by 
adding  to  about  3  c.c.  of  solution  No.  2  a  drop  of  the  nitrate  solution 
(No.  1).  Equal  parts  of  urine  and  of  the  reagent  are  mixed  and  then 
quickly  supersaturated  with  ammonia.  The  characteristic  reaction  now 
consists  in  the  mixture  turning  more  or  less  intensely  red,  the  foam  which 
forms  upon  shaking  being  tinged  from  a  rose  to  deep  red  ;  the  reaction 
is  then  positive.  The  brownish-yellow  color  which  appears  when  the 
test  is  performed  with  any  normal  urine  must  not  be  mistaken  for  the 
characteristic  rose-red  coloration.  AVhen  the  test  is  positive  and  the 
mixture  is  allowed  to  stand,  after  some  time  a  precipitate  forms,  whose 
upper  margin  exhibits  a  dark  zone  of  a  green  or  greenish-black  or  even 
violet  shade.  Any  deviation  from  the  above  procedure  will  produce 
other  results,  and  should  therefore  be  avoided — e.  g.,  the  supersaturation 
with  ammonia  must  be  done  at  once,  and  not  drop  by  drop. 

Although  it  mav  be  incorrect  to  assume  that  the  diazo-reaction  is 
dependent  upon  an  increased  excretion  of  uroproteic  acid,  the  reaction 
may  nevertheless  be  regarded  as  an  indication  of  a  pathologic  decom- 
position of  the  proteids. 

1  ZeJts.f.  klin.  Med.,  vol.  v.,  p.  285,  1882. 

^  Almost  simiiltaneouslv  bv  Bondzvnski  and  Gottlieb  and  bv  M.  Cloetta. 


500  URINARY  EXAMINATION. 

So  far  as  the  clinical  results  are  concerned,  Ehrlich  claims  that  the 
reaction  is  never  found  in  healthy  individuals,  and  in  non-febrile  dis- 
eases only  exceptionally,  and  in  the  following  instances:  1,  In  advanced 
cardiac  disease  ;  2,  in  chronic  hepatitis  ;  3,  in  carcinoma,  especially  of 
the  pylorus  ;  4,  in  leukemia  ;  5,  in  marasmus  senilis  ;  6,  in  the  cachexia 
of  malaria ;  7,  in  cold  abscesses.  So  far  as  febrile  affections  are  con- 
cerned, they  may  be  divided  into  three  subdivisions  :  1,  Those  in  which 
the  reaction  is  almost  always  absent — e.  g.,  joint  rheumatism,  meningitis  ; 
2,  those  in  which  it  may  occur  sometimes  more  often,  sometimes  less 
often,  according  to  the  nature  of  the  attack — e.  g.,  pneumonia,  scarlet 
fever,  diphtheria,  erysipelas,  phthisis  ;  3,  those  in  which  it  is  of  nearly 
constant  occurrence — e.  g.,  typhoid,  typhus,  measles. 

The  occurrence  of  the  reaction  in  either  of  the  first  two  categories 
of  febrile  disorders  appears  to  render  the  prognosis  more  grave. 

In  typhoid  the  reaction  may  be  of  diagnostic  value  in  one  of  two 
ways  :  First,  the  persistent  absence  of  this  reaction  in  a  disease  which 
simulates  a  severe  typhoid  speaks  considerably,  although  not  absolutely, 
against  such  diagnosis.  Secondly,  typhoid  recurrences  or  relapses  may 
be  distinguished  by  this  reaction  from  intercurrent  lung  affections  and 
other  febrile  complications.  With  a  recurrence  or  a  relapse  the  reaction 
will  return  or  be  increased  ;  otherwise,  this  is  not  the  case. 

The  reaction  is  found  quite  frequently  in  phthisis,  especially  in  severe 
and  progressive  cases.  Here  it  suggests  a  bad  prognosis,  and  is,  as  it 
were,  an  index  to  the  general  serious  condition.  Unfortunately,  the 
reaction  does  not  seem  to  be  of  any  value  in  differentiating  acute  miliary 
tuberculosis  from  typhoid,  as  it  is  often  present,  and  very  intense  in  the 
former. 

In  puerperal  infection  the  appearance  of  the  reaction  is  coincident 
with  the  fever. 

Riittimeyer  has  also  observed  the  reaction  in  pulmonary  actinomy- 
cosis. 

The  diazo-reaction  must  be  considered  as  a  metabolic  symptom  of 
certain  diseases,  which  (like  splenic  swelling  and  fever)  is  not  of  diag- 
nostic value  in  itself,  but  only  when  considered  in  connection  with  the 
other  symptoms.  It  should  also  be  noted  that  a  similar  reaction  may 
be  obtained  after  the  administration  of  opium,  morphin,  chrysarobin, 
naphthalin,  heroin,  dionin,  tannic  acid,  alcohol  in  large  quantities,  phe- 
nol, cresol,  creosote,  and  guaiacol.  This  fact  must  consequently  be 
borne  in  mind  before  drawing  conclusions  as  to  the  diagnostic  value  of 
the  diazo-reaction. 

The  so-called  egg-yellow  reaction,  as  described  by  Ehrlich,  is  said  to 
be  somewhat  characteristic  of  pneumonia  just  before  and  during  the 
crisis.  It  is  a  preliminary  reaction — i.  e.,  a  diazo-reaction  which  occurs 
before  the  addition  of  ammonia.  The  urine  becomes  deep  yellow  after 
the  addition  of  the  reagent,  the  color  showing  most  distinctly  in  the 
foam.  It  does  not  turn  red  when  ammonia  is  added,  but  becomes  lighter 
yellow.  Oppenheim  found  it  constantly  in  28  of  his  cases  at  the  crisis. 
In   some  conditions  we  might  predict  the    crisis    from  this  reaction. 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE   URINE.   501 

Ehrlich  claims  that  the  chromogen  of   urobilinogen   is  an    alteration 
product  of  the  bilirubin  arising  from  the  hemoglobin  in  the  exudate. 

EXAMINATION   OF  THE    URINE    FOR    SUBSTANCES    INTRODUCED 
INTO  THE  BODY  FROM  WITHOUT   (DRUGS  AND  POISONS). 

DETECTION  OF  LEAD. 

A  shining  strip  of  magnesium  free  from  lead  is  placed  in  the  urine  and  left 
there  for  some  time  ;  the  deposit  is  dissolved  in  nitric  acid  and  then  tested  accord- 
ing to  the  rules  of  inorganic  chemistry.^  If  the  urine  contains  but  a  small  amount 
of  lead,  this  method  will  not  give  the  desired  result ;  a  larger  quantity  of  the 
urine  must  be  used,  the  organic  substances  destroyed  with  hydrochloric  acid  and 
potassium  chlorate,  and  the  lead  sought  for  in  the  evaporated  residue.^ 

DETECTION  OF  MERCURY. 

To  500  to  1000  c.c.  of  urine  are  added  2  to  4  c.c.  of  hydrochloric  acid  (Fiir- 
bringer).  It  is  then  digested  at  60°  to  80°  C  for  five  to  ten  minutes  in  a  flask 
with  \  to  \  gm.  of  brass-wool,  and  frequently  skaken.  The  metal  is  washed  first 
with  water,  then  with  alcohol,  and  finally  with  ether,  and  dropped  into  a  glass 
tube  of  high  melting-point,  which  has  been  prolonged  into  a  capillary  tube  at  the 
upper  end.  It  is  there  brought  to  a  red  heat,  the  capillary  end  being  kept  upj^er- 
most.  The  mercury,  which  has  become  amalgamated  with  the  brass-wool,  becomes 
volatile  and  will  be  deposited  as  a  mirror  at  the  capillary  end  of  the  tube.  If  a 
particle  of  iodin  is  evaporated  in  the  tube,  the  deposit  will  be  colored  red  by  the 
formation  of  iodin  of  mercury.  (In  reference  to  other  methods,  see  Spath,  p. 
399  et  seq.) 

DETECTION  OF   IODIN. 

Iodin  occurs  in  the  urine  as  potassium  iodid  after  the  internal  and  external 
administration  of  iodin  or  one  of  its  preparations.  It  may  be  easily  demonstrated 
as  follows  :  A  few  cubic  centimeters  of  urine  are  boiled  with  a  piece  of  starch 
about  the  size  of  a  pea  until  the  latter  is  dissolved.  After  cooling  the  fluid  is 
carefully  stratified  over  concentrated  nitric  acid.  If  iodin  is  present,  a  blue-vio- 
let ring  that  gradually  disappears  is  formed  at  the  line  of  junction  of  the  two 
fluids.  In  this  test  iodin  is  liberated  from  the  potassium  iodid  by  the  nitric  acid, 
and  unites  with  the  starch  to  form  blue  iodid  of  starch. 

Another  way  is  to  add  to  the  urine  5  to  10  drops  of  crude  nitric  acid  and  \ 
c.c.  of  chloroform,  and  then  shake  gently.  If  iodin  is  present  the  chloroform 
which  settles  to  the  bottom  will  be  colored  a  rose  red  to  violet,  due  to  the  solu- 
tion in  the  chloroform  of  the  free  iodin. 

To  prove  that  a  patient  has  really  taken  a  drug  prescribed,  introduce  a  grain 
or  two  of  potassium  iodid  into  the  prescription.  Iodid  should  then  be  demon- 
strated both  in  the  urine  and  in  the  saliva. 

Both  the  above  tests  are  very  delicate.  But  if  the  urine  contains  but  a  very 
slight  trace  of  iodin,  the  chloroform  test  may  not  be  very  specific,  since  the  nitric 
acid  may  set  free  indol  and  skatol  pigments  as  well  as  urorosein  (see  p.  478),  and 
so  tinge  the  chloroform  reddish.  But  in  this  case  the  urine  itself  usually  appears 
more  deeply  colored  than  the  chloroform.  The  starch  reaction  may  not  be  of  much 
help  in  deciding  in  such  a  case,  because  the  blue  ring  of  the  iodid  of  starch  may 
be  simulated  by  an  indican  reaction,  for  in  a  urine  so  rich  in  such  chromogen  not 
only  calcium  chlorid,  but  sometimes  even  nitric  acid  (see  p.  477),  will  produce 
the  change.  Here,  however,  it  is  easy  enough  to  show  tliat  the  nitric  acid  alone 
is  capable  of  producing  this  blue  ring  without  the  addition  of  any  starch. 

Palladium  chlorid  furnishes  still  another  iodin  reaction.    The  urine  suspected 

^  Salkowski,  Practicum  der  physiol.  u.  path.  Chemie,  2d  ed.,  1900. 

^  For  the  accumte  procedure,  see  Lehmann,  Zeitfs.  f.  phymol.  Chemie,  vol.  vi.,  p.  4, 1882. 


602  URINARY  EXAMINATION. 

to  contain  iodin  is  strongly  acidulated  with  hydrochloric  acid,  and  then  a  few 
drops  of  a  moderately  saturated  solution  of  palladium  chlorid  in  hydrochloric 
acid  1  are  added. 

If  iodin  is  present  a  brown  discoloration  occurs,  and  gradually  a  black  pre- 
cipitate. This  reaction  has  but  one  meaning,  but  it  is  much  less  delicate  than 
the  starch  or  the  chloroform  reaction. 

DETECTION  OF  BROMIN. 

The  test  for  bromin  is  performed  in  exactly  the  same  way  as  the  iodin  test 
with  chloroform,  except  that  a  few  drops  of  a  calcium  chlorid  solution  and  hydro- 
chloric acid  are  used  to  liberate  the  bromin.  If  bromin  is  present  the  chloroform 
will  be  colored  yellowish  brown  by  the  free  bromin.  This  test,  although  much 
less  delicate  than  the  iodin  test,  is  sufficiently  accurate  to  recognize  the  thera- 
peutic ingestion  of  large  doses  of  bromin  salts.  To  add  to  the  uncertainty  of 
this  test,  we  must  remember  that  the  chloroform  can  also  be  tinged  yellow  by 
some  of  the  urinary  coloring  matters.  To  prevent  this  latter  source  of  error,  IQ 
c.c.  of  the  urine,  to  which  have  been  added  2  c.c.  of  caustic  potash  and  2  c.c. 
of  potassium  nitrate,  are  incinerated,  the  ash  dissolved  in  water,  and  the  result- 
ing solution  tested  for  bromin,  as  above. 

A.  Jolles^  has  described  an  admirable  test  which  is  quite  simiDle.  It  depends 
upon  the  fact  that  bromin  can  be  freed  from  the  urine  by  potassium  permanganate 
in  acid  solution,  and  that  such  free  bromin  gives  a  red  color  with  jo-dimethylphe- 
nylendiamin.  Filter  paper  is  moistened  with  an  aqueous  solution  of  the  hydro- 
chlorid  of  ^-dimethylphenylendiamin,  dried,  and  cut  into  strips.  Ten  cubic  cen- 
timeters of  urine  are  acidulated  in  a  narrow-necked  flask  with  H^SO^,  saturated 
with  potassium  permanganate.  The  color  is  now  a  permanent  red.  A  moist 
strip  of  the  above  test  paper  is  suspended  in  the  neck  of  the  flask,  and  the  latter 
is  warmed  over  a  water  bath.  If  bromin  is  present  the  paper  will  be  colored 
from  violet,  through  blue  and  green,  to  a  brown.  Iodin  and  chlorin  present  other 
brownish  shades  different  enough  not  to  be  confusing. 

The  demonstration  of  bromin  in  the  urine  is  of  no  special  interest  except,  of 
course,  in  verifying  a  diagnosis  of  suspected  bromism. 

DETECTION  OF  SALICYLIC  ACID. 

Ferric  chlorid  is  added  to  the  urine  drop  by  drop.  If  the  latter  becomes  a 
more  or  less  intense  deep  violet,  the  reaction  is  positive.  It  is  very  delicate,  and 
can  be  used  in  the  same  way  as  the  iodin  reaction  to  control  the  ingestion  of  drugs. 
Salicylic  acid  and  its  salts,  in  which  latter  form  the  administered  salicylic  acid 
partly  appears  in  the  urine,  both  give  this  reaction.  (Compare  p.  496  with 
reference  to  the  differentiation  of  the  salicylic  acid  reaction  from  the  similar 
reaction  of  diacetic  acid.) 

DETECTION  OF   PHENOL. 

Phenol  appears  in  the  urine  largely  as  phenol  sulphate.  Ferric  chlorid  will 
produce  a  violet-blue  color  in  the  distillate  from  a  phenol  urine  to  which  5  per 
cent,  sulphuric  acid  has  been  added.  Phenol  urine  turns  dark  to  black  upon 
exposure  to  the  air.  This  is  due  to  the  fact  that  it  contains  hydroquinone  and 
pyrocatechin,  which  form  dark-colored  derivatives  upon  oxidation. 

DETECTION  OF  ANTIPYRIN. 

The  urine  appears  dark  and  is  dichroic — in  reflected  light  greenish,  in  trans- 
mitted light  reddish.  A  brownish-red  color  gradually  appears  upon  the  addi- 
tion of  ferric  chlorid  solution. 

'  This  solution  is  prepared  by  adding  1  gra.  of  palladium  chlorid  to  a  ^vf  dropsof 
hydrochloric  acid,  allowing  it  to  stand  for  a  day,  and  then  diluting  the  resulting  solution 
with  enough  hydrochloric  acid  to  make  a  faintly  transparent  brown  solution. 

2  Wien.  Mm.  Rundschau,  1898,  No.  12. 


QUALITATIVE  CHEMICAL  EXAMINATION  OF  THE   URINE.  503 

DETECTION  OF  THALLIN. 

The  urine  is  yellowish  green  to  dark  brown,  and  turns  brownish  red  upon  the 
addition  of  ferric  chlorid  solution.  If  the  urine  is  shaken  with  ether,  the  latter 
will  be  tinged  green  ^  upon  the  addition  of  ferric  chlorid. 

DETECTION  OF  PHENACETIN. 

The  urine  is  dark  yellow,  and  turns  reddish  brown  upon  the  addition  of  ferric 
chlorid  solution.     The  color  gradually  becomes  black  after  prolonged  standing. 

DETECTION  OF  ANTIFEBRIN. 

The  urine  is  extracted  with  chloroform,  and  to  the  extract  mercuric  nitrate  is 
added.  The  mixture  is  then  heated,  and  if  a  green  color  is  produced  2  antifebrin 
is  present.  ^ 

DETECTION  OF  PYRAMIDON. 

The  urine  is  frequently  clear,  purplish  red  in  color,  and  deposits  a  sediment 
consisting  of  small  red  needles.  If  the  urine  be  mixed  with  an  equal  volume  of  a 
2  per  cent,  solution  of  ferric  chlorid,  a  dark-brownish  amethyst  color  is  produced. 
According  to  Jolles,  a  violet  ring,  gradually  becoming  red,  is  obtained  when  the 
urine  is  carefully  covered  by  a  layer  of  dilute  alcoholic  solution  of  iodin  (a  10 
per  cent,  tincture  of  iodin  diluted  with  10  parts  of  alcohol). 

DETECTION  OF  TANNIN. 

Tannin  is  eliminated  in  the  urine  partly  as  gallic  acid.  Urine  which  con- 
tains  tannic  and  gallic  acids  will  turn  blue  black  upon  the  addition  of  ferric 
chlorid  solution  (ink  reaction). 

DETECTION   OF   BALSAM   OF  COPAIBA  AND  SANDALWOOD  OIL. 

After  the  administration  of  balsam  of  copaiba  the  urine  will  reduce  cupric 
oxid  (Trommer's  test)  but  not  bismuth  (Nylander's  test).  If  hydrochloric  acid 
is  added  to  the  urine  drop  by  drop,  a  precipitate  of  resinous  acids  api3ears  with  a 
reddish  to  violet  coloration.  Also  after  the  use  of  sandalwood  oil  the  urine  pos- 
sesses reducing  properties,  and  will  exhibit  a  precipitate  of  resinous  acids  when 
hydrochloric  is  added,  but  with  a  reddish-brown  color.  Karo  claims  that  this 
color  is  not  characteristic.  Alexander  ■*  emphasizes  the  fact  that  the  intensity  of 
the  resinous  acid  precipitate  is  not  proportioned  to  the  color  reaction  produced, 
and  that,  with  regard  to  the  amount  of  the  resinous  acid  excreted,  individuals 
differ  greatly  when  the  same  dose  of  copaiba  balsam  or  sandalwood  oil  has  been 
administered. 

DETECTION  OF  SANTONIN. 

Santonin  urine  is  of  a  saffron-yellow  to  greenish  color.  The  addition  of 
sodium  hydrate  will  turn  it  a  rose-red  shade.  If  this  rose  pigment  is  shaken 
with  amylalcohol,  it  will  be  immediately  dissolved  by  the  latter,  giving  it  a 
beautiful  and  intense  coloring,  while  the  urine  will  become  decolorized. 

DETECTION  OF  EMODIN,  CHRYSOPHANIC  ACID,  AND  SUBSTANCES  RELATED 
THROUGH  THE  OXYMETHYLANTHRAQUINONE  GROUP,  RHUBARB. 
SENNA,    RHAMNUS    (Cascara    Sagrada),   ALOES. 

After  the  ingestion  of  rhubarb,  of  the  different  kinds  of  rhamnus  (E.  fran- 

gula  and  K.  purshiana  or  cascara  sagrada),  of  senna,  and  of  large  doses  of  aloes, 

the  urine  will  be  tinged  a  brownish  yellow,  and  upon  the  addition  of  an  alkali 

(sodium,  potassium,  or  ammonium  hydroxid)  will  become  more  or  less  distinctly 

'red.     This  peculiarity  depends  upon  the  presence  of  emodin  (trioxymethylanthra- 

^  V.  Jaksch,  Zeits.f.  klin.  Med.,  vol.  viii.,  p,  551. 
'■^  Yvon,  Jour,  de  Phann.  et  de  Chemie,  1887,  No.  1. 
»  Deutsch.  Med.  Wock,  1893,  No.  14,  p.  324. 


504  .         URINARY  EXAMINATION. 

quinone)  and  of  chrysophanic  acid  (dioxymetliylanthraquinone).  These  substances 
are  excreted  in  the  urine  partly  as  such  and  partly  in  combination.  Even  after 
the  external  use  of  chrysarobin  the  urine  sometimes  exhibits  the  same  i^eculiari- 
ties,  probably  because  chrysophanic  acid  is  formed  in  the  body  from  chrysarobin. 
Urine  containing  one  of  these  substances  differs  from  santonin  urine  in  this  respect : 
the  red  coloring  matter  j)roduced  by  the  addition  of  alkalies  will  not  dissolve  in 
the  amyl  alcohol.  The  reaction  common  to  chrysophanic  acid  and  emodin,  and 
recently  named  the  oxyriiethylanthraquinone  reaction,  has  been  modified  and 
made  more  delicate,  according  to  Tschirch,  by  boiling  the  urine  in  a  test  tube 
with  1  or  2  drops  of  caustic  potash,  in  order  to  split  up  the  combined  bodies,  then 
acidulating  with  HCl,  extracting  with  ether,  and  shaking  the  ether  with  ammonia. 
After  a  short  delay  the  ether  sej^arates  from  the  ammonia,  and  the  latter  is  tinged 
a  beautiful  cherry  red.  Chrysophanic  acid  passes  from  the  ether  into  the  ammonia 
with  dilEculty,  so  that,  if  the  ether  remains  yellow  despite  the  red  coloration  of 
the  ammonia,  we  are  justified  in  deciding  ujjon  the  presence  of  chrysophanic  acid 
instead  of  emodin. 

QUANTITATIVE   URINARY   ANALYSIS, 

Preliminary  Note. — Since  in  the  quantitative  analysis  of  any  urine 
the  amount  of  the  particular  constituent  excreted  in  twenty-four  hours 
is  required,  the  specimen  examined  must  be  a  portion  of  a  well-mixed 
twenty-four-hour  urine. 

QUANTITATIVE    ESTIMATION    OF   UROCHROME. 

Klemperer  ^  has  recently  made  a  noteworthy  attempt  to  attach  a  diagnostic 
value  to  the  amount  of  normal  urinary  pigment  contained  in  the  urine.  The 
normal  urinary  pigment,  and  trequently  the  only  one,  is  urochrome  ;  it  holds  a 
close  chemical  relation  to  urobilin,  into  which  it  may  be  converted  by  cautious 
oxidation.  According  to  Klemperer,  the  normal  color  of  the  urine  corresponds 
approximately  to  0.15  per  cent,  urochrome  solution.  He  determines  the  amount 
of  contained  urochrome  colorimetrically  by  comparison  with  a  solution  of  "  pure 
yellow"  ("Echtgelb"  of  Leitz).  Klemperer  prepares  his  solution  for  compari- 
son by  dissolving  0.1  gm.  of  dry  "pure  yellow"  in  a  liter  of  water,  and  diluting 
5  c.c.  of  this  solution  to  90  c.c.  According  to  Klemperer,  the  shade  of  this  solu- 
tion of  "pure  yellow  "  (1  :  180,000)  corresponds  to  a  0.1  solution  of  urochrome, 
and  by  diluting  the  urine  or  the  test  solution,  the  quantity  of  contained  urochrome 
may  easily  be  determined  by  the  colorimetric  method.  The  urine  and  the  test  solu- 
tion must",  of  course,  be  contained  in  vessels  of  the  same  shape  when  the  com- 
parison is  made.  Stronger  solutions  of  "pure  yellow "  cannot  be  employed,  since 
their  color  does  not  agree  with  that  of  urine.  Should  the  urine  contain  consider- 
able quantities  of  other  pigments,  such  as  urobilin  or  hematoporphyrin,  an  exact 
colorimetric  estimation  of  the  urochrome  is,  of  course,  impossible.  Klemperer 
nevertheless  believes  that  if  the  presence  of  these  other  pigments  is  not  disclosed 
by  absorption  bands  in  the  spectroscopic  examination  (urochrome  absorbs  light 
diffusely),  the  method  given  above  will  be  sufficiently  accurate.  He  also  believes 
that  the  estimation  of  the  daily  excretion  of  urochrome  furnishes  an  indication  of 
the  functional  activity  of  the  kidneys,  since  he  assumes  that  urochrome  is  formed 
in  the  kidneys.  It  is  nevertheless  clear  that  if  the  latter  assumption  be  incorrect, 
and  it  has  not  yet  been  proved,  the  amount  of  excreted  urochrome  is  not  of  such 
simple  significance,  since  it  would  not  depend  upon  the  kidneys  alone,  but  also 
upon  the  unknown  function  upon  which  the  formation  of  urochrome  in  the  body 
is  dependent.  The  fact  that  pale  urine  is  frequently  excreted  in  uremia  could 
also  be  due  to  the  fact  that,  in  addition  to  the  impairment  of  the  excretory  func- 
tion of  the  kidneys,  other  important  functions  holding  some  relation  to  the  forma- 
tion of  urochrome  are  also  implicated. 

1  Berlin,  klin.  Woch.,  1903,  No.  14,  p.  314. 


QUANTITATIVE   URINARY  ANALYSIS. 


505 


QUANTITATIVE  ESTIMATION  OF  PROTEIDS. 

ESTIMATION  BY  OBTAINING  AND  WEIGHING  PURE  (COAGULABLE)  PROTEID. 
OR  KJELDAHL'S  METHOD. 

An  exact  quantitative  estimation  of  coagulable  proteid  must  depend 
upon  a  complete  precipitation  of  the  proteid  by  boiling  after  the  addition 
of  dilute  acetic  acid  (2  per  cent.).  (See  Removal  of  Proteid  from  Urine, 
p,  463.)  The  precipitate  must  then  be  washed,  and  dried  upon  a  dry- 
weighed  filter  at  110°  to  120°  C.  to  a  constant  weight,  the  dried  residue 
weighed,  and  the  weight  of  the  dry  filter  subtracted.  To  save  time  in 
drying  the  precipitate,  the  amount  of  urine  should  be  small,  so  that  the 
weight  of  the  dry  proteid  will  not  exceed  0.2  to  0.3  gm.  (preliminary 
estimation).  (See  below.  Estimation  of  Quantity  of  Proteid  according 
to  Esbach.) 

Proteid  is  exceedingly  hydroscopic ;  hence,  the  weighing  should  be 
very  carefully  carried  out.  The  material  should  be  placed  between 
watch  glasses,  with  the  ground  edges  carefully  applied 
to  each  other.  For  very  great  accuracy  the  albuminous 
precipitate  must  be  first  washed  with  alcohol  and  ether, 
in  order  to  remove  the  fat  before  drying,  and  finally 
the  content  of  ash  determined  and  subtracted.  For 
most  clinical  purposes  this  method,  which  is  the  only 
one  absolutely  accurate,  is  too  complicated.  Approxi- 
mate estimations  usually  answer  the  purpose.  There 
are  quite  a  number  of  such  methods,  of  which  the  fol- 
lowing are  the  most  practicable  : 

ESBACH'S  ESTIMATION  OF  PROTEID. 

This  method  consists  in  determining  the  volume  of 
proteid  which  is  precipitated  from  a  definite  amount  of 
urine  by  a  certain  solution.  A  graduated  test  tube  of 
thick  glass,  called  an  albuminimeter  (Fig.  174),  is  filled 
to  the  mark  U  with  the  acidified  urine  to  be  examined, 
and  then  a  solution  (10  gm.  of  picric  acid  and  20  gm. 
of  citric  acid  in  1  liter  of  distilled  water)  for  precipi- 
tating the  proteid  is  added  up  to  the  mark  R.  The 
tube  is  closed  with  a  rubber  cork,  and  the  liquids  mixed 
by  repeated  inversion  without  shaking.  The  glass  is 
now  set  upright  in  a  test-tube  rack.  The  precipitated 
proteid  gradually  settles  to  the  bottom,  and  after  twenty- 
four  hours  the  height  of  the  layer  can  be  quickly  seen 
tions  indicate  the  grams  of  proteid  in  the  liter.  With  some  instruments 
the  graduation  reads  as  high  as  1.2  per  cent.  If  the  amount  of  proteid 
is  so  large  (0.>5  per  cent.)  that  the  precipitate  settles  unevenly,  it  is  safer 
to  dilute  the  urine  once  or  twice,  or  even  four  times,  before  performing 
the  test.  In  Esbach's  method  the  limit  of  accuracy  for  a  moderate 
amount  of  proteid  is  perhaps  0.1  per  cent.  If  the  amount  of  proteid 
is  large,  or  if  it  is  less  than  0.05  per  cent.,  the  chances  for  error  become 
considerable.     A  very  small  quantity  will  not  sediment,  so  that  it  cannot 


Fig.  174.— Esbach's 
albuminimeter. . 


The  gradua- 


506  URINARY  EXAMINATION. 

be  estimated  by  this  method.  The  empirical  graduation  of  Esbach's 
albuminimeter  presupposes,  of  course,  the  average  room  temperature. 
The  result  will  be  decidedly  diiferent  if  the  surrounding  temperature 
varies  much  from  the  normal.  If  the  urine  contains  a  considerable 
quantity  of  resinous  acids — e.  g.,  after  ingestion  of  the  balsams  or  of 
santalwood  oil — this  method  cannot  be  employed,  because  these  acids 
will  be  precipitated  by  the  picric  acid  along  with  the  proteid  (p.  463). 
Weighing  will  then  have  to  be  resorted  to,  and  any  resinous  acid  which 
may  happen  to  be  precipitated  will  be  removed  from  the  proteid  pre- 
cipitate by  the   washing  with  alcohol  and  ether. 

ROBERTS-STOLNIKOW'S    (BRANDBERG'S)    METHOD  FOR  THE  ESTIMATION 

OF  PROTEID. 

A  method  described  by  Eoberts  and  Stolnikow  simultaneously,  and  then  tested 
more  accurately  by  Brandberg,  can  be  recommended  if  we  do  not  happen  to  have 
an  albuminimeter.  This  test  depends  upon  the  fact  that  the  turbidity  of  proteid 
in  the  nitric  acid  test  appears  more  or  less  quickly  according  to  the  amount  of 
proteid  contained  in  the  urine.  If  the  urine  contains  0.0033  per  cent,  of  proteid, 
the  cloudiness  first  appears  within  two  and  one-half  to  three  minutes.  By  diluting 
the  urine  sufiiciently  to  cause  the  turbidity  to  appear  within  that  interval,  the 
amount  of  proteid  actually  contained  in  the  specimen  can  be  readily  determined. 
Naturally,  great  care  must  be  exercised  in  performing  the  reaction.  If  a  cloudi- 
ness occurs  inside  of  three  minutes,  we  employ  a  dilution  of  1  :  10  (A).  If  this 
dilution  is  still  not  sufficient,  mixture  B  may  be  prepared  by  diluting  1  part  of 
A  with  2  parts  of  water.  If  even  this  mixture  (B)  is  too  concentrated,  we  make 
up  a  third  dilution  (C),  consisting  of  1  part  of  B  with  4  parts  of  water ;  and 
again,  if  necessary,  a  fourth  dilution  (D),  consisting  of  1  part  of  C  with  1  part 
of  water. 

A  corresponds  to  0.033  per  cent,  of  proteid. 

B  "  0.10 

C  "  0.50 

D  "  1.00 

If  the  urine  contains  either  nucleo-albumin  or  resinous  acids,  this  method  is 
not  available,  because  nitric  acid  precipitates  both  of  these  bodies  along  with  the 
proteid  (p.  462). 

QUANTITATIVE    ESTIMATION  OF  DEXTROSE. 

In  diabetes  mellitus  the  amount  of  sugar  in  the  urine  generally 
ranges  from  4  to  5  per  cent.,  but  it  may  be  as  high  as  10  per  cent.,  so 
that  in  the  course  of  twenty -four  hours  1  kgm.  or  more  may  be  excreted. 

ESTIMATION    OF  THE  AMOUNT  OF    SUGAR   FROM  THE    SPECIFIC    GRAVITY 
AND  THE  QUANTITY  OF  IRON. 

Naunyn  constructed  an  approximately  accurate  table  for  estimating 
the  amount  of  sugar  in  diabetic  urine,  as  follows  : 
With  a  daily  quantity  of : 

2  litei-s  and  with  a  specific  gravitv  between  1028-1030,  about  2-3  per  cent. 

3  a     ^         u  'u  1028-1032       "     3-5        " 

5  "  "  "  1030-1035       "     5-7        " 

6  to  10  "  "  "  1030-1042       "     6-10      " 

The  percentage  of  sugar  in  the  urine  can  be  approximately  determined 
from  the  quantity  and  specific  gravity  if  we  deduct  as  much  from  the 
specific  gravity  found  as  would  represent  the  specific  gravity  of  a  normal 


QUANTITATIVE  URINARY  ANALYSIS.  507 

non-sugar  urine  diluted  up  to  the  same  quantity  by  the  excessive  inges- 
tion of  water.  For  instance,  if  2  liters  represent  the  amount  of  the 
twenty-four-hour  excretion,  the  specific  gravity  would  ordinarily  be 
about  1015.  Then  if  the  volume  is  still  further  increased  by  abundant 
water-drinking,  a  urine  whose  twenty-four-hour  quantity  amounts  to  3 
liters  will  have  approximately  a  specific  gravity  of 

2  X  1015  +  1000_  ^^^Q 


and  one  of  6  liters,  a  specific  gravity  of 
2  X  1015  +  4000 


1005. 


6 

Now,  suppose  a  diabetic  urine  (a),  whose  twenty-four  hour  amount  equals 
3  liters,  and  another  (6),  whose  twenty-four-hour  amount  equals  6  liters, 
have  the  same  specific  gravity,  1030.  The  sugar  contained,  then,  in  urine 
a  is  sufficient  alone  to  produce  a  specific  gravity  of  1030  —  1010  =  1020, 
and  in  urine  6  to  1030  —  1005  =  1025.  From  this  the  amount  of  sugar 
present  can  be  approximately  calculated  by  multiplying  the  last  two 
figures  of  the  specific  gravity  by  0.23.  (See  p.  513,/.,  Quantitative 
Areometric  Fermentation  Test.)  This  gives  for  urine  a  4.6  per  cent., 
and  for  urine  b  5.7  per  cent.  Such  an  estimate  is,  of  course,  inaccurate, 
if  for  no  other  reason  than  that  diabetes  mellitus  also  alters  the  amount 
of  urea  and  salts  eliminated,  which  in  turn  also  influences  the  specific 
gravity  of  the  urine. 

ESTIMATION  OF  THE  QUANTITY  OF  DEXTROSE   BY  TITRATION. 
Fehling-Soxhiet's  Method. 

Dextrose  will  reduce  cupric  oxid  in  an  alkaline  solution  to  cuprous  oxid. 
This  property  is  the  one  most  frequently  employed  in  titrating  for  sugar ;  because 
when  certain  conditions  are  maintained  the  reduction  of  the  alkaline  cupric  oxid 
solution  by  the  sugar  takes  place  quantitatively.  Fehling' s  solution  is  the  one 
generally  employed.     It  is  prepared  as  follows  : 

34. 64  gm.  purest  crystalline  copper  sulphate,  173  gm.  Eochelle  salt  (sodium 
potassium  tartrate),  100  c.c.  sodium  hydrate  solution  of  specific  gravity  1.34, 
distilled  water  up  to  1000  c.c. 

Fehling's  solution  cannot  be  preserved  in  its  original  form.  It  is  therefore 
advisable  to  keep  two  separate  solutions,  which  should  not  be  mixed  until  just  before 
using.  Solution  1  contains  34.64  gm.  of  copper  sulphate  dissolved  in  500  c.c.  of 
distilled  water  acidulated  with  a  drop  of  concentrated  sulphuric  acid.  Solution  2 
contains  173  gm.  of  Eochelle  salt  with  100  c.c.  of  NaOH  solution  (specific 
gravity  1.34),  and  the  volume  made  up  to  500  c.c.  with  water.  By  mixing  equal 
volumes  of  these  solutions,  a  fresh  Fehling's  solution  can  be  obtained  for  everj^  test. 
This  mixture  contains  sufficient  cupric  oxid,  so  that  10  c.c.  of  the  solution  when 
diluted  five  times  with  water  will  be  reduced  to  the  red  cuprous  oxid  when  boiled 
with  0.05  gm.  ,of  grape  sugar  (or,  according  to  Soxhlet,  0.0473  gm).  If  the  urine 
contains  more  than  1  y>^v  cent,  of  dextrose  it  should  be  diluted  with  water,  before 
titration,  until  it  does  not  contain  more  than  that  amount.  The  above-mentioned 
rules  for  approximately  estimating  the  amount  of  sugar  from  the  specific  gravity 
can  be  used  as  the  basis  for  this  procedure.  As  a  rule,  more  than  5  c.c.  of  urine  are 
required  to  reduce  the  10  c.c.  of  Fehling's  solution.  Albuminous  urine  must  be 
freed  from  proteid  by  boiling  the  acidified  urine,  and  filtering  before  titration 
(see  p.  463). 


608  URINARY  EXAMINATION. 

Metliod:  5  c.c.  of  solution  1  and  5  c.c.  of  solution  2  are  mixed  in  a  small 
flask,  diluted  with  water  up  to  50  c.  c. ,  heated  to  boiling,  and  the  urine,  approiDriately 
diluted,  added  a  few  drops  at  a  time  from  the  buret.  The  mixture  is  kept  boiling 
gently  until  it  is  approximately  decolorized  and  an  abundant  precipitate  of  the 
red  cuprous  oxid  has  appeared.  We  cannot,  of  course,  expect  to  obtain  accurate 
results  with  this  method  (Fehling's  original  method),  because  the  end-reaction 
cannot  be  recognized  accurately,  and  because  a  portion  of  the  suboxid  always 
dissolves  in  the  ammonia  liberated  from  the  urine  and  becomes  reoxidized.  This 
test  really  gives  only  approximate  values. 

For  accuracy  Soxhlet's  modification  should  be  resorted  to.  He  pours  the 
approximate  amount  of  urine  into  the  boiling  Fehling's  solution  at  once  (he  also 
uses  10  c.c.  of  Fehling's  solution  diluted  to  50  c.c.  with  water),  then  allows  the 
solution  to  boil  for  two  minutes,  and  then  takes  the  flame  away.  The  shming 
meniscus  at  the  upper  margin  of  the  fluid  is  his  index  of  the  end-reaction.  If 
this  persists  in  being  still  slightly  blue  he  I'epeats  the  test  with  a  fresh  and  slightly 
larger  volume  of  urine  and  fresh  Fehling's  solution  until  he  determines  the  exact 
amount  that  is  required  to  decolorize  the  fluid,  as  shown  by  the  meniscus. 

The  calculation  of  the  result  is  xerj  simple.  If  9  c.c  of  urine  diluted  10 
times  are  required  to  reduce  10  c.c.  of  Fehling's  solution,  then  0.9  c.c.  of  urine 
contains  0.05  gm.  of  dextrose. 

0.9  :  0.05  =  100  :  X 

X=  — -Q  =  5.5  gm.  of  grape  sugar 

— /.  e. ,  the  urine  contains  5. 5  per  cent,  of  dextrose. 

Or  if  we  employ  the  exact  figures  of  Soxhlet : 

0.9  :  0.0473  =  100  :  X 
^       4.73        .  _ 

Various  other  modifications  of  Fehling's  test  have  been  suggested  to  overcome 
the  diflBculty  of  sharply  determining  the  change  of  color  of  the  solution — ;.  e.,  the 
end-reaction.  Pavy's '  method,  one  of  the  best  known,  adds  a  certain  amount  of 
ammonia  to  the  Fehling's  solution  to  produce  a  colorless  cuprous  oxid  combina- 
tion. The  end-reaction  will  then  consist  in  a  complete  decoloration  of  the  blue 
copper  solution.  PaA-y  keeps  the  fluid  boiling,  and  adds  the  urine  from  a  buret, 
drop  by  drop.  The  difficulties  of  this  procedure  are,  however,  scarcely  less  than 
those  of  Fehling's  titration.  First  of  all,  air  must  be  excluded  during  the  titra- 
tion, so  that  the  buret  has  to  be  fastened  air-tight  into  the  flask,  otherwise  the 
colorless  solution  always  oxidizes.  Secondly,  the  ammonia  fumes  which  arise 
are  most  annoying.  Thirdly,  as  a  consequence  of  the  gradual  addition  of  the 
urine,  cuprous  oxid  will  be  precipitated  by  the  removal  of  ammonia  occasioned  by 
the  too-prolonged  boiling  of  the  solution.  Pavy's  method,  therefore,  necessitates, 
if  anything,  more  practice  than  Fehling'  s.  It  is  more  usefiil  when  Soxhlet's  modi- 
fication is  adopted  (addition  of  all  the  urine  at  one  time). 

Practically  speaking,  Soxhlet's  method  is  the  only  safe  one  for  the  practitioner  ; 
the  others  require  especial  practice  and  skill,  otherwise  they  are  too  uncertain. 
It  is  well  to  note  here  that  many  if  not  most  of  the  old  results  from  Fehling's 
method  were  probably  inaccurate ;  hence,  w^e  should  be  on  our  guard  against 
accepting  them  unreservedly. 

Dextrose  Titration  According  to  Drechsel-KIimmer. 
Klimmer  2  has  published  Drechsel's  method  for  sugar  titration  since  the  latter' s 
death.     It  seems  to  oflfer  a  sharp  end-reaction.     It  is  based  upon  the  fact  that  in 

'  "Phvsiologie  der  Kohlehydrate,"  fTerman  by  K.  Grube,  "Wien,  Deuticke,  1895. 

'■^  "Ist'Zucker  ein  norraaler  Bestandteil  des  Harnes  unserer  Haussiiugetiere?"  and 
"  Zwei  neue  klinische  Methoden  der  quantitativen  Zuckerbcstimmung  im  Harne,''  I.  A. 
D.  Bern,  1898. 


QUANTITATIVE   URINARY  ANALYSIS.  509 

the  presence  of  guanin  the  red  suboxid  which  is  formed  in  Trommer's  test  will 
unite  with  guanin  to  form  a  less  readily  oxidizable  combination  of  a  white  color, 
so  that  in  titration  with  Fehling's  solution  to  which  a  certain  amount  of  guanin 
has  been  added  the  solution  may  be  filtered  off  from  the  precipitate  and  tested  for 
copper.  For  all  clinical  purposes  the  decoloration  of  the  filtered  fluid  is  a  suffi- 
ciently sharp  end-reaction.  But  when  great  accuracy  is  essential  the  filtrate  must  be 
examined  for  copper  by  acidifying  and  then  adding  potassium  ferrocyanid  (brown 
precipitate  of  copper  ferrocyanid).  The  filtration  must  be  performed  through  a 
double  filter.  Albuminous  urine  must  be  freed  from  proteid.  The  technic  is  as 
follows  :  A  1  :  20  normal  guanin  solution  is  prepared  by  dissolving  9.  .375gm.  of 
guanin  hydrochlorid  in  1000  c.c.  of  1  j)er  cent,  solution  of  NaOH,  so  that  1  c.c. 
of  the  1  :  20  normal  guanin  solution  contains  0.00755  gm.  of  pure  guanin. 
Fifteen  cubic  centimeters  of  this  guanin  solution  are  added  to  10  c.c.  of  Fehling's 
solution,  and  the  mixture  then  diluted  with  25  c.c.  of  distilled  water.  Before 
titration  the  urine  should  be  diluted  so  that  it  does  not  contain  more  that  0. 5  to 
1  per  cent,  of  sugar.  The  total  amount  of  urine  employed  to  produce  the  end 
reaction  will  contain  0.05  gm.  of  dextrose.  If  the  reduction  produces  a  red 
color,  the  titration  must  be  repeated  with  the  addition  of  more  guanin  to  the 
Fehling's  solution.  For  a  very  exact  determination,  the  titration  should  be  per- 
formed before  and  after  fermentation,  in  order  to  eliminate  any  error  caused  by 
the  other  reducing  substances  of  the  urine,  and  then  the  difference  in  the  quantity 
of  urine  used  in  both  cases  made  the  bases  for  further  calculation. 

This  method  is  accurate,  but  only  when  very  pure  guanin  is  used,  and  that  is 
rather  expensive. 

LEHi«LA.NN'S    lODOMETRIC  TITRATION  METHOD    FOR   DEXTROSE.i 

In  this  method  a  definitely  measured  amount  of  urine  is  boiled  with  Fehling's 
solution  [just  as  in  Soxhlet-Allihn's  (p.  510)],  and  the  copper  which  remains  in 
solution  in  the  filtrate  is  titrated.  This  is  accomplished  by  adding  a  measured 
amount  of  potassium  iodid  solution  of  a  definite  specific  gravity  to  the  filtrate 
acidified  with  sulphuric  acid.  lodin,  which  is  set  fi-ee  according  to  the  equation 
2CuS0^  +  4KI  =  2K2SO^  +  CuJ^  +  \,  is  then  titrated  with  sodium  thio- 
sulphate,  using  starch  paste  as  an  indicator.  Every  atom  of  fi-ee  iodin  corresponds 
to  one  atom  of  copper  in  the  solution. 

In  addition  to  what  is  essential  for  Soxhlet's  estimation,  this  method  requires 
a  decinormal  sodium  thiosulphate  solution,  prepared  as  follows:  24.8  grams  of 
sodium  thiosulphate  and  2  gm.  of  ammonium  carbonate  are  each  dissolved  in 
water,  and  the  solution  diluted  up  to  one  liter.  One  cubic  centimeter  of  this 
solution  corresponds  to  0.00635  gm.  of  copper. 

A  good  asbestos  filter  is  also  necessary.  The  one  described  upon  p.  510  may 
be  employed.  However,  we  do  not  really  need  a  suction  filter  ;  and,  as  a  matter 
of  fact,  a  sufficiently  accurate  asbestos  filter  can  be  readily  constructed  by  shoving 
a  small  plug  of  glass-wool  into  the  opening  at  the  neck  of  an  ordinary  glass  funnel, 
in  order  to  support  the  asbestos,  and  then  pouring  upon  this  packing  a  finely 
divided  emulsion  of  asbestos  in  distilled  water  until  the  layer  of  filtering  asbestos 
is  .sufficiently  thick.  It  is  a  good  plan,  after  the  water  has  drained  away,  to  com- 
press the  asbestos  a  little  with  the  finger. 

We  now  mix  in  a  small  flask  10  c.c.  of  the  copper  sulphate  solution  used  for 
the  Soxhlet-Allihn's  solution  with  10  c.c.  of  the  corresponding  alkaline  tartrate 
solution,  and  add  30  c.c.  of  water,  heat  to  boiling,  and  then  pour  in  10  c.c.  of 
the  urine  to  be  examined.  This  urine  ^  must  be  free  from  proteid,  and,  if  neces- 
sary, must  be  diluted  sufficiently  not  to  contain  more  than  1  per  cent,  of 
dextrose  (see  p.  507).     After  the  addition  of  the  urine  the  mixture  is  allowed  to 

^  Arch.  f.  Hyijiene,  vol.  xxx.,  and  Zeits.  f.  anal.  Cheniie,  1898,  part  4,  and  Pharmac. 
Post,  1898,  No.  30.  Cf.  also  E.  Riegler,  Zeits.  f.  anal.  Chemie,  1898,  part  1,  and  Benjamin, 
BeutKch.  med.   WocL,  1898,  No.  35,  p.  552. 

'^  The  urine  mu.st  fii-st  be  freed  from  proteid,  because  otherwise  the  reduced  copper 
oxid  would  not  filter  off. 


510  URIXABY  EXAMINATION. 

boil  for  two  minutes  more  ;  then  the  cupric  oxid  which  has  been  formed  is  filtered 
oiF  by  the  asbestos  filter  and  finally  washed  with  water. 

The  filtrate  is  iodometrically  examined.  For  this  purpose  2  c.c.  of  concen- 
trated sulphuric  acid  are  added  to  it,  and,  after  cooling,  1  gm.  of  potassium 
iodid  dissolved  in  about  10  c.c.  of  water.  lodin  immediately  separates  out  with  a 
change  of  color.  Xow  we  deliver  from  a  buret  enough  decinormal  sodium 
thiosulphate  solution  to  make  the  fiuid  begin  to  clear  up,  then  (or  if  preferred 
even  before  beginning  to  add  the  thiosulphate)  add  a  few  cubic  centimeters  of  a 
thin  starch  paste  as  an  indicator,  and  titrate  again  until  the  blue  coloration  dis- 
appears. According  to  the  author's  experience,  the  thiosulphate  solution  should 
not  be  added  too  quickly,  because  the  decoloration  does  not  take  place  im- 
mediately. Shortly  after  the  blue  color  has  disappeared  (it  very  frequently  soon 
reappears)  to  estimate  the  end-reaction  we  must  be  very  careful  to  see  that  the 
decoloration  persists  for  at  least  five  minutes. 

In  making  the  calculation  it  must  be  remembered  that  the  10  c.c.  of  the 
copper  solution  which  we  have  employed  corresponds  to  27.8  c.c.  of  a  decinormal 
thiosulphate  solution.  If  v  equals  the  number  of  cubic  centimeters  of  thiosulphate 
solution  employed,  then  27.8  —  v  equals  the  number  of  cubic  centimeters  of  thio- 
sulphate solution  which  correspond  to  the  amount  of  reduced  copper ;  consequently, 
27.8  —  V  X  0.00635  is  the  amount  of  reduced  copper.  The  amount  of  sugar  cor- 
responding to  this  reduction  will  be  found  in  Allihn's  table,  p.  512. 

According  to  the  tests  which  the  author  has  made  with  this  method  he  believes 
that  it  can  be  recommended  as  one  of  the  most  trustworthy  and  convenient  of  the 
clinical  methods  for  the  determination  of  sugar.  The  only  real  difiiculty  is  the 
preparation  of  the  asbestos  filter  ;  but  after  a  little  practice  this  can  be  done  easily 
enough  if  the  directions  given  above  are  followed. 

SOXHLET-ALLIHN'S  METHOD  OF   DEXTROSE  ESTIMATION.^ 

This  is  a  thoroughly  accurate  method,  perhaps  the  most  reliable  of  all,  and 
certainly  to  be  recommended  for  scientific  investigation.  It  is  rather  too  compli- 
cated for  the  practising  physician,  but  in  a  clinical  laboratory,  after  the  necessary 
apparatus  is  once  put  together,  it  may  be  performed  in  a  reasonably  short  time. 
In  this  method  a  definite  excess  of  Fehling'  s  solution  is  partly  reduced  by  a  meas- 
ured volume  of  urine  ;  after  filtering  ofi"  the  solution  the  red  cuprous  oxid  previ- 
ously formed  is  collected  upon  an  asbestos  filter,  reduced  in  a  current  of  hydrogen, 
and  the  resulting  metallic  copper  weighed,  from  which  the  amount  of  sugar  con- 
tained in  the  urine  can  be  calculated.  Albuminous  urine  must  first  be  freed  from. 
proteid  (compare  p.  463  et  seq.).     The  following  two  solutions  are  required  : 

Solution  1:  173  gm.  of  Eochelle  salts,  125  gm.  of  potassium  hydroxid  dissolved 
in  water,  and  the  volume  made  up  to  500  c.c. 

Solution  2  :  34.6  gm.  of  crystallized  copper  sulphate  dissolved  in  water  and 
the  A'olume  made  up  to  500  c.c. 

Both  solutions  are  preserved  separately,  and  are  mixed  in  equal  volumes  for 
use.  The  technic  of  the  determination  is  as  follows:  60  c.c.  of  alkaline  cop- 
per solution  (30  c.c.  Eochelle  salt  solution,  30  c.c.  copper  sulphate  solution) 
are  placed  in  a  beaker  holding  about  300  c.c,  diluted  with  60  c.c.  of  water, 
and  then  heated  to  boiling  over  the  free  flame  or  on  a  sand  bath.  Twenty-five 
cubic  centimeters  of  urine  are  then  added  to  the  actively  boiling  fluid.  The 
urine  must  not,  of  course,  contain  more  than  1  per  cent,  of  sugar  ;  otherwise  it 
must  be  diluted  according  to  the  rules  given  on  p.  507  et  seq.  The  boiling  is  allowed 
to  continue  for  two  minutes.  The  precipitated  red  oxid  is  then  immediately  fil- 
tered ofl".  The  asbestos  suction  filter  recommended  by  Soxhlet  is  the  best  for  this 
purpose.  It  consists  of  a  small  tube  of  hard  glass,  15  cm.  long,  one  half  of  which 
has  a  lumen  of  about  2  cm.  diameter,  which  suddenly  diminishes  to  a  lumen  of 
about  h  cm.  in  the  other  half.  The  wide  half  is  filled,  perhaps,  2  cm.  deep  with 
long-fiber  asbestos.  A  little  glass-wool  is  first  placed  over  the  constricted  portion 
in  order  to  furnish  the  asbestos  a  better  hold.  Upon  this  glass-wool  enough  long- 
'^  Jour.  f.  praktische  Chemie,  Neue  Folge,  vol.  xxii.,  1880,  p.  52. 


QUANTITATIVE   URINARY  ANALYSIS.  511 

fiber  asbestos  is  poured  in  to  make  the  filter  sufiiciently  thick,  then  a  thoroughly- 
shaken  emulsion  of  short-fiber  asbestos  is  added.  If  the  precipitate  escapes 
through  the  filter,  the  layer  of  asbestos  can  be  made  sufiiciently  compact  by  press- 
ing it  down  with  a  glass  rod.  We  must  first  wash  the  asbestos  with  pure  dilute 
hydrochloric  acid,  and  then  wash  it  free  from  the  chlorin.  To  pour  the  fiuid  in 
more  conveniently,  a  small  funnel  can  be  inserted  into  the  wide  end  of  the  filter 
tube  with  the  aid  of  a  perforated  rubber  stopper.  The  constricted  portion  is 
placed  vertically  in  the  perforated  cork  of  a  suction  bottle,  and  the  latter  connected 
with  a  suction  pump.  Before  using  the  asbestos  filter,  it  must  always  be  dried  at 
120°  C,  cooled  in  the  exsiccator,  and  then  weighed.  The  fiuid  can  then  be  rap- 
idly sucked  through.  After  the  cuprous  oxid  has  been  removed  to  the  asbestos 
filter,  alcohol  is  allowed  to  fiow  through,  and,  then  the  filter  is  dried  in  an  air 
bath  at  120°  C.  for  about  one-half  hour.  By  means  of  its  perforated  rubber  stop- 
per and  a  small  glass  tube,  the  filter  is  next  connected  with  the  rubber  tube  of  a 
Kipp  hydrogen  apparatus,  and  hydrogen  is  passed  through.  The  hydrogen  must 
first  have  been  thoroughly  purified  by  passing  it  through  concentrated  sulphuric 
acid  and  then  through  a  potassium  permanganate  solution.  While  the  hydrogen 
is  being  passed  through,  the  filter  tube  should  be  so  placed  that  the  narrow 
half  is  a  little  lower  than  the  wide  one,  so  that  the  heavier  air  can  be  more  readily 
and  completely  displaced  by  the  hydrogen.  After  a  few  minutes  a  test  can  be 
made  to  see  whether  the  hydrogen  comes  through  the  filter  free  from  air.  For 
this  purpose  a  narrow  test  tube  is  held  vertically  over  the  opening  for  a  few 
moments,  its  mouth  carefully  closed  with  the  thumb,  and  the  contained  hydro- 
gen then  ignited  by  holding  the  mouth  of  the  tube  near  a  flame.  If  all  the  air 
has  been  displaced  from  the  apparatus,  the  hydrogen  will  explode  with  but  a  slight 
noise,  and  afterward  a  small  blue  flame,  hardly  visible  by  daylight,  will  travel 
slowly  and  gently  to  the  bottom  of  the  tube.  But,  on  the  other  hand,  if  the 
hydrogen  which  escapes  from  the  filter  still  contains  air,  the  fiame  will  immedi- 
ately shoot  into  the  tube  with  a  loud  whistling  noise,  and  then  instantly  die  out. 
In  such  an  event  hydrogen  must  be  passed  through  until  the  last  vestige  of  air 
has  been  removed  from  the  tube,  so  that  all  danger  of  explosion  from  the  subse- 
quent heating  of  the  asbestos  may  be  entirely  avoided.  As  soon  as  we  are  sure 
of  this  freedom  from  air,  the  asbestos  end  of  the  tube  is  fastened  over  a  gas  flame, 
and  kept  at  a  red  heat  in  the  current  of  glowing  hydrogen  until  all  of  the  brick- 
red  cuprous  oxid  has  become  reduced — i.  e. ,  until  the  precipitate  upon  the  filter 
has  changed  to  a  characteristic  brown  rec^the  color  of  metallic  copper.  The 
completion  of  the  reduction  may  also  be  recognized  by  the  fact  that  no  more  tiny 
drops  of  water  form  at  the  cold  end  of  the  tube,  and  that  when  the  hydrogen  is 
ignited  at  the  small  end  of  the  tube  it  no  longer  burns  with  an  increasing  flame. 
The  tube  is  now  allowed  to  cool  in  the  current  of  hydrogen,  and  is  then  set  in 
the  exsiccator  until  weighed.  The  weight  of  the  reduced  copper  can  then  be 
readily  determined.  The  empirical  table  (next  page)  compiled  by  Allihn  shows  at 
a  glance  the  amount  of  sugar  corresponding  to  a  given  weight  of  the  copper. 

If  Allihn's  directions  are  adhered  to  exactly,  and  particularly  if  the  filtration 
is  performed  immediately  after  tivo  minute.-i'  boiling  of  the  fluid,  these  figures  are 
accurate. 

S.  Pfliiger  has  careftilly  criticized  Soxhlet-AUihn's  method.  His  article  (weigh- 
ing the  cuprous  oxid  found)  also  includes  his  improvement^  upon  the  cuprous 
oxid  method,  Prager's  method  ^  (transforming  the  cuprous  oxid  to  cupric  oxid  and 
then  weighing),  and  Volhard's  estimation  of  cuprous  oxid  as  cyanid.  Pfliiger 
recommends  an  appropriate  modification  of  the  asbestos  filter.  (See  p.  439  of  the 
first-mentioned  article.) 

Ambiihl  ^  has  more  recently  demonstrated  that  a  more  practical  method  is  to 
omit  the  reduction  of  the  cuprous  oxid  to  copper,  which  Allihn  recommends,  and 
to  wash  the  cuprous  oxid  immediately  with  hot  water,  alcohol,  and  ether,  and  then 
to  weigh  it  after  having  dried  it  for  an  hour  at  98°  C.  to  a  constant  weight.     From 

1  Arch.  f.  d.  gesamte  Physiol,  vol.  Ixix.,  1898.        ^   ^  Cf.  Ibid.,  vol.  Ixvi.,  1897. 
^  Cheraiker-Zeitumj,  vol.  xxi.,  I.  Sem,  p.  137. 


512 


URINARY  EXAMINATION. 


this  the  corresponding  amount  of  sugar  can  be  calculated.  According  to  Ambiihl's 
table,  the  difference  in  the  amount  of  sugar  found  by  his  method  and  that  of 
Allihn's  ordinarily  amounts  to  less  than  0.1  per  cent.  Multiplying  the  amount 
of  cuprous  oxid  (Ambiihl's  method)  by  0. 888  will  give  the  corresponding  weight 
of  copper,  and  then  Allihn's  table  can  be  employed  to  estimate  the  corresponding 
amount  of  sugar. 


Copper 
(milligrams). 

10  .  . 

20  .  . 

30  .  . 

40  .  . 

50  .  . 

60  .  . 

70  .  . 

80  -  . 

90  .  . 

100  .  . 

110  .  . 

120  .  . 

130  .  . 

140  .  . 

150  .  . 

160  .  . 

170  .  . 

180  .  . 

190  .  . 

200  .  . 

210  .  . 

220  .  - 

230  .  . 

240  .  . 


Dextrose 
(m.iUigrams) 

.       6.1 

.     11.0 

.  16.0 
.    .    20.9 

.    25.9 

.    30.8 

-    35.8 

.  40.8 
,  .  45.9 
,  .  50.9 
,    .    50.0 

.  61.1 
,  .  66.2 
,  .  71.3 
.  .  76.5 
,  .  81.7 
,  .  86.9 
,  .  92.1 
,  .  97.3 
,  .  102.6 
,  .  107.7 
.  .  113.2 
,  .  118.5 
,    .  123.9 


Copper  Dextrose 

(milligrams),  (milligrams). 

250 129.2 

260 134.6 

270 140.0 

280 144.5 

290 151.0 

300 156.5 

310 162.0 

320 167.5 

330 173.1 

340 178.7 

350 184.3 

360 190.0 

370 195.7 

380 201.4 

390 207.1. 

400 212.9 

410 218.7 

420 224.5 

430 230.4 

440 236.3 

450 242.2 

460 248.1 

463 249.9 


COLORIMETRIC  ESTIMATION  OF  DEXTROSE. 

Because  of  the  blue  color  peculiar  to  combinations  of  dextrose  in  alkaline 
solution  with  copper,  and  the  blue  color  of  copper  combinations  in  general,  the 
writer  has  made  an  effort  to  utilize  this  color  in  one  way  or  another  for  the  pur- 
pose of  estimating  colorimetrically  the  quantity  of  dextrose  in  the  urine.  He 
has  conducted  numerous  experiments,  and  will  briefly  report  the  results. 

A  conceivable  method  is  to  add  to  a  constant  amount  of  sodium  hydroxid  a 
constant  amount  of  copper  sulphate  solution,  which  is  so  chosen  that  the  copper 
is  always  in  excess — i.  e. ,  when,  subsequently,  sugar  containing  urine  is  added, 
the  copper  cannot  be  held  entirely  in  solution,  but  is  sufficient,  in  spite  of  the 
sugar,  to  cause  a  precipitate  of  cupric  hydroxid.  Urine,  suitably  diluted,  if 
necessary,  is  added  in  measured  quantities,  and  the  precipitate  filtered  from  the  deep- 
blue  solution  by  means  of  an  asbestos  filter.  The  intensity  of  the  color  is  deter- 
mined colorimetrically  and  the  quantity  of  the  sugar  estimated  in  this  way.  The 
solution  may  be  diluted  and  compared  with  a  test  solution  of  copper  kept  in  a 
hermetically  sealed  tube.  It  has,  however,  been  proved  that  this  method  is  unre- 
liable. The  intensity  of  the  color  proves  to  be  quite  independent  of  the  amount 
of  sugar  added,  giving  the  impression  that  only  small  quantities  of  sugar  enter 
into  the  blue  combination.  For  instance,  we  found  that  it  was  quite  immaterial 
whether  a  0. 5  or  a  1  per  cent,  solution  of  sugar  was  added  to  the  constant  quantity 
of  sodium  hydrate  and  copper  sulphate. 

Another' method  of  colorimetric  estimation  proved  equally  unreliable.  Copper 
sulphate  solution  is  added  drop  by  drop  from  a  buret  to  a  solution  containing 
equal  parts  of  sodium  hydroxid  and  of  the  urine  to  be  examined  until  the  excess 
of  copper  commenced  to  separate  as  cupric  hydroxid.  The  shade  of  blue  is  esti- 
mated colorimetrically,  but,  just  as  before,  the  intensity  of  the  color  appears  to  be 
quite  independent  of  the  amount  of  sugar.  In  these  experiments  a  0. 5  and  1  per 
cent,  sugar  solutions  hold  in  solution  about  an  equal  amount  of  copper  oxid.     For 


QUANTITATIVE   URINARY  ANALYSIS.  513 

this  reason  one  may  not  draw  conclusions  as  to  the  quantity  of  sugar  contained 
in  the  urine  from  the  volume  of  copper  sulphate  solution  necessary  to  produce 
cloudiness. 

One  might  endeavor  to  utilize  the  reduction  test  colorimetrically.  After  per- 
forming the  reduction  (Soxhlet-Allihn  p.  510)  and  filtering  off  the  suboxid 
the  quantity  of  non-reduced  copper  in  the  filtrate  might  be  estimated  colori- 
metrically instead  of  iodometrically.  Even  this  method  is  not  practical,  for  we 
found  that  the  color-intensity  of  Fehling's  solution  with  constant  quantities  of 
alkali  and  Eochelle  salt  does  not  run  parallel  with  the  amount  of  copper  con- 
tained. 

However,  the  following  method  of  utilizing  the  reduction  test  colorimetrically 
gives  approximate  results.  The  test  is  the  same  as  Soxhlet-Allihn's,  up  to  the 
filtering  off  of  the  reduced  suboxid,  for  iodometric  estimation.  The  cuprous  oxid 
or  the  reduced  copper  is  not  determined  by  weighing,  but  nitric  acid  is  poured  on 
the  asbestos  filter  until  the  red  oxid  is  dissolved.  Water  is  next  poured  over  the 
filter,  and  the  quantity  of  copper  contained  in  the  solution  estimated  colorimetri- 
cally by  comparing  with  a  copjDer  solution  of  known  strength.  We  began  by 
using  a  solution  of  copper  nitrate,  so  as  to  have  exactly  comparable  conditions. 
We  found,  however,  that  its  color  was  exactly  that  of  a  copper  sulphate  solution 
containing  an  equal  amount  of  copper,  and  so  have  since  used  the  copper  sulphate 
solution  utilized  in  preparing  Fehling's  solution.^  In  two  graduated  cylinders  of 
equal  diameter  are  placed  respectively  some  copper  sulphate  solution  and  an  equal 
volume  of  the  nitric  acid  solution  of  cuprous  oxid.  Water  is  then  added  to  the 
darker  of  the  two  solutions  until  the  shade  of  color  of  the  two  is  the  same.  The 
amount  of  copper  contained  in  the  two  solutions  is  then  proportional  to  their 
volumes,  so  that  it  becomes  possible  to  estimate  not  only  the  amount  of  copj^er 
reduced,  but  also  the  amount  of  sugar  in  the  urine,  inasmuch  as  we  know  just  how 
much  dextrose  corresponds  to  each  cubic  centimeter  of  the  copper  sulphate  solu- 
tion. This  method  of  employing  graduated  cylinders  only,  and  without  accurate 
colorimetric  apparatus,  gives  only  approximate  values,  which  are  far  less  accurate 
than  the  results  obtained  by  weighing  the  copper  or  cuprous  oxid  or  by  iodo- 
metric titration.  The  practising  physician,  however,  who  is  not  familar  with  the 
technic  of  the  more  accurate  methods,  and  who  desires  a  method  more  raj^id  than 
the  fermentation  test,  may  obtain  with  this  method  fairly  satisfactory  approxi- 
mate results.  By  using  accurate  colorimetric  apparatus,  the  correctness  of  the 
values  obtained  is  much  greater. 

QUANTITATIVE  FERMENTATION  TESTS  FOR  DEXTROSE. 

Upon  the  addition  of  yeast,  dextrose  possesses  the  property  of  fer- 
mentation— i.  e.,  of  splitting  into  alcohol  and  carbon  dioxid.  Three 
tests  based  upon  three  different  results  of  this  property  have  been 
devised  to  determine  the  quantity  of  sugar  in  urine. 

Robert's  Quantitative  Areometric  or  Densimetric  Test. 
— This  is  based  upon  the  fact  that  fermentation  considerably  diminishes 
the  high  specific  gravity  of  sugar  containing  urine.  From  this  differ- 
ence in  specific  gravity  before  and  after  fermentation  the  percentage  of 
sugar  may  be  determined. 

The  technic  of  the  test  is  as  follows  :  The  specific  gravity  of  the 
diabetic  urine  is  estimated  in  the  ordinary  way.  A  piece  of  compressed 
yeast  (not  containing  sugar,  or,  if  so,  washed  out  with  water)  the  size 
of  a  hazelnut  is  then  added  to  a  definite  amount  of  urine  (about  100 
CO.  are  sufficient  for  testing  the  specific  gravity  readily).     The  mixture 

^  This  is  explained  by  the  assumption  that  the  color  is  dependent  only  on  the  copper 
ion  which  is  present  in  equal  quantities,  or,  at  least,  in  equal  dissociation  in  both  solu- 
tions. 

.^3 


514  URINARY  EXAMINATION. 

is  shaken  gently,  loosely  covered  with  a  piece  of  paper  or  an  inverted 
beaker,  and  allowed  to  remain  at  the  room  temperature  for  twent}^-four 
to  thirty-six  hours.  When  fermentation  is  complete,  the  yeast  will 
settle  to  the  bottom,  the  foam  will  no  longer  form  and  the  fluid  will 
become  clear  above.  To  be  perfectly  sure  that  the  fermentation  is  com- 
pleted, Trommer's  test  can  be  employed.  The  specific  gravity  of  the 
completely  fermented  urine  is  then  determined.  If  the  yeast  which  has 
settled  to  the  bottom  is  stirred  up,  the  urine  must  first  be  filtered.  If 
the  difference  between  the  two  specific-gravity  estimations  (before  and 
after  fermentation j  is  multiplied  by  the  empirical  number  0.230,  the 
product  equals  the  percentage  of  the  sugar  contained  in  the  urine.  Com- 
parative estimation  with  other  methods  has  shown  that  a  difference  in 
density  of  B  corresponds  to  a  sugar  content  of  0.230  per  cent.;  conse- 
quently a  difference  in  density  of  D  will  correspond  to  a  sugar-content  of 
D  X  0.230  per  cent.  If  a  very  accurate  estimation  is  necessary,  we 
must  determine  the  temperature  of  the  fluid  before  and  after  fermenta- 
tion, and  if  they  are  not  equal  must  make  a  correction.  If  the  tempera- 
ture is  higher  after  fermentation  than  before,  one-third  of  a  degree  of 
the  urinometer  scale  must  be  added  to  the  specific  gravity  determined 
after  fermentation  for  each  degree  of  temperature.  If  the  temperature 
after  is  lower  than  before  fermentation  a  similar  deduction  must  be 
made.  The  urinometer  should  be  very  accurate,  with  subdivisions  from 
1000  to  1050,  and  sufficiently  wide  apart  for  careful  reading;  the 
urinometer  glass  of  good  size,  so  that  the  amount  of  urine  is  considerable. 
An  excellent  plan  is  to  employ  one  urinometer  for  densities  between 
1000  to  1025,  and  a  second  for  those  between  1025  to  1050.  Many 
authors  have  proved  that  this  method  is  sufficiently  accurate  for  clinical 
purposes  (up  to  0.1  per  cent.),  although  it  has  been  often  questioned,^  and 
certainly  it  is  so  simple  as  to  be  very  practical  for  the  ordinary  physician. 
The  diminution  in  specific  gravity  can  be  determined  directly  with- 
out the  tise  of  au  urinometer  by  weighing  a  measured  quantity  of  urine 
upon  an  ordinary  apothecary's  hand-scale. 

Quantitative  Gas-volumetric  Fermentatioii  Test. — This  metliod  is  based 
upon  the  fact  that  the  amount  of  sugar  in  urine  can  be  computed  by  measuring 
the  volume  of  the  carbon  dioxid  which  is  evolved  by  fermentation.  To  obtain 
useful  results  with  this  method,  the  volume  of  the  carbon  dioxid  produced  in  the 
eudiometer  tube  must  be  read  off  with  all  the  precautions  necessary  in  gas-volu- 
metric analyses — /.  e.  with  consideration  of  the  barometric  pressure,  the  tempera- 
ture, the  tension  of  the  water  vapor,  the  weight  of  the  fluid  shutting  off"  the  gas  in 
the  eudiometer  tube,  etc.  The  gas,  too,  must  be  measm-ed  enclosed  in  mercury, 
on  account  of  the  solubility  of  carbonic  acid  in  water.  The  so-called  idiopathic 
fermentation  of  the  yeast  renders  the  accuracy  very  questionable,  and,  in  any 
event,  the  process  is  too  complicated  for  the  ordinary  practitioner.  Einhorn's 
attempt  to  simplify  the  method  for  the  practising  physician  the  author  regards  as 
a  failure. 

[AVe  must  disagree  with  the  author  in  this  statement.  The  results 
obtained  in  this  country  with  Einhorn's  saccharometer  have  been  found 

1  PflUger's  Archiv,  vol.  xxxiii.,  1884,  p.  211 ;  vol.  xxxvii.,  1885,  p.  479.  Lohnstein, 
Rerlin.  klin.  WocL,  1896,  No.  6,  p.  120. 


QUANTITATIVE   URINARY  ANALYSIS. 


515 


to  be  sufficiently  accurate  to  warrant  the  widespread  and  general  use  of 
the  apparatus.  Of  course,  when  the  fermentation  method  is  employed 
with  any  modification,  only  relative,  and  not  absolute,  amounts  can  be 
expected.  The  introduction  of  physical  details  into  the  procedure  is  an 
approach  at  accuracy  not  warranted,  on  account  of  the  basic  inaccuracy 
of  the  general  method. 

Einhorn's  saccharometer  is  shown  in  Fig.  175.  A  determination 
with  this  instrument  is  performed  as  follows  :  One  gram  of  yeast  {-^  of 
the  ordinary  cake  of  compressed  yeast  is 
about  equal  to  a  gram)  is  carefully  shaken 
with  10  c.c.  of  the  urine  to  be  examined, 
and  the  mixture  is  poured  into  the  bulb  and 
upright  tube,  completely  filling  the  latter. 
No  bubbles  of  air  must  be  allowed  to  re- 
main at  the  top  of  this  tube,  nor  should  any 
collect  there  within  the  first  few  minutes  after 
the  filling  of  the  apparatus.  It  is  always 
advisable  to  make  a  control  test  with  normal 
urine  or  with  water.  The  apparatus  is  then 
allowed  to  stand  at  30°  C.  for  twelve  hours, 
after  which  a  reading  on  the  graduation  must 
be  made.  The  scale  is  calibrated  directly 
into  percentages  of  sugar  (dextrose)  in  the 
urine.  It  must  be  emphasized  that  the  total 
volume  of  the  twenty-four-hour  excretion  of 
urine  must  be  taken  into  consideration  in  order  to  calculate  the  quantity 
of  sugar  eliminated  in  the  twenty-four  hours.  Percentage  results  are  of 
no  value  as  aids  to  diagnosis. — H.  C.  J.] 

Lohnstein's  Accurate  Fermentation  Saccharometer.^ — Lohnstein's  Accu- 
rate Fermentation  Saccharometer  is  constructed  upon  manometric  principles, 
measuring  the  pressure  produced  by  the  development  of  the  carbonic  acid.  Its 
only  disadvantage  is  that  one  of  its  parts  cannot  be  regulated  by  the  experimenter, 
who  is  consequently  dependent  upon  the  maker  of  the  instrument.  The  writer 
will  omit  a  description  of  the  saccharometer.  It  is  easily  used,  and  is  praised  by 
many  authors  as  an  accurate  instrument. 

The  presence  of  proteid  in  the  urine  does  not  in  any  way  disturb  the 
technic  or  accuracy  of  the  fermentation  tests.  This  is  a  great  advantage, 
because  with  most  other  methods  of  determining  the  amount  of  sugar 
the  urine  must  be  first  freed  of  proteid. 

Compressed  yeast  is  employed  so  universally  now  throughout  America 
that  it  seems  hardly  necessary  to  suggest  any  substitute. 

POLARIMETRIC   ESTIMATION   OF   DEXTROSE. 

The  polarimetric  estimation  of  dextrose  is  probably  the  most  convenient  of 
all.  It  does,  however,  require  a  rather  expensive  apparatus,  and  it  fails  to  estimate 
very  small  quantities.  Almost  any  of  the  polariscopes  are  good  enough,  but  the 
author  especially  recommends  Wild's  polaristrobometer.     The  principle,  which 

1  Allg.  med.  Centralzeit.,  1899,  No.  101,  1900,  No.  30,/. 


Fig.  175.— Einhorn's  saccha- 
rometer. 


516  URINARY  EXAMINATION. 

is  the  same  with  all  polariscopes,  depends  on  the  fact  that  a  solution  of  dex- 
trose has  the  power  to  turn  the  plane  of  polarized  light  to  the  right.  The  angle 
of  deflection  is  proportionate  to  the  amount  of  sugar  in  the  solution.  It  is 
known  that  when  a  ray  of  polarized  light  is  taken  up  by  an  analyzing  Nicol 
jjrism,  the  portion  of  light  which  passes  through  the  analyzing  Nicol  varies 
decidedly  according  to  the  position  of  the  Nicol  relative  to  the  plane  of  vibration 
of  the  polarized  ray  of  light.  If  the  plane  of  vibration  of  the  analyzing  Nicol  is 
parallel  to  that  of  the  i^olarized  ray  of  light,  the  maximum  amount  of  light  will 
be  transmitted  ;  if  at  right  angles  to  it,  the  minimum  of  light.  If  the  position  of 
the  analyzing  Nicol  is  now  determined  for  this  maximum  or  minimum,  then  the 
interposition  of  an  optically  active  substance — e.  g.,  a  solution  of  dextrose — will 
rotate  the  plane  of  the  polarization  of  the  ray  of  light  with  relation  to  the 
analyzing  Nicol.  Then  to  determine  again  a  maximum  or  minimum  of  light 
intensity,  the  Nicol  itself  must  be  rotated  through  a  certain  angle.  The  size 
of  this  angle  will  be  proi^ortional  to  the  amount  of  the  interposed  substance — e.  g. , 
sugar  ;  this  amount  can  therefore  be  calculated  from  the  angle  through  which  it 
is  necessary  to  rotate  the  Nicol  to  produce  the  maximum  or  minimum  of  light. 
All  polariscopes  constructed  for  quantitative  analysis  depend  upon  this  j)rinciple. 
Their  only  difierences  dei^end  upon  the  employment  of  various  optical  contri- 
vances in  order  to  facilitate  the  determination  of  the  position  of  the  planes  of 
vibrations  to  each  other — e.  g.,  the  interi^osition  of  doubly  refracting  bodies, 
peculiarly  ground  plates  of  quartz,  etc.  They  produce  peculiar  optical  appear- 
ances, according  to  the  position  of  the  Nicol,  colors,  stripes,  etc. 

Wild's  instrument  uses,  as  an  indicator  of  the  position  of  the  planes  of  vibra- 
tion, the  system  of  parallel  dark  bands  which,  in  a  homogeneous  polarized  light 
(sodium  flame),  are  made  by  two  crossed  quartz  plates  cut  at  an  angle  of  45°  to  the 
axis.  The  advantage  of  homogeneous  light  and  parallel  bands  without  color,  which 
appear  simply  dark  upon  a  light  background,  is  that  the  test  depends  upon  the 
examiner's  sensibility  to  light  alone,  and  not  to  color.  The  test  with  other 
instruments — e.  g. ,  Soleil- Ventzke'  s — depends  upon  the  sensibility  of  the  eyes  to 
color.  Fig.  176  shows  Wild's  instrument.  The  analyzing  Nicol  prism  and  the 
quartz  plates  are  set  in  the  tube  a  c,  and  the  polarizing  Nicol  prism  in  the  tube  d  e. 
In  looking  through  the  instrument,  in  a  dark  room,  from  a  to  the  sodium  flame  at 
b,  with  the  Nicols  parallel  and  crossed,  the  parallel  bands  will  appear  upon  the 
bright  background  of  the  field  of  vision  (Fig.  176,  IV.).  If  one  of  the  Nicols  is 
rotated  45°  by  means  of  the  screw  /,  the  bands  will  disappear ;  further  rotation 
will  bring  them  back. 

It  should  be  noted  that  Pfister  and  Streit,  of  Bern,  are  now  supplying  Wild' s 
instrument  with  a  number  of  marked  improvements  which  increase  its  accuracy, 
and  make  it  possible  by  employing  the  so-called  half-shadow  principle  to  use 
a  non-homogeneous  strong  light,  and  under  some  circumstances  to  omit  entirely 
decolorizing  the  urine. 

To  estimate  the  amount  of  dextrose  by  polarization,  50  c.c.  of  urine  are  decol- 
orized by  shaking  with  about  i  of  this  volume  of  the  best  animal  charcoal  and  then 
filtering.  If  the  urine  is  dark-colored  it  must  sometimes  be  allowed  to  stand  for 
several  hours  with  the  animal  charcoal,  during  which  time  it  is  fi-equently  shaken  ; 
or  it  may  be  necessary  to  boil  the  urine  containing  the  charcoal  for  a  brief  period. 
The  decolorization  should  be  complete.  As  Spath  fears  that  some  of  the  dextrose 
may  be  absorbed  by  the  charcoal,  he  recommends  the  following  method  of  Patein 
and  Dufau  for  decolorization  of  the  urine  :  A  solution  of  mercuric  nitrate  is  pre- 
pared by  dissolving  200  gm.  of  acid  nitrate  of  mercury  in  500  to  600  gm.  of 
water,  and  sodium  hydroxid  is  added  until  a  slight  precipitate  results.  Sufiicient 
water  is  added  to  bring  the  quantity  up  to  1  liter,  and  the  mixture  is  filtered. 
Small  quantities  of  this  solution  are  added  to  50  c.c.  of  urine  until  no  further 
precipitation  occurs  ;  a  dilute  solution  of  sodium  hydroxid  is  added  drop  by  drop 
until  the  reaction  of  the  mixture  is  neutral  or,  at  most,  feebly  alkaline  ;  the  quantity 
is  brought  up  to  100  c.c.  by  adding  sufficient  water  ;  and  the  mixture  is  filtered. 
No  precipitate  should  be  produced  by  the  addition  of  sodium  hydroxid  to  the 
filtrate. 


QUANTITATIVE    URINARY  ANALYSIS. 


517 


m\ 


II. 


IV. 


Fig.  176.— Wild's  polaristrobometer. 


518 


URINARY  EXAMINATION. 


A  metal  tube  (200  mm.long)  (Fig.  176,  II.) ,  which  can  be  closed  at  both  ends  with 
parallel  plain  glass  disks  and  metal  caps,  is  filled  with  the  decolorized  urine.  We 
must  be  careful  not  to  include  any  air  bubbles,  and  not  to  press  the  glass  plates  by 
screwing  the  metal  caps  too  hard,  because  under  pressure  the  glass  becomes  doubly 
refractive,  and  the  dark  bands  will  not  disappear  with  any  position  of  the  Nicol. 
When  so  arranged  the  tube  will  contain  a  layer  of  urine  exactly  200  nmi.  thick. 
The  instrument  is  adjusted  with  a  sodium  flame  in  a  dark  room  so  that  the  par- 
allel bands  absolutely  disappear,  and  the  tube  which  contains  the  urine  is  then  set 
upon  the  rest  c,  d.  If  the  urine  contains  sugar  the  bands  will  immediately  reappear. 
They  are  then  made  to  disappear  by  rotating  the  polarization  plane  with  the 
polarizing  Nicol  by  means  of  the  screw/.  At  the  moment  when  they  disap- 
pear, the  size  of  the  angle  through  which  the  Nicol  prism  has  been  rotated  is 
read  off  through  the  telescope  g  h,  upon  the  scale  i,  by  means  of  the  vernier  k. 
The  gas  flame  at  I  serves  to  illuminate  the  scale.  When  the  amount  of  sugar  con- 
tained is  very  great,  the  tube  III.  is  substituted  for  tube  II.  In  the  latter,  one  of 
the  parallel  glass  disks  is  placed  at  M,  so  that  the  thickness  of  the  urine  is  M  m — 
i.  e.,  100  mm.  The  part  Mo  is  simply  an  empty  continuation  of  the  tube  necessary 
for  its  adjustment.  The  angle  of  rotation  is  read  off"  and  the  amount  of  sugar  in 
tenths  of  1  per  cent,  calculated  directly  from  the  following  table  : 


Angle  of  rotation. 


1  degrees 

2  " 

3  " 

4  " 

5  " 

6  " 

7  " 

8  " 

9  " 
10  " 


Thickness  of  urine  layer,  Thickness  of  urine  layer, 

100  mm.  (length  of  tube).  200  mm.  (length  of  tube). 

1.984  per  cent,  dextrose 992  per  cent,  dextrose. 


.968 
.  5.952 
.  7.936 
.  9.920 
.  11.904 
.  13.888 
.  15.872 
.  17.856 
.  19.840 


1.982 
2.976 
3.968 
4.960 
5.952 
6.944 
7.936 


9.920 


The  scale  of  the  instrument  is  not  graduated  in  minutes  and  seconds,  but  in 
tenths  of  degrees.  Hence,  the  figures  in  the  above  table  indicating  the  amounts 
of  sugar  corresponding  to  each  degree  can  be  used  directly  to  express  the  amounts 
of  sugar  corresponding  to  tenths  of  degrees  by  simply  moving  the  decimal  point 
one  place  to  the  left.  If,  for  instance,  8°  rotation  with  a  layer  100  mm.  thick 
corresponds  to  5.952  per  cent,  of  dextrose,  then  0.3°  will  correspond  to  .5952  per 
cent.  The  calculation  then  becomes  extremely  easy — e.  g.,  if  the  rotation  equals 
3.2°, 

3.0°  =  5.952    per  cent. 

0.2°  =    .3968       " 

3.2°  =  6.3488  per  cent. 

The  polarimetric  estimation  of  the  percentage  of  sugar  can  be,  therefore,  very 
speedily  performed. 

Proteids,  contrary  to  dextrose,  are  levorotatory  ;  hence,  to  obtain  correct  results 
with  albuminous  diabetic  urine  (see  p.  463  et  seq. ),  the  proteid  must  first  be 
removed.  Polarimetric  estimation  of  sugar  is  accurate  to  about  0.5  per  cent., 
w^hich  suffices  for  all  practical  j^urposes,  although  results  by  means  of  the  areo- 
metric  fermentation  test  have  a  still  narrower  limit  of  error.  With  the  polari- 
metric method,  mistakes  are  apt  to  occur,  due  to  the  occurrence  in  the  urine  of 
levogyrate  substances  (levulose,  combined  glycuronates,  and  /3-oxybutyric  acid). 


QUANTITATIVE  DETERMINATION  OF  UREA. 

Normal  human  urine  contains  up  to  4  per  cent,  of  urea.     The  aver- 
age amount  of  urea   excreted   in   twenty-four   hour.s  ^   for  a   man  on  a 
mixed  diet  is  about  33  gm.,  varying  between  24  and  40,  with  starva- 
1  Vierordt,  Daten  und  Tabellen,  1888. 


QUANTITATIVE  URINARY  ANALYSIS.  519 

tion  and  non-nitrogenous  diet,  15  to  20  gm.  Women  excrete  from  20 
to  32  gm.  Upon  a  very  rich  proteid  diet  even  as  much  as  100  gm. 
has  been  excreted.  Quantitative  estimations  of  urea  are  most  essential 
in  all  metabolic  investigations. 

The  urea  estimation  may  also  be  used  to  test  the  capability  of  complete  diges- 
tion— e.  g.,  a  very  rich  proteid  diet  is  ingested  for  one  day  by  an  individual 
in  a  condition  of  approximate  nitrogenous  equilibrium.  We  then  estimate  the 
total  amount  of  urea  for  that  day  and  the  day  following,  and  determine  whether 
it  is  excreted  in  an  amount  proportionate  to  the  ingested  food.  By  far  the  greater 
part  of  the  nitrogen  introduced  in  the  form  of  proteid  is  eliminated  as  urea,  and 
at  most  only  a  small  amount  of  proteid  will  be  stored  up  in  one  day  ;  hence, 
nearly  the  whole  of  the  ingested  nitrogen  must  appear  as  urea  in  the  urine  of  the 
particular  day,  and  perhaps  of  the  following,  provided  proteid  food  has  been  well 
utilized. 

Following  the  suggestion  of  F.  Hirschfeld,  a  patient  ingests  during  one  day  a 
test  diet  of  500  gm.  of  meat  (106.25  gm.  of  proteid),  8  eggs  (48  gm.  of  proteid), 
and  200  gm.  of  bread  (18  gm.  of  proteid),  or  a  total  of  172.25  gm.  of  proteid.  If 
the  proteid  is  well  utilized  the  patient  will  excrete  at  least  59  gm.  of  urea  (27. 5  gm. 
of  nitrogen).  If  he  does  not  not  excrete  as  much  as  that  the  utilization  is  incom- 
plete. Hirschfeld  considers  such  a  condition  of  insufficient  utilization  character- 
istic of  certain  cases  of  diabetes  mellitus,  and  is  inclined  to  attribute  it  to  some 
functional  disturbance  of  the  pancreas.  As  a  consequence  of  the  slight  elimi- 
nation of  urea,  such  cases  are  usually  supposed  not  to  present  any  increase  in 
the  quantity  of  urine. 

ESTIMATION  OF  THE  AMOUNT  OF  UREA  BY  MEANS  OF  THE  SPECIFIC 
GRAVITY  OF  THE  URINE. 

Urea  affects  the  specific  gravity  of  urine  more  than  any  other  con- 
stitutuent ;  hence,  the  specific  gravity  of  the  urine  will  furnish  an 
approximate  measure  of  the  amount  of  urea,  provided,  of  course,  that 
sugar  is  absent.  Experience  has  shown  that  a  specific  gravity  of  1014 
corresponds  to  about  1  per  cent,  of  urea;  of  1014  to  1020,  to  about 
1.5  per  cent. ;  of  1020  to  1024  to  about  2.25  per  cent.  ;  of  1028,  to 
about  3  per  cent.  This  estimate  must  be  modified  in  fever  and  in 
cachexia,  in  both  of  which  the  chlorid  excretion  is  diminished. 

If  sugar  is  present,  it  must  first  be  removed  by  fermentation  before  we  can 
judge  of  the  amount  of  urea  from  the  specific  gravity.  In  such  an  event  it 
is  better  at  the  same  time  to  employ  the  areometric  method  for  the  estimation 
of  sugar  (p.  513  et  seq.),  and  then  to  recalculate  the  specific  gravity  found 
after  fermentation,  since  the  alcohol  lowers  this  to  some  extent.  The  degree  in 
which  the  specific  gravity  is  thus  lowered  can  be  best  determined  by  calculating 
the  amount  of  alcohol  from  the  result  of  the  areometric  estimation  of  sugar. 
Eemembering  that  approximately  equal  amounts  by  weight  of  alcohol  and  car- 
bon dioxid  are  produced  in  the  fermentation  of  dextrose,  and  having  already  deter- 
mined the  percentage  of  dextrose,  we  can  easily  get  the  amount  of  alcohol  in  the 
fermented  urine,  for  it  will  equal  about  half  the  amount  of  sugar  found — e.  g. ,  after 
fermentation,  approximately  a  1.5  per  cent,  solution  of  alcohol  will  result  from  a 
diabetic  urine  containing  3  per  cent,  of  dextrose.  According  to  Hirschfeld  ^  the 
following  specific  gravities  apply  to  watery  solutions  of  alcohol  at  15°  C.  (water  = 
1000):  1  per  cent,  998.5  ;  2  per  cent.,  997;  3  per  cent,  995.6;  4  percent, 
994.2.  The  specific  gravity  of  the  urine  is  thus  diminished  about  1.5  for  every 
per  cent,  of  alcohol  in  solution.  Therefore  the  specific  gravity  of  the  fermented 
urine  must  be  increased  by  1.5  for  every  per  cent,  of  alcohol  contained  before  we 
can  estimate  the  urea  by  the  above  method. 

1  Zeits.f.  Mm.  Med.,  1891,  vol.  xix.,  p.  338. 


520 


URINARY  EXAMINATION. 


LIEBIG'S  METHOD  FOR  UREA  BY  TITRATION. 

Liebig  precipitates  the  urea,  in  the  form  of  urea  mercuric  nitrate,  by  means 
of  a  solution  of  mercuric  nitrate.  In  its  original  form  the  method  is  very  simple 
and  convenient,  but  unless  performed  very  carefully  many  errors  may  arise,  and 
even  with  the  greatest  care  a  number  of  corrections  should  be  made.      On  account 

of  these  difficulties  several  modifications  have 
been  suggested,  all  of  which  furnish  better  re- 
sults, but  which  are  more  complicated  and  re- 
quire more  technical  skill  than  the  original 
process.  As  a  matter  of  fact,  moreover,  Lie- 
big's  method  has  been  abandoned  because  it 
does  not  estimate  the  amount  of  urea  in  the 
I A  urine,  but  rather  the  approximate  amount  of 

total  nitrogen  (see  p.  526). 


KNOP  -  HUFNER'S     METHOD     OF 
TING  THE  UREA. 


ESTIMA- 


This  is  not  only  the  simplest,  but  also  the 
most  accurate,  of  all  methods.  It  is  to  be 
recommended  for  clinical  purposes.  It  de- 
pends upon  the  decomposition  of  urea  into 
carbon  dioxid,  water,  and  nitrogen  by  means 
of  a  solution  of  sodium  hypobromite  in  an 
excess  of  sodium  hydroxid.  The  nitrogen 
liberated  from  a  definite  amount  of  urine  is 
measured  volumetrically,  and  from  this  the 
corresponding  amount  of  urea  is  calculated. 
The  carbon  dioxid  is  absorbed  by  the  excess 
of  sodium  hydroxid.  For  veiy  accurate  anal- 
ysis the  barometer  and  temperature  must  be 
considered.  Other  nitrogenous  constituents- 
of  the  ui'ine  (uric  acid,  kreatin,  etc. )  are  par- 
tially broken  up  at  the  same  time,  liberating 
nitrogen  ;  hence,  the  method  is  not  absolutely 
accurate.  Nevertheless,  if  the  j^roteid  is  first 
removed,  these  other  constituents  will  not  add 
much  to  the  figures  for  urea. 

Hiifher's  aj^j^aratus,  represented  in  Fig. 
177,  has  been  modified  again  and  again  to 
more  or  less  advantage.  It  consists  of  three 
separate  parts  : 

1.  The  dilated  glass  receptacle,  C,  con- 
nected by  means  of  a  ground-glass  stopjaer 
with  a  smaller  one,  D,  which  holds  fi-om  6 
to  7  c.c. 

2.  The  bell-shaped  glass  vessel,  B,  open  at. 
both  ends,  and  connected  with  the  upper  end 
of  C  by  means  of  a  perforated  hard-rubber 
stopper. 

3.  The  eudiometer  tube.  A,  divided  into 
centimeters  and  fractions,  to  be  placed  when  in 
use  within  vessel  B  over  the  upper  end  of  C. 

Preparation  of  the  sodium  hypobromite  solution  :  70  c.c.  of  a  30  per  cent, 
sodium  hydroxid  solution  are  mixed  with  180  c.c.  of  water  and  5  c.c.  of  bromin. 
The  latter  dissolves  with  the  formation  of  sodium  bromid  and  sodium  hypobromite. 

2  NaOH  +  Br^  =  NaBrO  +  H,0  +  NaBr. 

As  soon  as  the  bromin  has  dissolved,  the  reagent  is  ready  for  use.     It  should 


Fig.  177. 


-Hiifner's  apparatus  for  estima- 
tion of  urea. 


QUANTITATIVE   URINARY  ANALYSIS. 


521 


be  freslily  prepared  every  day  or  two,  because  tbe  hypobromite  gradually  becomes 
decomposed.  It  should  also  be  kept  in  a  cool,  dark  place — best  of  all  in  an  ice- 
chest — and  never  employed  when  warm  from  mixing.^ 

Technic  of  the  Method. — The  amount  of  urea  in  the  urine  to  be  examined 
is  first  approximately  estimated  by  the  specific  gravity  (p.  519  et  seq.),  and  then, 
if  necessary,  the  urine  is  diluted  so  that  the  amount  of  urea  present  is  not  above 
1  per  cent.  Five  cubic  centimeters  of  the  urine,  or  of  a  diluted  portion  (when 
necessary),  are  removed  in  a  long,  thin  pipet  and  allowed  to  run  into  the  vessel  D, 
carefully  avoiding  wetting  the  sides  of  C.  In  the  same  pipet  is  then  sucked  up  1 
to  2  c.  c.  of  water,  in  order  to  remove  any  urine  adhering  to  its  sides.  The  recep- 
tacle JD  is  then  filled  with  the  contents  of  the  pipet  exactly  to  the  upper  margin 
of  the  bore  in  the  glass  stopcock.  This  is  now  shut  oflF.  Then  the  vessel  C  is 
filled  to  overflowing  with  the  hypobromite  solution,  and  next  the  vessel  B,  as  well 
as  the  eudiometer  tube,  is  filled  with  concentrated  sodium  chlorid.  The  tube  is 
inverted  over  the  opening  of  the  vessel  C  under  the  level  of  the  liquid  in  B,  its 
opening  having  been  first  closed  with  the  thumb,  and  the  inclusion  of  air  avoided. 
A  is  now  held  in  position  by  the  retort  stand,  which  also  supports  the  other  parts. 
Now,  as  soon  as  the  stopcock  is  opened,  the  heavy  hypobromite  solution  in  C  be- 
comes mixed  with  the  lighter  urine  in  jD,  and  nitrogen  develops  actively.  This 
gas  accumulates  in  the  eudiometer  tube,  gradually  displacing  the  salt  solution. 
The  decomposition  is  complete  in  from  twenty  minutes  to  one-half  hour.  The 
bubbles  adhering  to  the  sides  of  the  vessel  are  then  gently  shaken  into  the  eudi- 
ometer tube,  which  is  closed  under  the  level  of  the  salt  solution  with  the  thumb. 
It  is  then  removed,  and  submerged  as  completely  as  possible,  opened  downward,  in 
a  large  cylinder  filled  with  water  at  the  room  temperature.  After  about  fifteen 
minutes  the  eudiometer  tube  and  its  contents  will  be  at  the  same  temperature  as 
the  surrounding  water.  The  tube  is  then  lifted  far  enough  out  of  the  water  to 
equalize  the  levels  of  the  fluid  inside  and  outside,  and  at  this  moment  the  volume 
of  the  enclosed  nitrogen  is  read  off".  The  temperature  of  the  water  and  the  baro- 
metric pressure  should  also  be  recorded.  The  volume  of  gas  estimated  must  now, 
for  the  purpose  of  calculation,  be  reduced  to  0°  C,  760  mm.  barometric  pressure, 
and  absolute  dryness,  according  to  the  formula  : 

760  (1  +  0.00366  t) 
V  (b  —  w) 
v^  =  Reduced  volume  desired. 
V  =  Volume  read  off". 

b  =  Barometric  pressure  at  the  time  of  reading,  in  mm.  Hg. 
IV  =  Tension  of  water  vapor  at  a  temperature  t,  in  mm.  Hg. 
t  =  Temperature  of  water  at  time  of  reading. 
0.00366  =  CoeflBcient  of  expansion  of  gases  for  1°  C. 
The  values  for  w  corresponding  to  the  temperatures  usually  met  with  are  as 
follows: 


10°  C 9.126 

11°  C 9.751 

12°  C 10.421 

13°  C 11.130 

14°  C 11.882 

15°  C 12.677 

16°  C 13.519 

17°  C 14.009 


18°  C 15.351 

19°  C. 16.345 

20°  C 17.396 

21°  C 18.505 

22°  C 19.675 

23°  C 20.909 

24°  C 22.211 

25°  C 23.582 


^  [The  method  of  preparation  of  the  hypobromite  solution  as  outlined  by  Rice  can 
be  highly  recommended.  Two  solutions  are  necessary,  and  may  be  retained  for  any 
ordinary  length  of  time. 

1.  A  solution  of  125  gm.  of  bromin  and  125  gm.  of  sodium  bromid  in  sufBcient 
water  to  make  the  volume  up  to  1000  c.c. 

2.  A  solution  of  sodium  hydroxid  of  a  specific  gravity  of  1250  (22.5  per  cent.).  To 
prepare  the  hypobromite  for  use,  mix  equal  volumes  of  the  two  solutions,  and  dilute 
with  1^  volumes  of  water. — Ed.] 


522 


URINARY  EXAMINATION. 


One  gram  of  urea  furnislies  354.3  c.c.  of  nitrogen  (a  little  less  than  the 
theoretic  quantity) ;  hence,  the  following  proportion  will  determine  the  amount  of 
urea  {x)  in  the  5  c.c.  of  urine  employed. 


354.3:  \  =  v'  -.x 

X  ^  v' 


354.3  grams. 

The  percentage  of  urea  contained  in  the  urine  can  be  very  easily  determined 
by  multiplying  this  number  by  20.  Of  course,  if  the  urine  was  diluted  before 
the  estimation,  this  dilution  must  also  be  considered. 

The  author  considers  that  Gerrard'  s  ^  improvement  upon  Hiifoer'  s  apparatus 
has  been  shown  to  be  the  most  practical  for  the  practitioner  (Fig.  178). 

A  graduated  glass  tube,  a,  fixed  in  a  wooden  stand,  is  connected  at  the  lower 


Fig.  178.— Gerrard' s  apparatus  for  estimation  of  urea. 


Fig.  179.- 


-Dupri^'s  apparatus  for  esti- 
mating urea. 


end  by  means  of  a  side  projection  and  a  rubber  tube  with  a  vessel,  6,  which  is 
open  at  the  top,  and  at  its  upper  end  with  a  wide-necked  bottle,  d,  by  means  of  a 
perforated  rubber  stopper,  c,  and  a  rubber  tube.  Vessel  h  may  be  raised  or  lowered 
upon  the  graduated  tube  by  the  metal  spring  clamp  e.  The  wide-necked  bottle,  d 
is  filled  with  100  c.c.  of  sodium  hvpobromite  solution;  5  c.c.  of  urine  are  poured 
into  the  small  test  tube,  /,  which  is  carefully  placed  in  bottle  rf,  so  as  to  be,  for 
the  time  being,  protected"  from  the  hypobromite  solution.     The  bottle  is  then  con- 

1  Lancet,  1884,  ii.  p.  952. 


QUANTITATIVE   URINARY  ANALYSIS.  523 

nected  with  the  rest  of  the  apparatus  by  means  of  the  perforated  rubber  stopper 
g  and  tube  gh.  Next,  the  stopper  c  is  removed  and  vessel  a  is  filled  with  water 
up  to  the  zero  mark  of  the  scale.  Of  course,  the  communicating  vessel  b,  which 
has  been  pushed  up  toward  the  top,  also  fills  to  the  same  level.  The  stopper  c  is 
now  replaced.  While  this  is  being  done  the  spring  clamp  ^,  which  closes  the 
rubber  tube  attached  to  the  glass  tube  h,  is  opened  carefiilly  so  that  at  the  moment 
of  replacing  c  there  will  be  no  increase  of  pressure  of  the  air  upon  the  level  of 
the  water.  The  fluid  therefore  remains  at  the  same  level  in  the  communicating 
vessels  a  and  b.  The  spring  clamp  i  is  now  very  carefully  closed  again.  After 
the  apparatus  has  been  connected  in  this  fashion,  the  urine  in  the  little  glass  /  is 
easily  poured  out  into  the  bromin  solution  by  repeatedly  tipping  the  vessel  d. 
The  development  of  gas  follows  immediately.  Bottle  d  is  placed  in  a  large  vessel 
of  water  at  the  room  temperature  (15°  C.)  while  the  development  of  gas  con- 
tinues. To  make  it  sink,  the  bottle  is  fiirnished  with  a  lead  framework,  as  shown 
in  the  picture.  The  object  of  having  the  gas  develop  under  water,  at  the  tem- 
perature of  the  room,  is  to  distribute  the  heat  which  arises  as  the  result  of  the 
chemical  reaction  of  the  hypobromite  solution.  This  heat  will  not  only  influence 
the  decomposition,  but  will  also  increase  the  volume  of  the  liberated  nitrogen  gas. 
We  need  not  correct  the  gas  volume,  since  both  the  gas  and  the  apparatus  may  be 
considered  to  be  at  the  room  temperature  of  15°  C.  The  nitrogen  set  fi-ee  accumu- 
lates in  the  upper  part  of  the  graduated  tube  a,  gradually  elevating  the  level  of 
the  water  in  b.  The  evolution  of  the  gas  may  be  materially  hastened  by  gently 
shaking  the  bottle  d.  When  the  decomposition  is  complete,  the  gas  can  be  put 
under  ordinary  atmospheric  pressure  by  lowering  vessel  b  sufficiently  to  equalize 
the  level  of  the  fluid  in  a  and  b  again.  Then  the  volume  of  the  nitrogen  is 
read  off". 

The  scale  upon  the  English  instrument  indicates  empirically  the  amount  of 
urea  at  room  temperature  and  normal  barometric  pressure  (760  mm.).  Mariott's 
law  can  then  be  made  use  of  to  correct  the  reading  according  to  the  barometric 
pressure — viz. : 


V  and  b  and  v^  and  b^  represent  the  corresjionding  gas  volumes  and  barometric 
pressures.  V  and  v''  may  be  directly  replaced  by  the  amount  of  urea  proportion- 
ate to  them,  so  that  the  formula  then  becomes,  when  h  and  b  represent  the  amounts 
of  urea  corresponding  to  the  barometric  pressures. 

It  is  advisable  to  control  the  empirical  scale  by  adding  a  scale  in  cubic  centi- 
meters on  tube  a.  Then  the  calculation  for  any  temperature  or  barometric  press- 
ure can  be  made  in  the  same  manner  as  with  Hiifiier's  apparatus  (see  p.  521). 
The  same  rules  for  dilution,  of  course,  apply  for  this  apparatus  as  for  Hiifiier's. 

Not  only  is  Gerrard's  instrument  more  compact  than  Hiifiier's,  but  the  gas 
can  be  entirely  evolved  within  a  few  moments  by  shaking  bottle  d. 

The  weak  point  of  the  apparatus  is  the  closure  of  the  upper  end  by  a  stop- 
cock, which  may  easily  allow  of  the  escape  of  gas,  and  consequently  give  rise  to 
an  erroneous  result.  Dupre's  modification  of  Hiifiier's  apparatus  (Fig.  179)  can 
be  thoroughly  recommended,  and  is  the  one  which  is  employed  in  the  author's 
clinic.  The  illustration  should  be  sufficient  without  further  description.  It  differs 
from  Gerrard's  apparatus  in  that  the  reduction  of  the  gas  to  atmospheric  pressure 
is  accomplished  by  moving  the  buret  in  which  the  gas  collects,  and  which  is  sus- 
pended in  a  cylinder  filled  with  water.  In  this  instrument  the  stopcock  at  the 
upper  end  of  the  buret  should  be  carefully  tested,  in  order  to  avoid  losing  any  of 
the  gas. 

[Two  modifications  of  the  method  of  Knop,  which  depends  upon  the  decom- 
position of  the  urea  by  sodium  hypobromite  or  hypochlorite,  have  received  especial 


624 


URINARY  EXAMINATION. 


attention  in  this  country,  and  appear  to  be  sufficiently  accurate  for  relative  values, 
so  that  they  have  been  almost  universally  employed  in  this  determination.  The 
simplest  procedure  is  that  which  makes  use  of  the  apparatus  of  Doremus  (Fig. 
180),  or  the  modification  of  this  by  Hinds  (Fig.  181). 

The  Doremus  ureometer,  as  seen  in  the  figure,  consists  of  a  bulb  with  an 
upright  graduated  tube,  which  can  be  obtained  so  as  to  rest  upon  a  stand.  The 
graduation  reads  in  grams  of  urea  per  cubic  centimeters  of  urine.  When  a  deter- 
mination is  to  be  made,  the  upright  tube  and  about  one-half  to  two-thirds  of  the 
bulb  are  filled  with  the  hypobromite  solution  (for  preparation  see  above,  p.  521). 
Care  must  be  observed  that  no  air  remains  at  the  top  of  the  upright  tube.  The 
1  c.c.  pipet,  which  is  provided  with  a  small  nipple,  is  filled  with  urine  to  the 
mark  (1  c.c),  and  the  tip  carefully  introduced  into  the  bulb  and  as  far  into  the 
bend  as  it  will  go.  The  urine  in  the  pipet  is  then  completely  delivered,  but  cau- 
tion must  be  observed  not  to  expel  any  air  with  it.  The  pipet  is  then  withdrawn, 
and  after  the  evolution  of  the  gas  has  stopped  (fifteen  to  twenty  minutes)  the 
meniscus  of  the  solution  is  read  off"  upon  the  scale.     This  value  multiplied  by  the 


Fig.  180.— Doremus  ureometer. 


Fig.  181. — Hinds'  modification  of  the 
Doremus  ureometer. 


number  of  cubic  centimeters  in  the  twenty-four  hours  will  give  the  daily  excretion 
of  urea  in  grams. 

The  directions  for  using  the  Hind's  modification  are  as  follows  :  The  tube  c 
and  the  lumen  of  the  stopcock  b  are  filled  with  urine  to  be  examined.  Tube  a  is 
then  washed  out  thoroughly  with  water  and  filled  completely  with  the  hypo- 
bromite solution.  The  bulb  attached  to  a  should  contain  enough  of  the  solution 
to  prohibit  the  passage  of  any  air  back  into  tube  a.  A  reading  is  then  made  on 
tube  c,  and  1  c.c.  of  the  urine  is  allowed  to  pass  into  a  by  means  of  the  stopcock 
b  (if  the  urine  is  concentrated,  dilute  with  equal  volume  of  water).  After  all  the 
bubbles  of  gas  have  collected  at  the  top  of  tube  a  a  reading  is  taken.  The 
graduation  corresponds  to  grams  in  1  c.c.  of  urine. 

Another  apparatus  is  that  of  Squibb.  The  chemical  basis  of  this  method  is 
the  same  as  that  of  the  preceding,  but  the  manipulation  is  somewhat  more  com- 
plicated, even  though  accuracy  is  not  increased  (see  Fig.  182).  There  are 
required  two  2-ounce  bottles  (a  and  b),  each  of  which  is  supplied  with  a  well-fitting 
double-bored  rubber  stopper.  One  opening  of  the  stopper  for  a  is  left  open  for 
the  subsequent  introduction  of  a  2  c.  c.  pipet,  closed  at  one  end  with  a  nipple  ; 


QUANTITATIVE   URINARY  ANALYSIS. 


525 


into  the  other  opening  is  put  an  L-shaped  glass  tube,  to  which  is  attached  a  piece 
of  rubber  tubing  c.  One  opening  of  the  stopper  for  b  is  supplied  with  a  straight 
piece  of  glass  tubing,  and  the  other  wdth  an  L-shaped  piece,  which  is  attached  to 
a  rubber  tube.  This  latter  tube  must  be  so  placed  that  the  free  end  just  clears  the 
the  bottom  of  the  graduate  cylinder  g.  This  free  end  is  also  provided  with  a 
glass  plug.     The  operation  is  as  follows  : 

The  bottle  b  is  filled  with  water  at  room  temperature,  and  after  the  rubber 
stopper  with  glass  tubes  has  been  put  in  place  sufficient  water  is  allow  to  escape 
from  the  bottle  into  the  rubber  tube,  to  fill  the  latter  completely.  The  glass 
plug,  e,  is  then  put  into  position,  and  the  bottle  placed  upon  its  side  as  in  the 
figure.  Into  bottle  a  are  put  10  to  15  c.c.  of  the  solution  of  chlorinated  soda  or 
lime  (for  preparation  see  below)  (the  hypobromite  is  also  employed  in  this  appa- 
ratus, but  not  frequently),  and  the  rubber  stopper  for  b  is  screwed  tightly  into 
position  after  the  pipet,  filled  with  urine  up  the  2  c.c.  mark,  has  been  pressed  into 
the  vacant  opening.  The  rubber  tubing  c  is  then  connected  with  the  straight 
glass  tube  emerging  from  the  stopper  of  b,  and  the  glass  plug  removed  fi-om  the 
end  of  tube  d.     A  few  drops  of  water  will  flow  out  of  the  free  end  of  the  tubing, 


Fig.  182.— Squibb's  urea  apparatus  for  the  approximate  estimation  of  urea  in  urine. 

but  the  flow  must  completely  cease  in  a  few  seconds.  This  indicates  that  the 
apparatus  is  tight.  The  empty  graduated  cylinder  must  be  placed  under  the  open 
end  of  tube  d.  Finally  the  urine  in  the  pipet  is  completely  but  careftilly  deliv- 
ered. During  the  operation  the  contents  of  bottle  a  should  be  shaken  from  side 
to  side  in  such  manner  that  no  fluid  can  get  into  the  rubber  tube  c.  Agitation  of 
the  contents  of  a  must  be  continued  as  long  as  bubbles  of  gas  come  over  into 
bottle  b.  This  usually  requires  twenty  to  thirty  minutes.  If,  however,  bottle  a 
is  placed  in  a  water  bath  at  about  35  to  40°  C.,  the  reaction  will  be  more  rapid 
and  complete  in  from  six  to  eight  minutes.  In  the  latter  event  the  bottle  a  must 
be  cooled  down  to  18°  C.  for  about  five  minutes. 

The  nitrogen  gas  which  has  been  evolved  during  the  reaction  has  replaced  its 
own  volume  of  water  in  the  bottle  b.  This  volume  has  escaped  in  the  graduated 
cylinder  g,  and  the  value  can  be  read  off  on  the  graduation  and  referred  to  the 
urea  table  (p.  521) ;  from  this,  and  from  the  volume  of  the  twenty-four-hour  sample, 
can  be  calculated  the  number  of  grams  excreted  in  the  twenty-four  hours  . 

The  solution  of  chlorinated  soda  can  be  prepared  as  follows  :  Shake  20  gm. 
of  chlorinated  lime  (chlorid  of  lime,  bleaching  powders)  in  a  bottle  with  45  c.c.  of 


526  URINARY  EXAMINATION. 

water  until  the  powder  is  thoroughly  disintegrated.  Let  this  settle  a  few  minutes, 
and  then  filter  oiF  the  supernatant  fluid  into  a  flask  having  a  capacity  of  about 
100  c.c.  Wash  the  residue  still  in  the  bottle  with  30  c.c.  of  water,  and  filter  this 
oflF  through  the  same  paper  into  the  same  flask.  Then  dissolve  40  gm.  of  sodium 
carbonate  in  30  c.c.  of  hot  water,  and  add  this  to  the  solution  already  in  the 
flask.  Filter  this  mixture  into  a  100  c.c.  graduated  flask,  and,  after  the  solution 
has  drained  through,  wash  the  precipitate  with  enough  water  to  make  the  volume 
in  the  flask  up  to  exactly  100  c.c.  Ten  to  15  c.c.  of  this  solution  are  sufficient 
for  each  determination. 

The  solution  of  chlorinated  lime  is  prepared  as  follows  :  Shake  40  gm.  of 
chlorid  of  Lime  with  120  c.c.  of  water.  After  allowing  this  to  settle,  filter  the 
supernatant  fluid  off"  into  a  200  c.c.  graduated  flask.  Wash  the  residue,  shake 
with  80  c.c.  of  water,  and  again  filter  into  the  flask  through  the  same  filter 
paper.  After  the  second  portion  has  well  drained,  pour  water  on  to  the  residue 
upon  the  paper  until  the  volume  of  the  solution  in  the  flask  is  just  equal  to  200 
c.c.  Ten  cubic  centimeters  of  this  solution  are  required  for  each  determination. 
It  remains  active  for  a  month. — Ed.] 

ESTIMATION  OF  UREA  BY  SCHONDORFF'S  METHOD. 

The  principle  of  this  method  is  as  follows:  The  urine  is  precipitated  by 
phosphotungstic  acid  containing  hydrochloric  acid,  during  which  the  urea 
remains  in  solution.  The  filtrate  is  then  heated  mth  phosphoric  acid;  ammo- 
nium phosphate  is  formed,  and  the  ammonia  is  freed  from  this  compound  by 
the  addition  of  caustic  potash.  The  ammonia  is  then  removed  by  distillation 
and  determined  by  titration,  as  in  Kjeldahl's  method  (see  below). 

As  the  opinions  in  reference  to  the  value  of  this  method  are  still  very  con- 
tradictory,! it  will  suffice  to  refer  the  reader  to  the  original  work  of  Schondorff" 
{Pfluger's  Archiv.,  vol.  Ixii)  ;  to  Jaksch  Klin.  Diagnostik  innerer  Krankheiten, 
5th  ed. ;  to  Pfaundler,  Zeits.  f.  physiol.  C hemic,  1900,  vol.  xxx.,  and  to  Folin, 
ibid.,  1901,  vol.  xxxii. 

ESTIMATION    OF    THE   AMOUNT    OF   TOTAL   NITROGEN    IN    THE 
URINE  BY  KJELDAHL'S  METHOD. 

Approximate  values  for  the  amount  of  total  nitrogen  in  the  urine  may  be 
obtained  from  the  estimation  of  the  amount  of  urea  (Knop-Hiifner' s  method). * 
In  the  calculation  we  must  assume  that  15  parts  of  urea  contain  7  parts  of 
nitrogen,  and  in  this  calculate  the  amount  of  nitrogen  belonging  to  the  urea 
present.  This  amount  must  then  be  multiplied  empirically  for  normal  urine  by 
1.136,  and  for  fever  urine  by  1.18.  This  will  approximately  furnish  the  amount 
of  total  nitrogen  excreted. 

Liebig's  method,  the  so-called  urea  titration,  also  approximately  estimates 
the  amount  of  total  nitrogen.  The  figures  found  for  the  quantity  of  urea  by  this 
method  are  too  high,  so  that,  in.  fact,  the  nitrogen  obtained  from  the  calculation 
of  the  urea  supposed  to  be  present  really  corresponds  approximately  to  the  total 
nitrogen  contained  in  the  urine. 

For  a  perfectly  exact  estimation  of  the  amount  of  total  nitrogen  in  the  urine, 
Kjeldahl's  method  is  to-day  almost  exclusively  employed.  The  principle  of  the 
method  is  that  the  organic  constituents  of  the  urine  are  destroyed  by  oxidation 
when  the  urine  is  heated  with  concentrated  sulphuric  acid,  and  that  the  nitrogen 
of  those  substances  which  do  not  contain  it  combined  with  oxygen  appears  as 
ammonium  sulphate.  The  urea  is  changed  directly  into  carbon  dioxid  and 
ammonia.  The  nitrogen  is  estimated  by  liberating  the  ammonia  fi-om  the  acid 
solution  mth  pota.ssium  or  sodium  hydroxid,  distilling  it  off",  and  passing  it  into 
a  measured  amount  of  acid.     The  acid  remaining  is  then  titrated  with  an  alkali. 

!  See  Spiith,  Die  chemische  u.  mikroslcopische  Untersuchung  des  Harnes,  2d  ed.,  1903. 
*  Of.  Anleitung  zur  qualitativen  wad  quantitativen  Harnanalyse  von  Neubauer  und  Vogel, 
Keubearbeitet  von  H.  Huppert,  1890,  p.  531. 


QUANTITATIVE   URINARY  ANALYSIS.  527 

The  details  of  the  method,  including  certain  modifications  recommended  by 
Wilfahrt  and  by  Salkowski,  are  as  follows :  The  acid  used  for  oxidizing  pur- 
poses is  a  mixture  of  500  c.  c.  of  concentrated  sulphuric  acid  and  100  gm.  of 
phosphoric  anhydrid.     Pure  sulphuric  acid  may  be  employed,  but  oxidization 

N  .       . 

takes  longer.     It  is  also  necessary  to  have  a  —  oxalic  acid  solution  prepared  by 

^  N 

diluting  the  normal  acid  with  an  equal  amount  of  water.     A  —  solution  of 

sodium  hydroxid  is  also  essential.     This  is  prepared,  according  to  Salkowski,  in 

the  following  manner :  i  Enough  water  is  added  to  80  c.  c.  of  sodium  hydroxid 

solution,   free    from    COj   and    at    1340    specific   gravity,  to    make    the   volume 

1100  c.  c.   This  is  well  stirred  and  a  portion  placed  in  a  buret.      10  c.  c.  of 

N  '   .        . 

the   —oxalic  acid  are  placed  in  a  beaker,  and  a  few  drops  of  rosolic  acid  or 

phenolphthalein  solution  added.     The  sodium  hydroxid  solution  is  added  until 

the  end  reaction  is  reached — i.  e. ,  until  the  mixture  becomes  a  permanent  red. 

The  sodium  hydroxid  must  be  diluted  until  10  c.c.  correspond  to  exactly  10  c.c. 

N 
of  the  —  oxalic  acid  solution.     The  volume  of  water  (x)  to  be  added  is  estimated 

according  to  the  formula :  x  =  — ^  in  which  v  =  the  volume  of  the  sodium 

a 

hydroxid  solution  diluted  (1100  c.c),  and  a  =  the  number  of  c.c.  used  to  bring 

about  the  end  reaction. 

10  c.  c.  of  urine  (or  5  c.c.   of  concentrated)  are  put  into  a  Kjeldahl  flask 

with  round  bottom  and  long  neck,  to  which  are  added  10  c.c.  of  the  sulphuric 

acid  mixture,  after  about  0.4  gm.   of  finely  divided  mercuric    oxid  have  just 

been  placed  in  the  flask.     This  mercury  acts  catalytically  in  aiding  oxidation. 

The  flask  is  next  loosely  closed  with  a  glass  ball,  and  heated  in  a  special  frame 

while  kept  somewhat  tilted.     The  flame  should  not  be  too  high  and  should  be 

applied  until  the  solution  is  colorless.     Even  the  slightest  tinge  of  yellow  suggests 

that  oxidation  is  not  complete  unless  iron  compounds  are  present  in  rather  large 

quantities.     As  a  rule,  it  takes  at  the  most  three  hours  to  complete  the  oxidation. 

The  mixture  is  now  allowed  to  cool,  and  is  poured  into  a  distilling  flask  by  means 

of  a  funnel.     The  digestion-flask  and  the  round  glass  stopper  are  rinsed  with  100 

c.c.  of  water,  which  is  added  to  the  contents  of  the  distillation-flask.     Next  40 

c.c.  of  sodium  hydroxid  solution  of  specific  gravity  1340  are  added  and  (in  order 

to  precipitate  the  mercury,  which  otherwise  would  form  amido  compounds  with 

the  ammonia)  this  is  followed  by  25  c.c.  of  potassium  sulphid  solution  (4  gm.  to 

the  liter).     The  flask  is  now  quickly  connected  with  the  distilling  tube.     This 

tube  passes  through  a  condenser,  and  the  end  is  placed  in  an  Erlenmeyer  flask  of 

N 
about  200  to  300  c.c.  capacity.     This  latter  vessel  contains  20  c.c.  of  the  — 

oxalic  acid,  and  just  enough  water  to  keep  the  end  of  the  condenser  tube  sub- 
merged. 

Distillation  is  continued  until  no  more  ammonia  escapes  and  the  distilled 
steam  no  longer  develops  ammonium  chlorid  fumes,  when  a  glass  rod,  moistened 
with  HCl,  is  held  in  front  of  the  open  end.  This  condition  of  affairs  usually 
obtains  when  about  100  c.c.  of  fluid  have  been  obtained  by  distillation.     Several 

N 
drops  of  a  methyl-orange  or  cyanin  solution  are  now  added  to  the  —  oxalic  acid 

solution  to  act  as  indicator,  and  the  amount  of  contained  ammonia  is  determined 

N 
by  titration  with  an  -—  sodium  hydroxid  solution.     The  amount  of  nitrogen  in 

the  quantity  of  urine  employed  may  then  be  calculated  from  the   amount  of 

N 
ammonia.     The  number  of  cubic  centimeters  of  _-  sodium  hydroxid  solution  used 

^  Prac.  der  physiol.  u.  path.  Chemie,  2d  ed.,  1900. 


528 


URINARY  EXAMINATION. 


is  deducted  from  20  c.c,  and  the  diflference  multiplied  by  7.02  gives  the  number 
of  milligrams  of  nitrogen  in  the  quantity  of  urine  emi^loyed. 

This  test  is  best  performed  with  the  commercial  Kjeldahl  apparatus,  which 
permits  the  oxidation  and  distillation  of  a  number  of  specimens  at  the  same  time. 
This  shortens  very  much  the  amount  of  time  necessary,  especially  as  one  is  usually 
obliged  to  make  a  series  of  tests. 

In  this  form  the  method  is  perhaps  rather  too  complicated  for  clinical  purposes  ; 


Kjeldahl  flasks. 


Condenser. 


Receivers. 


Fig.  183.— Kjeldahl's  apparatus:  a.  Apparatus  for  the  simultaneous  oxidation  of  six  specimens  ; 
6,  apparatus  for  the  simultaneous  distillation  of  six  specimens. 


Henninger^  and  Schonherr's  modification  is  more  practical.  The  amount  of 
ammonia  produced  by  the  destruction  of  the  organic  substances  is  estimated  azo- 
tometrically,  and  the  distillation  is  omitted,  as  in  Knop-Hiifner's  method  of  esti- 
mating urea.  The  ammonia  is  decomposed  by  sodium  hypobromite  solution,  and 
liberated  nitrogen  is  measured  volumetrically. 

The  technic  for  the  procedure  is  as  follows  :  After  the  oxidation  of  5  to  10 

'  Compt.  rend,  de  la  soc.  de  biol.,  1884,  p.  474  ;  Jahresbericht  f.  Thierehemie,  1884,  p. 
205.     O.  Schonherr,  "  Chemikerzeitung  12,  217,"  Chem.  Centralbl.,  1888,  p.  420. 


QUANTITATIVE   URINARY  ANALYSIS.  529 

c.c.  of  urine  according  to  the  method  given  above,  the  solution  is  diluted  with  a 
little  water,  and  partially  neutralized  with  potassium  or  sodium  hydroxid  until  the 
reaction  is  only  faintly  acid,  and  then  the  volume  made  up  to  50  c.  c.  For  azo- 
metric  analysis  we  use  20  c.c.  (corresponding  to  2  or  4  c.c.  of  urine)  of  this  solu- 
tion and  treat  it  exactly  like  the  urine  in  Knop-Hiifner's  method  (p.  520), 
although,  of  course,  the  size  of  the  apparatus  must  be  changed  somewhat.  With 
Gerrard's  or  D  up  re's  modification  this  can  be  accomplished  very  simply  by  select- 
ing a  tube  (Figs.  178  and  179)  which  will  contain  20  c.c.  instead  of  5  c.c. 

The  total  elimination  of  nitrogen  in  the  urine  generally  runs  parallel  to  the 
urea  excretion,  which,  of  course,  contains  the  greater  share  of  the  nitrogen.  In 
acute  yellow  atrophy  of  the  liver,  however,  the  comparison  of  the  total  amounts  of 
nitrogen  and  of  urea  elimination  shows  a  strikingly  different  result.  In  this  dis- 
ease the  major  portion  of  nitrogen  is  eliminated  as  leucin  and  tyrosin,  and  little  or 
no  urea  is  excreted  in  the  urine. 


QUANTITATIVE   ESTIMATION   OF   URIC   ACID. 

A  healthy  adult  excretes  0.2  to  1  gm.  of  uric  acid  in  the  urine  dur- 
ing the  course  of  twenty-four  hours.  The  amount  increases  physiologi- 
cally with  increased  ingestion  of  food,  and  pathologically  with  increased 
metabolism  of  nitrogen  in  about  the  same  proportion  as  urea.  The 
amount  of  uric  acid  in  normal  urine  varies  with  its  specific  gravity. 
The  last  two  numbers  of  the  specific  gravity  (calculated  to  four  places) 
multiplied  by  2  gives  approximately  the  number  of  centigrams  of  uric 
acid  in  the  liter.  The  daily  excretion  of  uric  acid  is  pathologically 
increased  in  fever  and  in  leukemia.  Opinions  still  differ  about  uric 
acid  excretion  before,  during,  and  after  attacks  of  gout.  Recent  inves- 
tigations probably  disprove  the  old  theory — that  in  gout  more  uric  acid 
is  permanently  produced  than  normally  (so-called  uric  acid  diathesis). 
According  to  Haig,  the  amount  of  uric  acid  formed  in  the  body  bears  a 
constant  ratio  to  the  amount  of  urea  (1  :  35  both  under  physiologic  and 
under  pathologic  conditions — e.  g.,  even  in  gout).  He  claims  that  vari- 
ations in  this  ratio  are  due  chiefly  to  irregularities  of  elimination,  which 
in  their  turn  depend  principally  upon  the  varying  degree  of  alkalinity 
of  the  blood.  Again,  the  elimination  of  uric  acid  will  be  increased, 
ceteris  paribus,  by  the  ingestion  of  uric  acid  and  other  xanthin  bodies, 
as  well  as  by  food  substances  rich  in  nuclein  (rich  in  cells). 

According  to  Gubler,^  the  amount  of  uric  acid  in  the  urine  may  be 
approximately  estimated  by  stratifying  upon  a  layer  of  nitric  acid  a 
specimen  of  urine  in  a  test  tube  so  that  the  volume  of  urine  shall  be  to 
the  volume  of  acid  as  3  :  2.  After  a  short  interval  uric  acid  will  pre- 
cipitate out  as  a  cloudy  ring  at  the  junction  of  the  two  fluids.  If  the 
amount  of  uric  acid  is  increased,  the  precipitation  will  be  plain  within 
five  minutes  ;  if  diminished,  not  until  later.  Of  course,  this  test  applies 
only  when  the  daily  volume  of  urine  is  normal.  If  the  volume  is 
diminished,  the  urine  must  be  diluted  up  to  the  normal  amount  with 
water.  Albuminous  urine  must  first  be  freed  from  proteid  by  boiling, 
after  slight  acidification. 

Heintz's  quantitative  method  of  estimating  the  amount  of  uric  acid 
1  Laquer,  Schmidts  Jahrbiicher,  1892,  vol.  236,  No.  10,  p.  78. 
34 


530  URINARY  EXAMINATION. 

has  been  abandoned  entirely.     It  is  not  trustworthy.     The  followmg 
two  roethods  are,  however,  quite  accurate : 

THE  LUDWIG-SALKOWSKI   METHOD    OF   ESTIMATING   THE    AMOUNT    OF 

URIC  ACID. 

This  method  gives  the  most  accurate  results  in  the  estimation  of  uric  acid. 
The  principle  is  as  follows: 

Uric  acid,  even  if  present  only  as  a  trace,  will  be  precipitated  from  the  urine 
as  silver  urate  upon  the  addition  of  a  mixture  of  a  solution  of  ammoniacal  silver 
nitrate  and  of  ammoniacal  magnesia  solution.  The  precipitate  is  treated  with 
an  alkaline  sulphid  solution  and  so  decomposed.  Silver  sulphid  and  ammonium 
urate  will  be  formed  ;  the  latter  is  filtered  off.  The  uric  acid  separates  fi-om  the 
solution  upon  evaporation  with  hydrochloric  acid,  and  is  then  dried,  and  weighed. 

The  precipitation  of  uric  acid  by  the  addition  of  ammoniacal  magnesia 
solution  has,  aside  from  the  advantage  of  the  slight  solubility  of  the  double  com- 
bination of  urate,  the  additional  advantage  that  triple  phosphate  is  precipitated, 
at  the  same  time  mixing  with  the  otherwise  gelatinous  urate  precipitate  and 
making  it  less  tenacious  and  more  easy  to  be  washed. 

For  the  procedure,  the  following  solutions  must  be  prepared : 

1.  Ammoniacal  silver  solution :  Twenty-six  grams  of  silver  nitrate  are  dis- 
solved in  distilled  water,  and  enough  ammonia  added  to  the  solution  to  redissolve 
the  precipitated  silver  oxid.     The  mixture  is  then  diluted  with  Avater  up  to  1  liter. 

2.  Ammoniacal  magnesia  solution :  One  hundred  grams  of  magnesium  chlorid 
are  dissolved  in  an  appropriate  amount  of  water.  About  200  c.  c.  of  a  cold  satu- 
rated ammonium  chlorid  solution  are  added,  and  then  enough  concentrated 
ammonium  hydroxid  to  give  the  mixture  a  strong  ammoniacal  odor.  This  mix- 
ture contains  a  double  salt  of  magnesium  chlorid  and  ammonium  chlorid,  which 
is  not  precipitable  by  ammonia.     The  mixture  is  diluted  with  water  up  to  1  liter. 

The  solutions  as  given  in  Ludwig'  s  directions  are  of  such  concentration  that 
10  c.c.  will  suffice  for  100  c.c.  of  urine. 

10  c.c.^  of  the  silver  solution  are  mixed  with  10  c.c.  of  the  magnesia  solution, 
and  the  resulting  precipitate  of  silver  chlorid  is  redissolved  by  the  addition  of 
hydroxid.  If  the  precipitate  does  not  dissolve  perfectly  it  must  contain  magne- 
sium hydroxid,  which  can  be  dissolved  by  adding  ammonium  chlorid.  The  clear 
solution  is  poured,  with  stii-ring,  into  a  beaker  containing  100  c.c.  of  urine  ;  the 
precipitate  which  foiTQS  is  allowed  to  settle  a  little,  then  filtered  off  upon  a  suction 
filter,  and  washed  two  or  three  times  with  water  to  which  a  few  drops  of  ammonia 
have  been  added.  Any  of  the  precipitate  remaining  in  the  beaker  is  washed  out 
into  the  filter  with  wash- water.  Traces  of  the  precipitate  may,  however,  be  allowed 
to  remain  in  the  beaker,  because  all  of  the  precipitate  on  the  filter  is  to  be  removed, 
by  the  aid  of  a  glass  rod,  to  the  beaker  again,  after  it  has  become  partly  diy  on  the 
paper.     The  filter  paper  must  be  kept  intact. 

The  precipitate  is  now  placed  in  about  200  c.c.  of  water,  according  to  Sal- 
kowski,  acidulated  with  hydrochloric  acid,  and  the  mixture  saturated  with  hydi'o- 
gen  sulphid.  Shaffer  and  Folin  recommend  the  previous  addition  of  5  to  10  c.c. 
of  a  1  per  cent,  solution  of  cupric  sulphate,  after  w'hich  the  fluid  is  brought  to 
the  boiling-point.  After  the  saturation  with  hydrogen  sulphid,  the  fluid  is  again 
boiled  for  several  minutes,  and  the  hot  solution  of  uric  acid  is  then  filtered  from 
the  silver  sulphid.  The  precipitate  should  be  thoroughly  washed  with  hot  water. 
The  filtrate  is  perfectly  clear  and  throws  down  no  silver  sulphate  upon  evaporation, 
just  as  in  Ludwig' s  method,  in  which  the  silver  is  removed  by  an  alkaline  sul- 
phid solution.  The  fluid  is  now  placed  in  a  porcelain  dish  upon  a  water  bath, 
and  evaporated  to  10  to  15  c.c.  From  5  to  10  drops  of  hyckochloric  acid  are 
now  added,  the  mixture  is  allowed  to  stand  for  twelve  hours,  and  the  uric  acid 
crystals  are  collected  upon  a  weighed  filter  which  has  been  dried  at  110°  C.  The 
crystals  upon  the  filter  are  then  washed  with  a  small  quantity  of  water  until  they 

^The  following  description  is  partly  quoted  from  Huppert :  Anleitung  zur  qiialita- 
tiven  und  quantitativen  Harnanalyse  von  Neubauer,  neu  bearbeitet  durch  Huppert,  1890. 


QUANTITATIVE   URINARY  ANALYSIS.  531 

are  free  from  chlorin  ;  the  quantity  of  the  filtrate  together  ^dth  that  of  the  wash 
water  should  not  exceed  50  to  60  c.c.  The  crystals  are  again  washed  twice  with 
absolute  alcohol,  then  with  ether,  dried,  and  weighed. 

Any  sediment  of  urates  must  be  dissolved  by  heating  before  measuring  off  the 
urine.  Any  precipitated  uric  acid  can  be  dissolved  in  as  little  sodium  hydroxid 
as  possible  and  the  solution  then  mixed  with  the  urine.  Too  much  sodium 
hyctoxid  should  not  be  used,  for  it  would  cause  excessive  precipitation  of  phos- 
phates, which  would  not  allow  any  phosphate  to  remain  for  the  production  of  a 
triple  phosphate  sediment  with  the  silver  magnesium  precipitation.  Adding 
sodium  phosphate  to  the  urine  before  the  silver  precipitation  would,  however, 
prevent  this  difficulty. 

Stadthagen  claims  that  peptones  and  proteoses  do  not  influence  the  uric  acid 
precipitation,  but  the  urine  must  first  be  freed  from  proteid. 

THE  HOPKIN-WORNER  METHOD  OF  URIC  ACID  ESTIMATION.i 

This  method  is,  according  to  all  obsen^ers,  simple  and  perfectly  accurate.  It 
depends  upon  the  following  principle :  Ammonium  chlorid  precipitates  uric 
acid  quantitatively  from  the  urine  as  ammonium  urate.  The  determination 
is  carried  out  as  follows:  150  c.c.  of  urine  are  warmed  in  a  beaker  to  40°  to 
45°  C,  and  30  gm.  of  ammonium  chlorid  allowed  to  dissolve  in  it.  The  pre- 
cipitate of  ammonium  urate  which  results  after  one-half  to  one  hour's  stand- 
ing is  filtered  off,  and  washed  free  from  chlorin  with  a  10  per  cent,  solution  of 
ammonium  sulphate.  It  is  then  dissolved  upon  the  filter  by  a  warm  1  to  2 
per  cent,  solution  of  sodium  hydroxid,  the  filter  washed  afterward  with  hot  water, 
and  the  filtrate  and  wash-water,  collected  in  a  porcelain  dish,  heated  upon  a 
water  bath  long  enough  to  drive  off  all  the  ammonia.  The  alkaMne  solution  of 
uric  acid  is  then  decomposed  with  15  c.c.  of  concentrated  sulphuric  acid  and  some 
copper  sulphate.  2  After  adding  sodium  hydroxid  the  free  ammonia  is  estimated  in 
the  usual  manner.     Such  a  small  amount  of  ammonia  is  more  accurately  measured 

N  N 

by   employing  a  —  oxalic  acid  instead  of  a  — ,  as  is  usual,  and  also  by   retitra- 

N 
tion.     One  cubic  centimeter  --  oxalic  acid  corresponds  to  0. 0042  gm.  of  uric  acid. 

Strongly  acid  urines  under  some  conditions  prevent  the  precipitation  of  ammo- 
nium urate,  or  make  such  a  precipitation  incomplete ;  hence,  Levandowski  ^ 
recommends  that  the  urine  be  neutralized  before  the  precipitation.  If  performed 
in  this  way  the  method  should  be  very  exact  and  trustworthy. 

TITRATION    OF   URIC    ACID,   ACCORDING    TO    HOPKIN,    MODIFIED    BY 
O.    FOLIN    AND    TH.  A.   SHAFFER.* 

This  method  differs  from  the  preceding  in  that  the  ammonium  urate  is  not 

dissolved  by  a  solution  of  sodium  hydroxid,  but  is  washed  from  the  filter  by  100 

c.c.  of  water.     After  the  addition  of  15  c.c.  of  concentrated  sulphuric  acid,  the 

N 
solution  is  at  once  titrated  with  a  ~  potassium  permanganate  solution  (1.6  gm. 

of  crystalline  potassium  pemianganate  dissolved  in  water  and  the  volume  made 
up  to  1  liter).  Toward  the  end  of  the  titration  the  permanganate  solution  must 
be  cautiously  added  drop  by  drop.  The  end  reaction  is  the 'first  slight  permanent 
reddish  tinge  obtained  by  stirring  the  fluid.     The  permanganate  solution  may  be 

tested  by  a  normal  oxalic  acid  solution.     One  cubic  centimeter  of  a  -^  perman- 

ganate  solution  corresponds  to  0. 00375  gm.  of  uric  acid. 

'  Worner,  Zeits.  f.  phijsioL  Cheniie.,  vol.  xxix.,  p.  1. 

^  This  takes  the  place  of  the  oxid  of  mercury  (p.  527).  It  acts  catalyticallv,  and 
has  the  advantage  that  the  subsequent  treatment  with  alkalin  sulphid  becomes  unnec- 
essary.      ,   ..  .  .  ^  Zei'Is.  f.  kUn.  3Iefl.,  lUOO,  vol.  xl.,  pp.  8  and  4. 

*  E.  Spiith,  Die  chemische  und  mikroskopische  Unlersuchang  des  Ilarnes,  1903. 


532  URINARY  EXAMINATION. 

ESTIMATION  OF  THE  ALLOXURIC    OR   PURIN  BODIES   EN 
THE  URINE, 

Eecent  investigations  concerning  the  relation  of  purin  bodies  (this  word  is  now 
used  to  include  uric  acid  and  alloxuric  or  xanthin  bases)  to  the  nucleins — i.  e. ,  to  the 
cell  nuclei — have  been  mainly  conducted  by  Kossel,  Nencki  and  Sieber,  Stadthagen, 
Ebstein,  and  Horbaczewsky.  These  authors  have  shown  the  clinical  importance 
of  these  bases.  According  to  our  present  knowledge,  their  formation  depends 
upon  the  destruction  of  cellular  elements,  especially  of  the  cell  nuclei  rich  in 
nuclein.  The  following  scheme  may  help  the  reader  to  understand  the  derivation 
of  the  purin  bodies  more  clearly: 

iS^uclein 

Proteid  Xucleic  acid 

Phosphoric  acid  Unknown  substance 

Uric  acid  Alloxur  or  Purin  Bases 


(Alloxur  Bodies  or  Purin  Bodies). 


Kolish  considers  that  gout  is  due  to  an  increased  formation  of  the  purin  bodies, 
but  other  investigators  do  not  yet  agree  vrith.  him.  However,  in  farther  work 
upon  the  subject  of  gout  the  significance  of  the  purin  bodies  of  the  urine  will  be 
of  the  highest  interest.  Moreover,  since  we  already  know  the  relation  of  the 
purin  bodies  to  the  cell  nuclei,  the  quantitative  estimation  of  these  substances  will 
be  the  source  of  much  interest  in  the  different  conditions  of  disease. 

Until  lately,  Kruger  andWulff's  ^  method  has  been  generally  used  to  estimate 
the  total  amount  of  the  pui'in  bodies.  But  it  has  been  proved  inaccurate,  and  so 
will  not  be  described. 

Salkowski's  method  is  exact.  It  depends  upon  the  precipitation  of  the  purin 
bases  by  an  ammoniacal  silver  solution.  It  determines  the  purin  bases  alone,  and 
is  analogous  to  the  Ludwig-Salkowski  method  for  estimating  uric  acid.  Deniges' 
method  is  employed  at  the  Bern  Clinic  quite  successfully,  and  will  also  be  described. 

SALKOWSKI'S    METHOD    OF    ESTIMATING    THE    PURIN   BASES.^ 

The  precipitate  obtained  from  the  urine  (at  least  500  to  1000  c.c.)  by  precip- 
itating with  the  silver  magnesia  solution  is,  after  carefully  washing,  decomposed 
by  hydrogen  sulphid  (just  as  in  the  Ludwig-Salkowski  uric  acid  method,  p.  530  et 
seq.).  The  filtrate  is  evaporated  to  dryness,  and  the  residue  extracted  with 
2  to  3  per  cent,  sulphuric  acid.  The  latter  dissolves  the  purin  bases  and  leaves 
the  uric  acid  undissolved.  To  be  absolutely  sure  that  at  the  most  only  traces  of 
uric  acid  become  dissolved,  Salkowski  delays  filtering  until  the  following  day. 
The  filtrate  is  now  rendered  alkaline  with  ammonia,  and  precipitated  again  with 
the  silver  solution.  The  amount  of  silver  present  in  the  precipitate  is  determined 
(after  washing)  by  titration  with  ammonium  sulphocyanate.  From  the  amount 
of  silver  present  in  the  precipitate  can  be  calculated  the  quantity  of  xanthin  or 
purin  bases  present. 

The  amount  of  xanthin  is  either  figured  out  or  the  xanthin  bases  are  separated 
directly  from  the  second  silver  precipitate  and  weighed.  Salkowski  believes  that 
the  larger  part  of  the  purin  bases  does  not  consist  of  xanthin,  but  rather  of  bodies 
similar  to  hypoxanthin,  as  described  by  him  in  Virchow's  Archiv.,  vol.  1. 

'  Zeits.  /.  physiol.  Chemie,  vol.  xx.,  p.  176. 

"^  Deutsch.  med.  TUocA..  1897,  No.  14,  and  Centralbl.  f.  d.  med.  Wissensehaften,  1894, 

No.  30. 


QUANTITATIVE   URINARY  ANALYSIS.  533 

METHOD  FOR  THE  DETERMINATION  OF  PURIN  BODIES,  INCLUDING  URIC 
ACID,  ACCORDING  TO  DfiNICSS.' 

This  method  is  based  on  the  fact  that  the  purin  bases  and  uric  acid  are  precipi- 
tated quantitatively  by  an  ammoniacal  solution  of  silver  nitrate,  ammonium 
chlorid,  and  magnesium  chlorid,  and  that  a  permanent  precipitate  of  silver  iodid 
is  produced  by  silver  nitrate  in  an  ammoniacal  solution  of  potassium  cyanid  and 
potassium  iodid  only  after  all  potassium  cyanid  has  been  changed  to  potassium  silver 
cyanid.     This  test  furnishes  the  quantity  of  purin  bodies,  including  uric  acid. 

The  following  solutions  are  necessary  : 

N 

1.  A  —  ammoniacal  silver  magnesia  solution.    In  a  graduate  of  1  liter  capacity 

are  placed  150  gm.  of  pure  ammonium  chlorid  and  100  gm.  of  pure  magnesium 

chlorid  ;  it  is  then  filled  three-quarters  full  with  ammonium  hydroxid.    This  is  gently 

treated  on  the  water  bath  until  the  salts  are  dissolved.     After  cooling,  600  c.c.  of 

N 
this  fluid  are  mixed  with  500  c.c.  of  a  —  solution  of  silver  nitrate. 

2.  A  —  solution  of  potassium  cyanid.  Ten  grams  of  KCN  are  dissolved  in  about 
1  liter  of  water,  to  which  are  added  10  c.c.  of  ammonium  hydroxid,  and  the  whole  is 
then  filtered.  This  solution  is  too  concentrated.  It  is  so  diluted  with  a  —  solu- 
tion of  silver  that  10  c.c.  of  the  latter  correspond  exactly  to  20  c.c.  of  the  potassium 
cyanid  solution,  since  2  molecules  of  potassium  cyanid  react  with  one  molecule  of 
silver.  (Formation  of  potassium  silver  cyanid,  KAgCN^. )  To  standardize  the 
potassium  cyanid  solution  20  c.c.  are  placed  in  a  beaker,  and  100  c.c.  of  water,  10  c.c. 
of  ammonia,  and  a  few  drops  of  potassium  iodid  solution  are  then  added.     Next 

N 
a  sufficient  quantity  of  the     .  silver  solution  is  added  to  produce  a  slight  but  per- 
sistent cloudiness.     If  we  assume  that  for  this  purpose  it  is  necessary  to  use  10  + 
n  c.c.  of  the  silver  solution,  then  there  must  be  added  to  the  potassium  cyanid 
solution  water  in  the  proportion  2  /i  c.c.   to  each  20  c.c.     A  potassium  cyanid 

N 
solution  so  prepared  will  correspond  to  an  equal  volume  of  the  —  silver  solution. 

3.  A  solution  of  potassium  iodid  prepared  by  dissolving  20  c.  c.  of  potassium 
iodid  in  100  c.c.  of  water  and  adding  2  c.c.  of  ammonium  hydroxid. 

N 

4.  A  —  silver  solution.     Seventeen  grams  of  pure  and  dry  silver  nitrate  are 

dissolved  in  1  liter  of  water. 

These  solutions  are  utilized  in  the  following  manner  to  determine  the  purin 
bodies  of  the  urine.     To  100  c.c.  of  urine  there  are  added  25  c.c.  of  the  ammoni- 

N  . 

acal  —  silver  magnesia  solution.  This  is  well  shaken  and  the  precipitate  (con- 
sisting of  silver  combinations  of  the  purin  bases)  filtered  off.  To  100  c.c.  of  the 
filtrate,  which  correspond  to  80  c.c.  of  urine  and  20  c.c.  of  the  silver  solution,  are 
added  20  c.c.  of  the  potassium  cyanid  solution.  This  volume  of  potassium  cyanid 
solution  would  react  exactly  with  20  c.c.  of  the  silver  solution  if  a  part  of 
the  silver  had  not  been  used  up  by  the  purin  bases,  and  thus  been  removed  by 
filtration  Ina.smuch  as  the  quantity  of  silver  is  less,  there  will  be  an  excess  of 
potassium  cyanid.     This  excess  is  estimated  by  adding  as  an  indicator  a  few  drops 

N 
of  potassium  iodid  solution,  and  then  from  a  buret  --  silver  solution  until  a  per- 
manent cloudiness  is  produced.  The  amount  of  silver  solution  added  will  correspond 
exactly  to  the  amount  of  silver  held  in  combination  by  the  purin  bodies.  By  far 
the  greater  part  of  the  purin  precipitate  is  made  up  of  uric  acid,  so  that  the  final 
result,  so  far  as  uric  acic  is  concerned,  may  be  figured  as  follows  : 

'  After  C.  Vieillard,  L'urine  humaine,  Paris,  1898 ;  original  in  Bull,  de  la  soc.  de 
pharm.  de  Bordeaux,  1884,  p.  137. 


534  URINARY  EXAMINATION. 

N 
Eacli  cubic  centimeter  of  the  --  silver  solution  corresponds  to   0.0168   gm. 

of  uric  acid.     If  n  c.c.  silver  solution  have  been  used,  these  80  c.c.  of  urine  will 

0.0168  X  1000  X  n 

contain  n  X  0.0168  and  1  liter  of  urine —  0.21  X  n  purin 

80 
bodies  in  terms  of  uric  acid. 

ESTIMATION  OF  THE  KREATININ  IN  THE  URINE. 

Kreatinin  in  the  urine  is  probably  derived  from  the  kreatin  of  the  muscles. 
Kreatinin  is  the  anhydrid  of  kreatin.  Normal  urine  probably  does  not  contain 
kreatin.  The  excretion  of  kreatinin  generally  runs  parallel  to  the  excretion  of 
urea.  An  increased  ingestion  of  meat,  and  in  all  probability  any  augmentation 
of  muscular  metabolism,  increases  the  excretion  of  kreatinin.  Here  lies  the 
clinical  interest  in  the  quantity  of  kreatinin  in  the  urine.  The  various  results  of 
experiment  as  to  whether  the  kreatinin  increases  in  amount  with  increased  muscular 
work  differ.  It  is  generally  assumed  that  the  excretion  of  kreatinin  is  not 
increased  by  muscular  exertion.  According  to  Thomas  and  Spath,'  the  daily  excre- 
tion of  kreatinin  of  healthy  men  is  about  1  gm.  The  excretion  of  kreatinin  in  dis- 
ease (in  spite  of  its  theoretic  interest)  has  not  been  followed  clinically  veiy  closely. 
A  pronounced  increase  has  as  yet  been  noticed  only  during  the  fever  of  acute 
diseases. 

An  accurate  quantitative  determination  of  kreatinin  may  be  got  (Neubauer)  ^  by 
preparing  and  weighing  the  kreatinin  zinc  chlorid  precipitated  from  the  urine. 
The  original  article  must  be  consulted  for  the  technic.  (Compare  Neubauer  and 
Vogel.)  ^ 

Kreatinin  can  be  demonstrated  qualitatively  in  the  urine  by  either  of  the  fol- 
lowing two  simple  methods,  which  may  also  be  used  for  a  quantitative  estimation  : 

Jaffe's  Reaction.* — The  addition  of  a  little  aqueous  solution  of  picric  acid 
and  a  few  drops  of  diluted  sodium  or  potassium  hydroxid  to  a  solution  of  kreat- 
inin will  immediately  produce  an  intense  red  color  even  when  the  amount  of 
kreatinin  in  the  urine  is  only  1  :  5000.  The  color  will  increase  for  a  few  moments, 
and  then  persist  unchanged  for  hours.  Acetone  also  gives  a  red  color,  although 
a  much  less  intense  one  ;  hence,  it  is  wise  first  to  remove  by  boiling  any  acetone 
that  may  be  present  in  the  urine. 

Th.  Weyl's  Reaction.* — A  few  drops  of  a  very  dilute  solution  of  sodium 
nitroprussid  is  added  to  the  urine,  and  then  some  diluted  sodium  hydroxid.  If 
kreatinin  is  present  a  ruby-red  color  will  result,  which  soon  changes  to  a  yellow. 
Up  to  this  point  the  reaction  is  identical  with  Legal' s  acetone  test  (p.  495  et  seq.). 
If,  however,  acetone  is  present,  the  fluid  turns  red  again  when  acidified  with 
acetic  acid  ;  this  is  not  the  case  with  kreatinin.  Salkowski  claims  that  if  kreat- 
inin is  present  the  addition  of  acetic  acid  and  subsequent  heating  produce  a 
greenish  and  then  bluish  coloration  (Prussian  blue).  Before  attemiiting  Weyl's 
test,  the  acetone  may  be  expelled  by  boiling  the  urine. 

QUANTITATIVE  ESTIMATION  OF  THE  CHLORIDS  IN  THE  URINE. 

The  amount  of  chlorid  eliminated  in  the  urine  of  a  healthy  adult  in 
twenty-four  hours  varies  between  11  and  15  gm.,  calculated  as  sodium 
chlorid.     Chlorids  of  the  urine  are  diminished  in  hunger  and  diarrhea, 

^  Harnanalyse  von  Neubauer  und  Vogel,  Neu  bearbeitel  von  Huppert  und  Thomas.  Kriedel, 
Wiesbaden,  1890. 

^  Ann.  der  Chemie.  u.  Pharm.,  1861,  vol.  cxix.,  p.  33.  Modification  der  Methode 
durch  Salkowski,  Zeits.f.  phys.  Chemie,  1886,  vol.  x.,  p.  113. 

^  Die  chem.  u.  mikroskopische  Untersuchunc/  des  Karnes,  1903. 

*  Zeits.  f.  phys.  Chemie.,  1886,  vol.  x.,  p.  399._ 

*  Th.  Weyl,  Ber.  d.  chem.  Oesellschaft,  vol.  xi.,  p.  2175. 


QUANTITATIVE   URINARY  ANALYSIS.  535 

from  the  formation  of  exudates  or  transudates  rich  in  sodium  chlorid, 
and  in  fever. 

It  has  been  assumed  that  the  diminution  of  chlorids  eliminated  in 
the  urine  in  fever  depends  entirely  upon  the  diminished  ingestion  of 
food.  This  is  certainly  wrong,  because  in  some  other  cases,  when  much 
less  food  is  ingested,  no  such  marked  diminution  of  the  chlorids  appears 
in  the  urine — e.  g.,  in  pneumonia.  Again,  in  pneumonia  the  amount  of 
chlorin  eliminated  increases  very  markedly  immediately  after  the  crisis 
without  any  increased  ingestion  of  food.  Xo  absolutely  correct  explana- 
tion of  the  diminution  of  chlorin  in  fever  has  yet  been  advanced.  One 
theory  suggests  that  in  fever  the  cell-proteids,  which  are  relatively  poor 
in  chlorin,  are  disintegrated  much  more  extensively  than  the  circulating 
proteids.  Another  theory  is  that  the  formation  of  inflammatory  exu- 
dates deprives  the  urine  of  a  considerable  amount  of  chlorin.  This 
agrees  very  well  wdth  the  fact  that  in  no  other  disease  is  there  so  great 
a  diminution  in  the  amount  of  chlorin  as  in  croupous  pneumonia,  where 
exudation  is  very  acute.  A  third  assumption  is  that  the  chlorids  are 
kept  back  as  a  sequence  of  the  supposed  retention  of  water  in  fever. 
Probably  several  of  the  above-mentioned  factors  act  together  in  febrile 
disturbances  to  diminish  the  chlorids  in  the  urine. 

It  is  practically  important,  however,  to  remember  that  in  febrile 
diseases  any  improvement  in  the  condition  will  increase  the  amount  of 
chlorids  in  the  urine,  and  often  before  any  improvement  is  indicated  by 
the  thermometer — e.  g.,  in  pneumonia.  Any  great  diminution  in  the 
amount  of  chlorids  in  non-febrile  disorders  always  poiuts  to  a  serious 
condition.  On  the  other  hand,  there  are  some  very  severe  general  con- 
ditions (the  author  has  paid  particular  attention  to  this  in  circulatory 
disorders)  in  which  no  diminution  of  chlorids  is  observed. 

A  pronounced  diminution  or  absence  of  chlorids  in  the  urine  in  a 
febrile  disorder  will  always  suggest  pneumonia,  because,  as  has  already 
been  mentioned,  the  greatest  degree  of  diminution  is  reached  in  this 
disease. 

For  practical  purposes  an  approximate  estimation  of  the  chlorids, 
made  as  follows,  will  suffice  :  A  specimen  of  urine  in  a  test  tube  is 
acidified  with  about  10  drops  of  pure  nitric  acid.  Then  a  single  drop 
of  silver  nitrate  solution  (1  :  10)  is  added.  If  the  chlorids  are  normal 
a  solid  ring,  a  ball,  or  one  or  more  compact  lumps  of  silver  chlorid  form 
and  settle  to  the  bottom;  if  diminished,  only  a  more  or  less  intense 
cloudiness  arises.  With  a  little  practice  the  relative  amount  of  chlorids 
may  be  judged  by  this  simple  test.  Nitric  acid  is  employed  because  it 
precipitates  any  proteid  present,  which  otherwise  would  be  precipitated  by 
the  silver  solution,  and  might  thus  lead  to  deception  ;  and  also  because  it 
prevents  the  precipitation  of  silver  phosphate,  which  might  be  mistaken 
for  the  silver  chlorid.  If  a  large  amount  of  proteid  appears  after  the 
addition  of  the  nitric  acid,  it  must  first  be  removed  by  filtering  or  by  let- 
ting it  settle  to  the  bottom  before  performing  the  chlorid  test. 

Volhard's  procedure  (titration  with  silver  and  annnonium  sulpho- 
cyanate  solution)  is  the  most  reliable  method.     It  is  described  in  con- 


536  UEINABY  EXAMINATION. 

nection  with  the  Liitke-Martius  method  of  estimating  the  hydrochloric 
acid  of  the  gastric  juice,  and  can  also  be  employed  for  the  urine  (see  p. 
380  et  seq.).  In  employing  this  method  it  is  best  to  use  the  urinary  ash^ 
since,  if  the  silver  solution  is  added  to  the  urine,  it  precipitates  not  only 
the  chlorids,  but  also  the  purin  bodies,  which  would  consequently  give 
rise  to  a  slight  error. 

QUANTITATIVE  ESTIMATION  OF  THE  PHOSPHATES  IN  THE 

URINE. 

The  daily  excretion  of  phosphoric  acid  in  the  urine,  in  the  form  of  phos- 
phates, amounts  normally  to  2  to  3  gm.  The  ratio  of  the  excreted  phosphoric 
acid  to  the  amount  of  excreted  nitrogen  is  normally  0.18  (15  urea  =  7  nitrogen). 

P  O 

This  ratio,   -^7-^,  is  termed  the  relative  value  of  the  phosphoric  acid  excreted.     In 

febrile  conditions  the  absolute  value  of  phosphoric  acid  elimination  may  be  di- 
minished or  increased  (more  frequently  the  first),  but  Ziilzer  claims  that  the 
relative  value  is  constantly  diminished.  In  convalescence  the  absolute  and  rela- 
tive values  immediately  increase  to  normal  or  sometimes  above.  According  to 
Fleischer,  a  considerable  diminution  in  the  absolute,  as  well  as  the  relative,  phos- 
phoric acid  values  seems  to  be  constant  in  nephritis. 

Quantitative  estimation  of  phosphates  in  so-called  phosphaturia — i.  e. ,  voiding 
of  a  urine  clouded  with  phosphates- — has  shown  that  this  condition  does  not  by 
any  means  signify  an  increase  of  the  daily  quantity  of  phosphates,  but  only  a  pre- 
cipitation of  the  phosphates  in  consequence  of  the  diminished  acidity  or  even 
alkalinity  of  the  urine  or  increase  in  the  quantity  of  the  alkaline  earths  present 
(see  p.  557,  et  seq.). 

The  quantitative  estimation  of  phosphates  is  accomplished  by  titration  with 
uranium  nitrate  in  a  solution  of  acetic  acid,  which  precipitates  all  the  phosphates. 

The  end  reaction  is  either  the  brown  color  which  is  produced  by  an  excess  of ' 
uranium  nitrate  in  the  presence  of  potassium  ferrocyanid,  or  the  green  color 
formed  by  tincture  of  cochineal  with  a  surplus  of  uranium. 

The  following  solutions  are  required : 

1.  A  solution  of  uranium  nitrate,  which  must  be  standarized  with  a  solution 
of  disodium  phosphate  of  known  strength.  About  35  gm.  of  uranium  nitrate  are 
dissolved  in  a  liter  of  water. 

2.  A  solution  of  disodium  phosphate,  so  prepared  that  50  c.c.  shall  contain 
0. 1  gm.  P2O5.  This  solution  is  prepared  from  the  ordinary  pure  disodium  phos- 
phate; but  since  this  salt  contains  a  varying  quantity  of  water,  and  consequently 
a  varying  amount  of  PjOg,  the  solution  must  be  standardized.  This  is  done  as 
follows :  Twelve  grams  of  pure  disodic  phosphate  are  dissolved  in  a  liter  of  water, 

N 
and  40  c.  c.  of  the  solution  are  titrated  with  —  hydrochloric  or  sulphuric  acid, 

alizarin  red  being  employed  as  an  indicator.     The  end  reaction  corresponds  to  the 

moment  when  all  of  the  disodium  phosphate  is  transformed  into  the  monosodium 

phosphate,  and  is  indicated  by  the  red  solution  turning  yellow.     If  the  solution  is 

correct — i.  e.,    if  50    c.c.    contain   0.1   PjO^ — the  40  c.c.   should  require  11.25 

N 
c.c.  —  hydrochloric  acid  before  the   end  reaction  occurs.     As  a  rule,  more  is 

required,  and  the  original  solution  must  consequently  be  diluted.     For  example, 

N 
if  13  c.c.  —  hydrochloric  acid  are  required,  and  x  represents  the  amount  of  fluid 

to  which  the  40  c.c.  must  be  diluted,  we  have  the  proportion : 

40  :  11.25  =  :r.- 13 

^^d^=    "^oxTs 
11.25 


QUANTITATIVE   URINARY  ANALYSIS.  537 

The  sodium  phosphate  solution  must  then  be  so  diluted  that  every  40  c.c.  is 
brought  up  to  the  volume  x.  If  the  solution  contains  too  little  phosphate,  it  must 
be  concentrated  by  evaporation  according  to  a  corresponding  proportion. 

3.  Acetic-acid  sodium  acetate  solution.  One  hundred  grams  of  sodium 
acetate  are  dissolved  in  800  gm.  of  water,  100  c.c.  of  a  30  per  cent,  acetic  acid 
solution  are  added,  and  the  mixture  is  diluted  to  1  liter. 

4.  Potassium  ferrocyanid  solution.  10  :  100  water  or  tincture  of  cochineal.  The 
latter  is  prepared  by  dissolving  6  gm.  of  powdered  good  cochineal  in  a  mixture 
of  300  c.c.  of  distilled  water  and  200  c.c.  of  alcohol.  The  mixture  is  kept  at  an 
ordinary  temperature  for  several  hours,  during  which  time  it  is  frequently  shaken, 
and  is  then  filtered. 

Preparation  of  the  TTraiiiuin  Nitrate  Solution. — Fifty  cubic  centimeters 
of  the  prepared  solution  of  sodium  phosphate  are  placed  in  an  Erlenmaier  flask, 
treated  with  5  c.  c.  of  the  acetic-acid  sodium  acetate  solution,  and  heated  to  the 
boiling-point.  A  solution  of  uranium  nitrate  (35 :  1000)  is  now  added  fi-om  a 
buret  as  long  as  there  is  a  distinct  precipitate  formed.  The  solution  should  now 
be  tested  after  the  addition  of  every  J  c.c.  by  taking  a  drop  of  the  fluid  out  of  the 
flask  by  means  of  a  glass  rod,  and  mixing  it  upon  a  porcelain  plate  with  a  drop 
of  a_  potassium  ferrocyanid  solution.  The  end  reaction  is  the  appearance  of  a 
reddish-brown  color.  A  simpler  method  of  attaining  the  same  end  is  to  add 
several  drops  of  the  tincture  of  cochineal  to  the  fluid  in  the  flask,  bring  it  to  the 
boiling-point,  and  add  the  uranium  nitrate  solution  until  a  permanent  pale-green 
color  is  obtained  after  mixing  and  reheating.  It  is  now  known  how  much 
uranium  nitrate  solution  is  necessary  for  the  precipitation  of  50  c.c.  of  the  sodium 
phosphate  solution,  and  the  uranium  solution  is  to  be  diluted  so  that  exactly  20 
c.c.  will  precipitate  50  c.c.  of  the  sodium  phosphate  solution.  The  20  c.c.  of 
uranium  solution  are  then  equivalent  to  0.1  P^O^,  or  1  c.c.  is  equivalent  to  0.005 
gm.  PjO.. 

Estimation  of  the  Total  Phosphates  in  the  Urine.— If  proteids  be  present 
they  must  be  removed;  sugar  does  not  interfere  with  the  reaction.  We  proceed 
with  the  urine  exactly  as  we  did  in  the  preparation  of  the  uranium  nitrate 
solution — i.  e.,  we  titrate  50  c.c.  of  the  urine  and  5  c.c.  of  the  acetic-acid  sodium 
acetate  solution  at  the  boiling-point  with  the  standardized  uranium  solution  until 
the  end  reaction  is  obtained  with  potassium  ferrocyanid  or  cochineal.  Every 
cubic  centimeter  of  the  uranium  solution  employed  then  corresponds  to  0.005 

Separate  Estimation  of  the  Earthy  Phosphates.— In  reference  to  so-called 
phosphaturia  (see  pp.  536  and  557),  it  is  of  interest  to  make  a  separate  estimation 
of  the  earthy  phosphates.  The  difference  between  the  total  phosphoric  acid  and 
the  earthy  phosphates  then  gives  the  alkaline  phosphates.  To  estimate  the 
earthy  phosphates  we  proceed  as  follows :  One  hundred  cubic  centimeters  of  urine 
are  rendered  alkaline  with  ammonia,  the  mixture  is  allowed  to  stand  for  twelve 
hours,  the  precipitate  removed  by  filtration  and  washed  with  ammonia  water. 
The  filter  is  now  perforated  with  a  glass  rod,  and  the  precipitate  is  washed  into  a 
beaker.  After  dissolving  the  precipitate  by  heat  in  as  small  a  quantity  of  acetic 
acid  as  possible,  the  solution  is  diluted  to  50  c.c.  with  water,  5  c.c.  of  "the  acetic- 
acid  sodium  acetate  solution  are  added,  and  the  mixture  is  titrated  with  the 
uranium  solution,  as  in  the  estimation  of  the  total  phosphates. 

QUANTITATIVE  ESTIMATION    OF   SULPHURIC  ACID  AND  OF  THE 
COMBINED  SULPHURIC  ACID. 

Although  the  total  amount  of  sulphuric  acid  eliminated  is  as  yet  of  no 
particular  clinical  importance, '  the  amount  of  the  combined  sulphuric  acid — i.  e., 
sulphuric  acid  united  with  organic  substances — e.  g.,  phenol,  indol,  etc. — to  form 
the  so-called  ethereal  sulphates  is  of  much  greater  interest. 

_  ^  The  so-called  total  sulphuric  acid  of  the  urine  consists  of  sulphuric  acid  in  the 
ordinary  sense  of  the  word,  and  of  sulphuric  acid  in  combination — i.  e.,  with  various 
organic  substances. 


538  URINARY  EXAMINATION. 

We  can  estimate  sulphuric  acid  proper  separately  from  combined  sulphuric 
acid  by  titration,  because  in  a  urine  which  either  is  not  acidified,  or  is  acidified 
entirely  by  acetic  acid,  barium  solutions  will  precipitate  only  the  sulphuric  acid 
proper  as  barium  sulphate;  whereas  in  the  presence  of  hydrochloric  acid  the 
ethereal  sulphuric  acid  will  be  freed  from  its  combinations  and  will  be  precipitated 
along  with  the  inorganic  sulphuric  acid.  By  subtracting  the  value  of  the  sul- 
phuric acid  proper  from  that  of  the  total  sulphuric  acid,  the  amount  of  combined 
sulphuric  acid  may  be  obtained. 

The  normal  daily  excretion  of  total  sulphates  in  the  adult  amounts  to  1. 5  to 
3  gm.  of  SO3,  and  parallels  the  quantity  of  proteid  decomposed.  The  normal 
ratio  of  the  daily  amount  of  the  total  sulphates  to  the  daily  quantity  of  urea  is 
about  1 :  5,  while  the  ratio  of  the  quantity  of  the  ethereal  sulphates  to  that  of  the 
remaining  sulphates  is  about  1:10. 

Many  processes  of  decomposition  within  the  body,  particularly  increased 
intestinal  putrefaction,  show  an  increase  in  the  amount  of  combined  sulphuric 
acid  at  the  expense  of  the  inorganic  sulphuric  acid.  An  abundant  administration 
of  phenol  (carbolic  acid  poisoning)  produces  the  same  effect. 

QUANTITATIVE   ESTIMATION    OF   AMMONIA   IN   URINE. 

The  normal  amount  of  ammonia  contained  in  adult  urine,  according  to 
Neubauer,  varies  in  twenty-four  hours  between  0.3  and  1.2  gm.,  and  averages 
0. 7  gm.  A  meat  diet,  the  ingestion  of  radishes,  the  breathing  of  air  saturated  with 
tobacco  smoke,  and  the  taking  of  ammonium  salts  and  mineral  acids  as  med- 
icaments increase  the  daily  amount  of  ammonia  excreted. 

The  quantitative  estimation  of  ammonia  in  the  urine  may  be  of  clinical 
interest  under  certain  circumstances.  We  know  that  the  human  organism,  like  that 
of  carnivora  in  general,  reacts  to  an  increased  ingestion  of  acid  or  increased  acid 
formation  by  an  increased  production  of  ammonia,  which  serves  the  purpose  of 
holding  the  otherwise  injurious  acids  in  combination.  Consequently,  the  amount 
of  ammonia  salts  contained  in  urine  is  an  important  indicator  of  acid  metabolism. 

The  daily  quantity  of  ammonia  excreted  is  increased  pathologically  in  diseases 
of  the  liver  and  in  acute  febrile  diseases,  such  as  pneumonia  and  typhoid  fever. 
The  increase  is  usually  at  the  expense  of  the  urea.  In  affections  of  the  liver 
there  is  a  specific  impairment  of  its  urea-forming  function ;  in  febrile  diseases  the 
increased  quantity  of  ammonia  is  the  effect  of  the  increased  formation  of  acids  in 
consequence  of  the  augmented  decomposition  of  proteid.  The  increase  in  the 
amount  of  excreted  ammonia  is  most  striking  in  diabetic  acidosis. 

This  is  of  practical  importance  in  diabetes  mellitus.  The  increased  elimina- 
tion of  ammonia  led  in  this  case  to  the  discovery  that  certain  diabetic  urines 
contain  /3-oxybutyric  acid  (compare  p.  539),  and  that  the  amount  of  ammonia 
eliminated  indicates  in  an  approximate  manner  the  degree  of  acidosis.^ 

To  be  sure,  the  amount  of  ammonia  in  the  urine  is  not  exactly  parallel  to  the 
acid  formation  in  the  organism,  because  the  ammonia  becomes  serviceable  for  the 
neutralization  of  acids  only  when  the  available  fixed  alkalies  are  no  longer  suffi- 
cient, 

Magnus  Levy  makes  the  following  estimation:  About  1  to  2  gm.  of  the 
ammonia  excreted  by  a  diabetic  are  for  the  purpose  of  neutralizing  the  fixed 
excess  of  acid  resulting  from  the  proteid  diet,  and  only  the  remainder  is  the 
measure  for  the  pathologic  excretion  of  acid.  A  diabetic  with  4  grn.  of 
ammonia  in  the  urine  is  consequently  excreting  not  twice,  but  nearly  three  times, 
as  much  pathologic  acid  as  one  with  2  gm.,  since  1  gm.  or  more  of  the  2  or  4 
respectively  is  combined  with  the  acids  normally  excreted.  According  to  this 
supposition,  when  2  gm.  of  ammonia  are  excreted,  about  1  gm.  is  utilized  for 
combination  with  the  two  pathologic  acids  of  diabetes  (oxybutyric  and  diacetic 
acid);  while  an  elimination  of  5  gm.  leaves  3  to  4  gm.  for  this  purpose.  An 
excretion  of  8gm.,  which  is  but  rarely  observed,  gives  6  to  7  gm.  of  ammonia  as 

1  Of.  Naunyn,  "Diabetes  Mellitus,"  in  Nothnagel's  SammeJwerk,  1898,  p.  179;  and 
Magnus  Levy,  Arch.f.  exp.  Path.,  1899,  vol.  xlii.,  p.  1981. 


QUANTITATIVE   URINARY  ANALYSIS.  539 

the  measure  of  the  pathologic  amount  of  acids.  These  figures  correspond  to  6, 
20,  and  36  to  40  gm.  of  /i-oxybutyric  acid.  Magnus  Levy  also  points  out  that 
such  an  estimation  of  the  acids  from  the  ammonia  is  of  value  only  when  an  aver- 
age is  taken  from  the  observations  extending  over  several  days,  since  the  amount 
of  ammonia  formed  in  any  twenty-four  hours  will  vary  considerably  as  the  result 
of  the  temporary  retention  or  excretion  of  alkalies.  The  large  quantity  last  men- 
tioned, of  40  gm.  of  oxybutyric  acid,  he  says,  represents  the  maximum  quantity 
of  acid  which  the  body  can  neutralize  by  producing  ammonia  and  without  the 
administration  of  sodium  bicarbonate.  By  administering  40  gm.  of  this  substance, 
however,  the  organism  may  eliminate  60  gm.  of  oxybutyric  acid  daily  in  the 
urine.  Magnus  Levy  believes  that  this  latter  quantity  is  exceeded  only  in 
diabetic  coma. 

Schlosing  has  described  the  simplest  method  for  estimating  the  amount  of 
ammonia.  It  depends  upon  the  fact  that  aqueous  solutions  of  ammonia  readily 
part  with  their  ammonia  when  exposed  to  the  air,  and  that  when  dilute  sulphuric 
acid  is  placed  in  a  closed  chamber  near  the  ammonia,  the  acid  quickly  and  com- 
pletely absorbs  the  ammonia.  Therefore,  if  we  free  the  ammonia  from  a  known 
quantity  of  urine  by  the  addition  of  lime  water,  and  then  allow  it  to  become 
absorbed  in  a  closed  space  by  a  known  amount  of  sulphuric  acid,  the  amount  of 
absorbed  ammonia  can  easily  be  determined  by  a  simple  acidity  titration. 
Neubauer  proceeds  as  follows:  A  shallow  dish  with  vertical  sides,  containing  25  c.  c. 
of  filtered  urine,  is  placed  upon  an  exsiccator  plate.  A  triangular  glass  is  set 
over  the  top  of  the  dish  and  holds  another  vessel  containing  10  c.c.  of  normal 
sulphuric  acid.  At  least  10  c.c.  of  lime  water  are  now  added  to  the  urine, 
and  the  whole  is  then  quickly  covered  with  the  glass  bell  of  the  exsiccator,  whose 
margin  is  greased  with  tallow.  All  the  ammonia  in  the  urine  will  be  absorbed  by 
the  acid  within  three  or  four  days.     Then,  using  methyl  orange  as  an  indicator, 

N 
the  acid  is  all  titrated  with  -—  sodium  hydroxid  till  the  red  color  turns  to  yellow. 

Every  cubic  centimeter  less  than  40  of  the  sodium   solution  employed  corre- 

17 
sponds  to   —  mg.  of  NH3. 

The  objection  to  Schlosing' s  method  is  the  length  of  time  required  for  the 
estimation.  Folin^  tried  to  shorten  the  period  by  forcing  the  freed  ammonia 
into  the  acids  by  a  current  of  air.  Nenski  and  Zaleski,'^  as  well  as  Soldner,* 
distil  the  freed  ammonia  in  a  vacuum  into  the  titrated  acids.  These  methods 
require  carefully  made  apparatus,  and  for  their  details  the  writer  must  refer  the 
reader  to  the  original  communications. 

Schmiedeberg'  s  *  platinum  chlorid  method  may  be  more  quickly  carried  out 
than  Schlosing' s,  but  it  is  also  more  complicated. 

QUANTITATIVE   ESTIMATION    OF  THE   /J-OXYBUTYRIC  ACID  IN 

THE   URINE. 

The  quantitative  estimation  of  /3-oxybutyric  acid  is  of  great  interest  in  diabetic 
acidosis.  Polarization  is  a  practical  chemical  method.  /J-oxybutyric  acid  is  levo- 
gyrate,  and  has  a  specific  rotating  power  of  23.4°  or  of  20.6°,  according  to  different 
authorities.  Fermented  urine  is  freed  from  proteid  and  decolorized  with  lead  ace- 
tate and  ammonia  or  mercuric  chlorid,  and  its  rotatory  power  is  then  determined 
(p.  516  et  seq.).  If  the  100  mm.  tube  of  the  polaristrobometer  is  used  (p.  517),  Min- 
kowski states  that  a  rotation  of  1°  will  correspond  to  -^— -  per  cent,  of  /3-oxybutyric 

acid  (about  5  per  cent.).  In  this  estimation  we  must  naturally  assume  that  the 
urine  does  not  contain  any  other  non-fermentable  substances  which  are  levogyrate, 

^  Zeits.  f.  phys.  Chem.,  1902,  vol.  xxxvii.,  p.  161. 
^Ibid.,  1901,  vol.  xxxiii,,  p.  237. 
^  Zeits,  f.  Biol.,  vol.  xxxviii.,  p.  237. 
*  Arch.  /.  ex}}.  Path.,  vol.  vii.,  p.  166. 


640  URINARY  EXAMINATION. 

such  as  the  combined  glycuronates,  etc.  A  positive  Trommer's  test  with  the 
fermented  urine  would  point  to  their  presence.  The  normal  constituents  of  the 
urine  which  turn  the  plane  of  polarized  light  to  the  left,  such  as  uric  acid  and 
kreatinin,  do  not  disturb  the  test,  because  the  rotation  caused  by  them  is  very 
slight,  and,  besides,  there  is  only  a  very  small  percentage  of  them  in  diabetic 
polyuria. 

Magnus  Levy  ^  regards  the  quantities  obtained  by  this  method  inaccurate,  and 
thinks  they  are  too  large,  but  is  unable  to  give  a  satisfactory  explanation  of  the 
marked  levogyration  found  in  these  cases. 

For  clinical  purposes  the  quantitative  estimation  of  the  excretion  of  ammo- 
nia is  the  best  indirect  means  for  determining  the  amount  of  /?-oxybutyric  acid 
excreted. 

Darmstadter's"'*  method  for  the  direct  estimation  of  the  ^-oxybutyric  acid 
seems  worthy  of  recommendation.  It  depends  upon  the  fact  that  /3-oxybutyric 
acid  is  broken  up  into  crotonic  acid  and  water  by  concentrated  mineral  acids. 
The  method  is  carried  out  as  follows:  100  c.c.  of  urine  are  rendered  alkaline 
with  sodium  carbonate  and  evaporated  almost  to  dryness  ;  the  residue  is  dis- 
solved in  150  to  200  c.c.  of  50  to  55  per  cent,  sulphuric  acid ;  300  to  350  c.c. 
are  now  distilled  from  this  mixture  within  two  to  two  and  one-half  hours,  the 
fluid  removed  being  replaced  by  water  ;  the  distillate  is  now  shaken  two  or  three 
times  with  ether,  the  ether  evaporated,  and  the  residue  heated  to  160°  C,  in 
order  to  remove  any  volatile  fatty  acids  which  may  be  present.  The  residue  is 
then  dissolved  in  50  c.  c.  of  water,  the  solution  filtered,  and  titrated  with  tenth- 
normal sodium  hydroxid  solution  :  1  c.c.  tenth-normal  sodium  hydroxid  solu- 
tion equals  0.0086  crotonic  acid;  1  part  crotonic  acid  equals  1.21  /?-oxybutyric 
acid. 

According  to  Magnus  Levy,  60  gm.  of  /3-oxybutyric  acid  may  be  excreted 
when  diabetic  coma  is  not  present,  while  in  coma  daily  amounts  of  over  150  gm. 
have  been  observed.  The  percentage  found  by  Magnus  Levy  in  diabetic  urine 
rarely  exceeded  0.5  to  1  per  cent. 

QUANTITATIVE  ESTIMATION  OF  THE  AMOUNT  OF  ACETONE  IN 

THE  URINE. 

Acetonuria  is  an  accompanying  phenomenon  of  diabetic  acidosis  ;  hence,  in 
addition  to  the  /3-oxybutyric  acid  estimation,  a  quantitative  acetone  estimation  is 
of  some  importance.  The  simplest  method  is  to  weigh  the  iodoform  which  is  pro- 
duced from  acetone  by  Lieben'  s  reaction.  One  hundred  cubic  centimeters  of  urine 
are  concentrated  in  vacuo  to  10  c.c,  and  well  cooled,  a  large  excess  of  sodium 
hydroxid  and  a  supersaturated  iodopotassium  iodid  solution  (p.  495,  Lieben' s 
Reaction)  are  then  added  to  the  distillate.  The  resulting  iodoform  is  allowed  to 
stand  twenty-four  hours  in  the  solution,  and  is  then  filtered  through  a  weighed 
filter  (glass-wool)  ;  the  precipitate  is  washed  with  a  little  cold  water,  and  then 
allowed  to  dry  for  a  short  time  over  sulphuric  acid.  One  gram  of  iodoform  cor- 
responds to  0.147  gm.  of  acetone.  It  is  simpler  to  extract  the  iodoform  by  means 
of  ether.  For  this  purpose  20  c.  c.  of  ether  free  from  alcohol  are  placed  in  the 
vessel  in  which  the  iodoform  is  formed,  the  mixture  is  well  shaken  and  10  c.c.  of 
the  ether  are  removed  by  means  of  a  pipet  and  evaporated  in  a  weighed  dish. 
The  residue  is  dried  over  sulphuric  acid  and  weighed. 

Acetone  and  diacetic  acid  usually  occur  together  in  the  urine  ;  hence,  the 
iodoform  obtained  includes  not  only  that  derived  irom  the  preformed  acetone,  but 
also  that  derived  from  the  acetone  formed  from  the  diacetic  acid  by  the  distilla- 
tion. Acetone  and  diacetic  acid  are  about  equally  valuable  in  diagnosis  (see  p. 
493),  so  this  is  no  particular  disadvantage.  Besides,  as  we  have  no  exact  method 
of  determining  the  amount  of  diacetic  acid,  the  estimation  of  the  acetone  is  the 
only  way  in  which  we  can  obtain  an  approximate  idea  of  the  amount  of  diacetic 
acid. 

^  Arch./,  exp.  Path.,  vol.  xlii.,  p.  167  et  seq. 

^  Zeits.  f.  physiol.  Chem.,  1902-3,  vol.  xxxvii.,  p.  355. 


QUANTITATIVE   URINARY  ANALYSIS.  541 

ESTIMATION  OF  THE  TOTAL  DRIED  RESIDUE  OF  URINE. 

Sometimes  this  is  of  clinical  interest.  The  author  has  demonstrated  that  a 
watery  diuresis— i  e.,  diuresis  produced  by  an  increased  consumption  of  water, 
more  especially  from  a  subcutaneous  or  intravenous  infusion  of  salt  solution — will 
increase  the  twenty-four-hour  excretion  of  solids  in  the  urine.  The  method  of 
determination  is  very  simple.  Fifty  cubic  centimeters  of  urine  in  a  crucible  are 
weighed  evaporated  to  a  syrupy  consistence  over  a  water  bath  at  a  very  moderate 
temperature  (not  over  60°  C.)  after  adding  2  or  3  drops  of  acetic  acid,  then  dried 
further  in  a  vacuum  over  sulphuric  acid  to  a  uniform  weight.  The  urme  must 
be  heated  above  60°  C,  as  otherwise  ammonia  will  be  given  off  from  the  urea. 
The  addition  of  acetic  acid  is  necessary  to  combine  with  any  ammonia  which  may 
have  been  liberated  in  spite  of  the  care  taken  when  evaporating. 

It  is  still  safer  to  dry  entirely  in  a  vacuum  without  heating,  but  then  a  much 
smaller  amount  of  urine  (at  most  5  c.c.)  should  be  employed.  A  drop  of  acetic 
acid  is  added  to  the  urine  in  a  very  shallow  dish,  along  with  a  generous  amount 
of  sulphuric  acid,  and  it  is  then  allowed  to  dry  in  the  vacuum  to  an  absolute 
weight.  If  necessary,  the  sulphuric  acid  can  be  replenished  and  the  vacuum 
restored  by  repeated  exhaustion.  ._.,,.         n 

An  approximate  estimation  of  the  total  amount  of  solids  m  1  liter  ot  urme 
can  be  obtained  from  the  specific  gravity  of  the  urine  (see  p.  451).      ■ 

URINARY  AQDIMETRY  AND  ALKALIMETRY, 

(Determination  of  Acidity  and  AlkaHnity.      Estimation  of  the  Acidic  and  Basic 

Points.) 

The  conditions  which  affect  the  reaction  of  the  urine  have  already  been 
discussed  upon  p.  455  et  seq.  The  reaction  of  individual  specimens  of  urine 
varies-  hence,  the  degree  of  acidity  must  be  determined  from  a  specimen  of  the 
mixed  twenty-four-hour  urine.  The  addition  of  a  few  drops  of  chloroform,  or 
keeping  the  urine  upon  ice,  will  prevent  any  change  in  the  reaction  due  to 
decomposition. 

The  quantitative  estimation  of  the  reaction  by  means  of  acidimetry  or  alka- 
limetry is  accomplished  by  titration.  Certain  objections  have  been  constantly 
raised  in  reference  to  the  possibility  of  titrating  the  acidity  of  the  urine,  and 
these  objections  have  also  been  fully  considered  in  Nageli's  ^  experiments  upon  this 
subject,  which  were  undertaken  at  the  writer's  request.  The  writer  fiiUy  real- 
izes the  theoretic  justification  of  all  these  objections,  which  arise  from  the  fact 
that  the  end  reactions  of  the  titration  of  the  phosphoric  acid  are  theoretically 
never  distinct,  and  not  always  so,  even  from  a  practical  standpoint.  The  reasons 
for  this  fact  have  been  clearly  explained  by  T.  Heffter.^  So  long  as  the  cheniist 
gives  us  nothing  better,  however,  we  are  forced  to  use  these  methods  in  practice, 
even  though  they  are  not  strictly  accurate,  and  Nageli  has  at  least  shown  that  it 
is  possible  to  obtain  approximate  values  for  the  acidity  of  the  urine  by  means  of 

titration.  .  . ,.      ,  • 

In  view  of  the  undeniable  difficulties  of  titrating  the  urine  acidimetri- 
cally  the  writer  thinks  it  is  entirely  beside  the  mark  to  attempt  to  replace  the 
classic  conception  of  acidity  by  an  entirely  different  one— namely,  the  concen- 
tration of  the  hydrogen  ions — instead  of  trying  to  improve  the  method  of  titra- 
tion. The  acidity  is  not  due  to  the  concentration  of  the  hydrogen  ions,  but  to 
the  number  of  hydrogen  atoms  capable  of  being  replaced  by  metals  and  contained 
in  a  given  quantity  of  a  fluid.  These  are  entirely  different  conceptions,  and,  since 
the  old  conception  of  acidity  is  still  upheld  by  the  teachings  of  physical  chem- 
istry, nothing  but  confusion  can  result  from  the  substitution  of  a  new  conception. 
For  this  reason  the  writer  believes  that  L.  v.  Eohrer's  ^  estimation  of  the  acidity 

1  Zur  Aciditatsbestimmung  des  Urines,  Zeils.  f.  physiol.  Chemie,  vol.  xxx.,  parts  3, 
4  and  5,  p.  366.  '^  Ergebnisse  der  Physiol.,  I.  Jahrg.,  1902. 

'  '    '  »  Pfliiger's  Archiv,  vol.  Ixxxvi. 


542 


URINARY  EXAMINATION. 


of  the  urine  by  determining  the  concentration  of  the  hydrogen  ions  tends  to  lead 
us  into  a  hopeless  tangle. 

Nageli  tested  a  large  number  of  indicators  in  reference  to  their  behavior 
toward  the  more  important  salts  occurring  in  the  urine,  and  ascertained  how 
much  information  could  be  obtained  from  them  by  any  change  of  color  they 
might  undergo  upon  titration  with  an  alkali  or  an  acid,  in  reference  to  the  chem- 
ical saturation  of  the  acidic  or  basic  affinities  of  the  urine.  The  following  discus- 
sion gives  the  essential  results  and  conclusions  obtained  by  Xageli. 

Only  two  reagents,  phenolphthalein  and  alizarin-red,^  are  of  any  value  for 
the  purpose  under  discussion.  Litmus  is  absolutely  useless  ;  it  never  shows  any 
sharp  change  of  color  when  titrating  phosphates.  When  phenolphthalein  is 
used  the  end  reaction  is  indicated  by  the  bright-red  color  sho\\Ti  by  this  indicator 

N         . 

when  the  acid  solution  becomes  alkaline  on  the  addition  of  -^   sodium  hydroxid 

solution.  (For  preparation  see  p.  378).  When  alizarin-red  is  employed,  the 
change  from  red  to  yellow  indicates  the  end  reaction  which  takes  place  upon 

adding    —  hydrochloric  acid  to  an  alkaline  solution,  the  moment  free  acid  is 

present.  Alizarin-red  does  not  react  to  acid  salts  nor  to  CO^.  The  following  table 
indicates  best  how  the  most  important  constituents  of  the  urine  react  on  titration 
toward  the  above  indicators : 


Titration    with     phenol- 
phthalein  and  --  XaOH. 

r 

Colorless  as  long  as  are  T  i 
present :  j 


Keutral  point :  

Eed,  as   soon   as  KaOH 
changes  all  to : 


Basic  point :  - 

(free  alkali) 
not  determinable. 


■S'aHjPO,,  KH,PO,.  XH.H^ 

PO^CafHjPO,)^^ 
H2CO3  (carbonic  acid) 


HPO4,  CaHPO,,  ^'aHC03 
KaHCO, 


Yellow  as  soon  as  free  HCl 
is  present. 

Acidic  point. 


Red. 

Titration    with   alizarin- 
red  and  ^jT  HCl. 


Urea,  chlorides,  sulphates,  urates,  oxalates,  kreatinin,  et  a!.,  remain  indifferent 
to  titration,  but,  on  account  of  their  small  quantity,  they  are  unimportant. 

The  above  table  shows  that  titration  of  urine  with  sodium  hydrate  and  phenol- 
phthalein to  determine  the  point  of  neutralization  gives  valuable  information 
as  to  acid  affinities  and  acid  equivalents.     The  value  found,   usually  expressed 

in  cubic  centimeters  of  ~-  sodium  hydroxid,  is  usually  termed  the  acidity  of  urine. 

This  does  not,  of  course,  indicate  the  amount  of  acid  excretion,  but  only  how 
much  the  acid  equivalents  contained  in  the  urine  exceed  the  basic  ecjuivalents. 
The  amount  of  acid  in  the  form  of  neutral  salts  (XaCl)  or  salts  reacting  alka- 
line to  phenolphthalein  (Xa^HPOJ  is,  of  course,  not  included  in  the  acidity. 
Besides  this,  it  should  be  remembered  that,  when  titrating  with  phenolphthalein, 
the  neutral  point  is  placed  where  all  phosphates  are  transformed  into  secondary 
salts  corresponding  to  the  formula  Xa^HPO^,  and  the  H^COg  is  changed  to 
NaHCOj.  In  this  sense  the  acidity  is  not  identical  with  the  basic  capacity, 
because  phosphates  with  the  formula  Xa^HPO^  can  still  take  up  one  more  basic 
atom.  The  basic  point — ;.  e. ,  the  moment  Ka^HPO^  is  changed  to  NajPO^  by 
the  addition  of  XaOH  and  free  alkali  becomes  present — cannot  be  determined  by 
any  indicator. 

^  Alizarin-red  of  Merck  (Alizarin  sodium  sulplionate). 


QUANTITATIVE  URINARY  ANALYSIS.  543 

N 
By  titration  witli  --  HCl  and  alizarin-red  one  obtains   in  a   similar  manner 

information  as  to  the  basic  equivalents  in  the  urine.     Just  as  the  acidity  is  meas- 

N  N 

ured  with  --  sodium  hydroxid,  the  basidity  is  measured  with  —  HCl.     The  acidity 

can  be  ascertained  only  to  the  neutral  point,  not  to  the  basic  point,  whereas  the 

total  basicity  may  be  determined,  because  the  moment  when  free  acid  appears, 

N 
following  the  addition  of  —  HCl  (acid  pointj,  is  indicated  sharply  by  alizarin-red. 

Leaving  out  of  consideration  the  urates  and  oxalates,  the  sum  of  the  values 
according  to  alizarin  and  phenolphthalein  corresponds  approximately  to  the  con- 
tents of  carbonic  and  phosphoric  acid  molecules  in  the  urine.  Finally,  the  two 
titrations  give  an  insight  as  to  the  amount  of  the  bases  which  are  excreted  com- 
bined witli  phosphoric  acid.  If  the  urates,  oxalates,  and  carbonates  are  not  con- 
sidered, this  amount  is  approximately  obtained  when  the  value  of  the  phenol- 
phthalein titration  is  added  to  double  that  of  the  alizarin  titration.  In  the 
titration  with  phenolphthalein,  as  much  alkali  equivalent  is  added  to  com- 
plete the  reaction  as  there  is  in  the  phosphates  corresponding  to  the  formula 
NaHjPO^  and  appearing  in  the  reaction ;  while  in  the  alizarin  reaction  one-half 
as  much  acid  equivalent  must  be  added  in  order  to  bring  about  the  end  reaction. 
This  calculation  contains  considerable  errors  only  when  there  are  present  in  the 
urine  relatively  large  quantities  of  carbonates,  oxalates,  or  urates,  which  may  enter 
into  the  reaction.     This  is  seldom  the  case,  however. 

Urines  which  reacted  alkaline  to  phenolphthalein  could  be  titrated  by  means  of 

N  ' 

--  HCl  with  the  indicator  and  the  neutralization  point  accurately  determined  if  the 

alkalinity  were  caused  hy  fixed  alkalies.     This  condition,  however,  has  never  been 
obsers'ed.     In  general,  a  mine  which  reacts  alkaline  to  phenolphthalein  contains 

N 
ammonium  carbonate,  and  in  this  case  the  addition  of  --  HCl  causes  the  forma- 
tion of  acid  ammonium  carbonate,  which  immediately  decomposes  and  liberates 
COj  and  NH^.  The  indicator,  being  much  more  sensitive  to  CO2  than  to  NH3, 
becomes  decolorized  (by  the  CO^)  long  before  the  NH3  in  the  urine  is  completely 
neutralized — i.  e. ,  before  all  the  (NH J^NCOg  is  transformed  into  (NH JHCO3.  The 
obtaining  of  an  accurate  end  reaction  with  phenolphthalein  under  these  conditions 
is  therefore  impossible.  Actually,  however,  this  difiiculty  presents  no  serious  dis- 
advantage, because  the  ammoniacal  character  of  urine,  with  the  exception  of  the 
presence  of  ammonium  carbamic  acid  as  the  result  of  calcium-feeding,  is  caused 
exclusively  by  the  bacterial  decomjjosition  of  urine.  In  such  cases  quantitative 
determinations  have  no  interest.  On  the  other  hand,  it  is  to  be  emphasized  that 
the  determination  of  the  acid  point — i.  e.,  the  point  at  which  all  the  NH^Cl 
is  transformed  into  HCl — presents  no  difficulties.  Such  determinations  acquire 
under  certain  conditions  clinical  interest  in  the  consideration  of  the  degree  of 
bacterial  decomposition  of  freshly  voided  urine  in  cystitis. 

On  the  other  hand,  it  is  conceivable  that  titration  with  HCl  in  the  presence 
of  alizarin  does  not  lead  to  accurate  results  if  the  urine  contains  large  amounts 
of  ammonium  salts,  as  is  the  case  in  diabetic  acidosis.  Niigeli  found  in  the 
titration  of  the  ammonium  salts  of  dibasic  acids — e.  g.,  ammonium  oxalate 
with  HCl — that  the  change  of  color  of  the  alizarin  into  yellow  does  not  take 
place  at  the  moment  of  the  appearance  of  free  acid,  but  as  soon  as  the  acid  salts 
are  formed.  The  color-change  is  also  too  gradual  to  allow  of  sharj)  reading. 
Nevertheless,  this  disturbance  of  the  reaction  does  not  come  into  play  in  the 
case  of  a  monobasic  acid,  such  as  /3-oxybutyric.  In  the  normal  condition  of  the 
excreted  ammonium  salts,  these  hardly  effect  the  determination  of  the  acid  point. 
In  cases  where  the  ammonium  content  of  the  urine  is  excessive,  the  determina- 
tion of  the  acid  point  can  be  performed  as  follows  :  In  a  portion  of  the  urine 
the  ammonium  is  quantitatively  determined  according  to  the  Schlosing  method 
(p.  539),  and  then  to  another  portion  is  added  the  equivalent  amount  of  NaOH, 


544  URINARY  EXAMINATION. 

sufficient  to  set  the  NH3  free.  This  ammonia  can  be  driven  oflf  by  heat,  and  the 
solution  then  titrated  in  the  usual  way. 

In  practice  the  titration  is  carried  out  in  the  following  manner :  To  2  por- 
tions of  10  c.c.  of  the  urine  are  added  respectively  phenolphthalein  and  alizarin. 

N 
The  first  is  titrated  with   --    NaOH   to   the    appearance   of    a   permanent   red 

N 
color.     To  the  second,  --  HCl  is   added  until  the  red   color   has   changed  to 

yellow.     The  color  of  the  urine  itself  does  not  interfere  in  the  titration  to  any 

noticeable  extent,  especially  if  there  is  placed  alongside  of  the  beaker  in  which 

the  titration  is  being  performed   a  second,  for  control,  with  equal  amounts  of 

urine  and  indicator  to  which  no  acid  or  alkali  is  added.     Both  solutions  should 

be    diluted  to  an    equal    extent.      Strongly  colored   urine    can   be  decolorized 

by  animal   charcoal  which  has  been  tested  and  found  to  be  neutral.     If  the 

end   reaction   is  not  sharp    and  the  cause   is   to  be   ascribed   to    the   presence 

of  ammonium  salts,   then  the  latter  may  be  removed  by  NaOH  in  equivalent 

amounts,   as  before  described.      For  the  technic  of  titration  and  preparation  of 

normal  solutions  see  pp.  378  and  381.     Proteid  must  be  removed  by  heat  and 

acetic  acid,  in  which  case  a  known  amount  of  the  acid  should  be  added,  and 

this  taken  into  consideration  in  the  titration.     The  values  found  in  these  titra- 

N 
tions  may  be  expressed  in  cubic  centimeters  of  --  NaOH,  or  calculated  in  grams 

N 
of  NaOH  (a  —  NaOH  solution  contains  in  a  liter  4  gm.  of  NaOH).     Haig 

found  that  the  average  acidity  of  the  daily  urines  of  healthy  persons  equalled  5.5 
gm.  of  oxalic  acid  or  3. 5  gm.  of  NaOH.  Spath,  however,  gives  a  daily  acidity 
of  1.45  gm.  of  HCl,  corresponding  to  1.60  gm.  of  NaOH. 

Freund  has  lately  suggested,  and  Lieblein  ^  has  agreed  with  him,  that  the  acidity 
of  the  urine  can  be  estimated  from  the  amount  of  acid  phosphates,  since  the  acid 
reaction  of  urine  is  due  mainly  to  these  salts. 

Lieblein  estimates  in  the  usual  way  the  total  amount  of  phosphoric  acid  in 
a  definite  volume  of  urine  by  means  of  uranium  nitrate  (compare  p.  536).  He 
then  removes  the  secondary  acid  phosphate  from  an  equal  amount  of  urine  by 
precipitation  with  barium  chlorid,  and  titrates  again  the  acid  phosphates  in  the 
filtrate.  Niigeli's  researches  have  raised  certain  objections  to  this  method,  how- 
ever. 

Nemmister^  suggests  a  method  to  prevent  the  phosphate  from  interfering 

with  all  acidity  titrations.     It  is  a  modification  of  Maly's^  old  procedure.     Fifty 

N 
cubic  centimeters  of  urine  are  rendered  strongly  alkaline  by  adding  25  c.c.  — , 

sodium  hydroxid,  the  mixture  is  heated  to  boiling,  25  c.c.  of  a  barium  chlorid 

solution  sufficiently  concentrated  to  precipitate  all  the  phosphoric  acid  are  then 

added.     The  resulting  mixture  is  shaken,  and  50  c.c.  are  filtered  through  a  dry 

filter  (equal  to  25  c.c.  of  the  urine)  ;  the  filtrate  is  colored  with  phenolphthalein 

N  .        . 

and    then    titrated   with  -—  sulphuric  acid  to  the  appearance  of  a  neutral  reac- 

tio'i.  The  less  sulphuric  acid  required,  the  stronger  the  acidity  of  the  specimen 
of  urine. 

Nageli  considers  this  modification  of  Maly's  original  method  to  be 
entirely  unreliable  {loc.  cit). 

^  Freund,  Ceniralbl.  f.  d.  med.  Wissenschaft,  1892,  p.  689 ;  Lieblein,  Zeiis.  f.  physiol. 
Chemie.,  vol.  xx.,  parts  1  and  2. 

^  Lehrbiich  d.  physiol.  Chemie,  1895,  vol.  ii.,  p.  225. 
'  Zeits.  f.  anal  Chemie,  vol.  xv.,  p.  417. 


QUANTITATIVE   URINARY  ANALYSIS.  545 

CRYOSCOPY    OF   THE   URINE;    OSMOTIC    PRESSURE   OR   THE 
MOLECULAR   CONCENTRATION    OF  THE   URINE. 

PREFATORY    NOTES. 

According  to  van  t'Hoff,  substances  held  in  solution  act  like  gases,  and  this 
observer  has  shown  that  the  laws  of  Boyle-Mariotte,  Gay-Lussac,  and  Avo- 
gadro  apply  to  these  substances  as  well  as  they  do  to  gases.  The  dissolved 
molecules  behave  exactly  like  the  molecules  of  a  gas,  which  exert  a  pressure 
upon  the  wall  of  the  containing  vessel  by  their  endeavor  to  diffuse  themselves 
through  the  greatest  possible  space.  This  pressure  of  dissolved  molecules  is  the 
osmotic  pressure,  and  this  pressure,  according  to  van  t'  HofF,  corresponds  to  the 
pressure  which  the  dissolved  substance  would  exert  as  gas  or  vapor  of  the  same 
molecular  concentration  and  in  the  same  space.  From  this  it  follows  that 
osmotic  pressure  shows  the  same  dependence  upon  the  temperature  as  does  the 
pressure  of  a  gas,  according  to  the  law  of  Gay-Lussac,  and  also  that  solutions 
which  contain  the  same  number  of  molecules  in  the  same  volume  of  fluid  pos- 
sess the  same  osmotic  pressure,  just  as  gases,  according  to  Avogadro's  law,  exert 
the  same  pressure  when  they  contain  the  same  number  of  molecules  in  the  same 
space.  If  we  apply  the  law  of  gases  to  solutions,  it  will  also  be  found  that  just 
as  every  gram  molecule  or  "mol"  of  a  gas — i.  e.,  the  quantity  which  weighs  as 
many  grams  as  there  are  units  in  the  molecular  weight — in  a  space  equivalent  to 
22.4  liters  at  0°  C.  exerts  a  pressure  of  one  atmosphere,  so  also  that  solutions 
which  contain  1  gram  molecule  of  substance  dissolved  in  22.4  liters  of  fluid  possess 
an  osmotic  pressure  of  one  atmosphere.  Vice  versa,  if  1  gram  molecule  be  dissolved 
in  a  liter  of  water,  the  osmotic  pressure,  corresponding  to  Mariotte's  law,  will  be 
22. 4  atmospheres.  From  this  it  will  also  be  observed  that  the  osmotic  pressure 
is  directly  proportional  to  the  concentration.  A  1  per  cent,  sugar  solution,  for 
example,  possesses  double  the  osmotic  pressure  of  a  0.5  per  cent,  solution. 
These  laws,  however,  apply  only  to  solutions  of  non-electrolytes.  Electrolytic 
substances,  such  as  acids,  bases,  and  salts,  when  in  solution  are  partly  dissociated 
into  ions,  and  a  comparison  of  the  osmotic  pressure  with  the  concentration  of  the 
ions  shows  that  in  such  solutions  the  osmotic  pressure  is  affected  by  the  ions  just 
as  it  is  by  the  molecules  (Arrhenius,  van  t'Hoff).  The  osmotic  pressure  of  a 
partly  dissociated  solution  is  consequently  proportional  to  the  sum  of  the  undis- 
sociated  molecules  and  of  the  ions.  The  osmotic  pressure  of  a  0. 5  per  cent, 
solution  of  sodium  chlorid,  unlike  that  of  a  sugar  solution  of  corresponding 
strength,  is  more  than  half  of  the  osmotic  pressure  of  a  1  per  cent,  solution, 
because  dilute  solutions  are  more  strongly  dissociated  and  contain  proportionately 
more  ions  than  do  concentrated  solutions. 

Under  ordinary  conditions,  osmotic  pressure  has  as  little  visible  effect  as  has 
the  pressure  of  a  gas  confined  within  a  vessel.  We  can,  however,  demonstrate 
the  effect  of  osmotic  pressure  by  carrying  out  certain  experiments.  For  example, 
if  we  place  a  watery  solution  of  a  substance  in  a  vessel  with  membranous,  yield- 
ing walls  which  will  allow  the  passage  to  water  but  not  to  the  dissolved  substance, 
and  place  this  closed  vessel  in  water,  the  dissolved  molecules  will  become  sep- 
arated in  proportion  to  the  amount  of  water  which  penetrates  the  membrane 
from  without.  By  this  means  the  osmotic  pressure  becomes  manifest,  and  there 
is  a  distention  of  the  elastic  vessel,  an  effect  of  pressure  in  the  ordinary  sense  of 
the  word.  The  latter  phenomenon  has  also  been  designated  as  a  result  of  the 
' '  attraction  of  the  solution  for  water ' ' ;  this  is  readily  understood,  but  it  does 
not  indicate  the  theoretic  point  involved.  The  amount  of  this  "attraction"  is 
equal  to  the  osmotic  pressure,  since  equilibrium  is  not  established  in  any  experi- 
ment until  the  hydraulic  pressure  has  become  equal  to  the  osmotic  pressure.  The 
osmotic  pressure  of  a  watery  solution  may  consequently  be  measured  hydraulically 
by  placing  the  particular  solution  in  a  tube,  the  lower  end  of  which  is  closed  by 
a  membrane  that  allows  the  water,  but  not  the  dissolved  substance,  to  pass  through 
it,  and  then  placing  the  lower  portion  of  this  tube  in  a  vessel  of  distilled  water. 
The  water  passes  into  the  tube  through  the  pores  of  the  membrane,  and  the  solu- 
35 


546 


URINARY  EXAMINATION. 


tion  continues  to  be  diluted  until  the  hydrostatic  pressure  in  the  tube  becomes 
equal  to  the  osmotic  pressure  of  the  original  solution.  In  this  experiment  the 
final  height  of  the  column  of  fluid  is  consequently  the  measure  of  the  osmotic 
pressure,  and  the  latter  may  be  correspondingly  expressed  in  atmospheres.  This 
method,  however,  is  not  very  practical,  and  the  osmotic  pressure  of  solutions  is. 
usually  determined  in  another  manner,  as  will  presently  be  shown. 


S^ 


METHOD  OF  DETERMINING  THE  FREEZING-POINT. 

In  medicine  we  are  chiefly  concerned  with  the  determination  of  the  osmotic, 
pressure  of  the  blood  and  of  the  urine,  more  rarely  with  that  of  other  fluids  of 
the  body.  The  best  method  for  this  purpose,  and  the  one  which  is  almost 
exclusivly  employed,  is  the  method  of  determining  the  freezing-point,  or  cryo- 
scopy.  The  method  depends  upon  the  fact  discovered  by 
Raoult,  that  the  lowering  of  the  freezing-point  of  a  wateiy 
solution,  as  compared  with  the  freezing-point  of  distilled 
water,  is  proportional  to  the  molecular  concentration  of 
the  solution — i.  e.,  to  the  number  of  molecules  contained 
in  a  unit  of  volume,  and  consequently  (see  above)  to  the 
osmotic  pressure.  We  must,  nevertheless,  remember  the 
fact  pointed  out  by  Arrhenius  and  van  t'HofF,  that  in 
partly  dissociated  solutions  the  ions  have  the  same  values 
as  the  undivided  molecules  in  determining  osmotic  press- 
ure, and  consequently  in  the  lowering  of  the  freezing- 
point.  It  will  be  seen  from  what  has  been  said  that  if 
one  watery  solution  has  a  freezing-point  of  —  1°  C,  and 
another  has  one  of  —  0.5°  C,  then  the  first  solution  pos- 
sesses double  the  osmotic  pressure  of  the  second.  The 
lowering  of"  the  freezing-point  is  usually  designated  by  A, 
and  the  minus  sign  is  omitted.  A  solution  which  freezes 
at  —  1°  C.  consequently  has  a  lowering  of  the  freezing- 
point,  A  =  1.  From  the  previously  stated  fact,  that  a 
gram  molecule  dissolved  in  a  liter  of  water  has  an  os- 
motic pressure  of  22.4  atmospheres,  it  is  easy  to  estimate 
the  osmotic  pressure  in  atmospheres  from  the  lowering  of 
the  freezing-point.  Since  a  gram  molecule  dissolved  in  a 
liter  of  water  produces  a  lowering  of  the  freezing-point 
indicated  by  A  =  1. 85,  it  follows  that  a  lowering  of  the 
freezing-point  of  1.85  corresponds  to  an  osmotic  pressure 
of  22.4  atmospheres.  Moreover,  since  the  lowering  of 
the  freezing-point  and  the  osmotic  pressure  vary  propor- 
tionately, the  correct  osmotic  pressure  of  any  solution 
may  be  estimated  in  atmospheres  from  the  freezing-point 
of  the  solution.  The  blood,  for  example,  has  an  osmotic 
pressure  of  about  7  atmospheres.  From  a  medical  stand- 
point, however,  we  are  more  interested  in  the  deviation  of 
the  fluid  examined  fi-om  the  normal^i.  e.,  in  a  relative 
value — and  consequently  the  freezing-point  is  not  usually 
calculated  in  pressure  values,  but  the  osmotic  pressure  is  simply  indicated  by  the 
lowering  of  the  freezing-point. 

The  freezing-point  is  usually  determined  by  means  of  Beckmann's  apparatus, 
Heidenhain's  modification  of  which  is  shown  in  Fig.  184.  The  instrument  is 
composed  of  the  following  parts :  a  is  a  battery  jar,  which  has  a  metal  cover  (b), 
perforated  in  the  middle.  This  jar  holds  the  freezing-mixture,  which  may  be 
stirred  by  the  strong  wire  loop  (c).  The  opening  in  the  lid  gives  passage  to  the 
wide  reagent  glass  (d),  in  which  the  actual  freezing-vessel  (e)  is  held  in  place  by 
a  perforated  cork.  This  freezing-vessel  has  a  lateral  prolongation  {/),  the  import- 
ance of  which  for  the  "inoculation  of  the  fluid  "  will  subsequently  be  pointed 
out.     Between  the  vessels  d  and  e  there  is  an  enclosed  layer  of  air,  which  is  for 


Fig.  184.— Beckmann- 
Heidenhain's  apparatus 
for  determining  the 
freezing-point  of  a  solu- 
tion. 


QUANTITATIVE   URINARY  ANALYSIS.  547 

the  purpose  of  allowing  the  cold  to  act  gradually  upon  the  fluid  contained  in  e. 
The  thermometer  (g),  divided  into  hundredths  of  a  degree,  is  held  in  the  freezing- 
vessel  by  means  of  a  perforated  cork,  which  also  gives  passage  to  the  platinum- 
wire  stirrer  (h).  The  thermometer  of  the  original  apparatus  does  not  possess  a 
fixed  zero,  since  in  purely  physical  experiments  it  must  be  used  not  only  for 
watery,  but  also  for  other  solutions  having  an  entirely  different  freezing-point. 
By  a  special  manipulation,  the  details  of  which  may  be  omitted,  the  amount  of 
mercury  in  the  thermometer  may  be  increased  or  diminished  from  a  specially 
constructed  reservoir  at  the  toi^  of  the  thermometer,  so  that  the  freezing-point 
of  the  particular  solvent  can  be  brought  within  the  scale.  The  freezing-point  of 
the  pure  solvent  is  first  determined,  and  then  that  of  the  solution.  The  difference 
obtained  is  the  lowering  of  the  freezing-point  in  hundredths  of  a  degree. 

This  procedure  with  the  original  instrument  of  Beckmann  is  too  complicated 
for  clinical  purposes,  and,  as  we  have  to  do  with  watery  solutions  only,  we  now 
usually  employ  a  thermometer  with  a  fixed  zero  (Heidenhain),  which  is  found  at 
the  upper  end  of  the  scale,  and  corresponds  to  the  freezing-point  of  pure  distilled 
water  (see  figure).  Below  this  point  the  scale  is  divided  into  hundredths  of  a 
degree.  The  upper  end  of  the  capillary  thermometer  tube  is  expanded,  so  that 
when  the  instrument  is  exposed  to  higher  external  temperatures  the  mercury  may 
accumulate  in  this  expansion  and  not  break  the  tube.  An  accurately  made 
instrument  of  excellent  quality  and  adapted  for  clinical  purposes  may  be  obtained 
from  the  glass-instrument  factory  of  Gotze,  Hertelstrasse  4,  Leijisic.  At  the 
writer's  request  this  firm  has  supplied  an  instrument  with  which  only  5  c.c.  of 
fluid  are  necessary  in  order  to  determine  the  freezing-point.  This  is  a  matter  of 
great  importance,  since  we  frequently  have  to  do  with  a  very  small  quantity  of 
fluid,  particularly  in  the  examination  of  the  blood. 

Since,  in  time,  all  thermometers  vary,  it  is  important  to  test  the  accuracy  of 
the  zero  mark  occasionally,  even  though  the  scale  were  originally  absolutely  cor- 
rect. This  is  done  by  determining  the  freezing-point  of  distilled  water  with  the 
instrument,  and,  when  it  does  not  agree  exactly  with  the  zero  mark,  adding  the 
correction  to  all  subsequent  readings.  In  doing  this,  however,  we  cannot  employ 
any  distilled  water  at  random.  After  a  time  distilled  water  absorbs  gases,  and  it 
also  takes  up  a  certain  amount  of  alkali  from  the  glass  container  ;  this  is  sufficient 
to  cause  a  distinct  lowering  of  the  freezing-point.  For  this  reason  the  distilled 
water  employed  must,  at  least,  be  freshly  boiled  or,  better  still,  freshly  distilled. 
In  this  distillation  the  receiver  should  consist  of  a  so-called  steamed  ffask — i.  e. , 
one  which  has  been  freed  from  soluble  alkali  by  means  of  a  current  of  steam. '^ 
If  it  be  desired  to  verify  not  only  the  zero  mark,  which  may  change  through  na 
fault  of  the  maker  of  the  instrument,  but  also  the  accuracy  of  the  scale,  this, 
may  be  done  by  also  determining  the  freezing-point  of  a  pure  1  per  cent,  sodium 
chlorid  solution.  According  to  Hamburger,  the  freezing-iaoint  of  such  a  solu- 
tion is  0. 589.  If  the  instrument  be  correct,  this  is  the  value  which  should  be 
found  after  making  the  necessary  correction  for  the  zero  mark. 

In  the  determination  of  every  freezing-point,  care  must  be  exercised  to  see 
that  small  particles  of  mercury  are  not  sticking  to  the  sides  of  the  upper  ex- 
panded portion  of  the  thermometer,  since,  if  this  were  the  case,  an  error  would 
arise  from  the  exclusion  of  this  part  of  the  mercury.  For  this  reason  the  expan- 
sion should  be  examined  with  a  lens  before  every  determination,  and  if  separate 
particles  of  mercury  are  found  they  must  be  united  with  the  mercurial  column, 
either  by  shaking  or  by  beating  the  instrument. 

In  determining  a  freezing-point  the  jar  {a)  is  first  filled  with  a  freezing-mix- 
ture. In  order  to  obtain  correct  results,  it  is  important  that  the  freezing-mix- 
ture be  correctly  prepared.  It  should  not  be  too  cold.  The  best  mixture, 
according  to  Hamburger,  ^  is  one  of  3  parts  of  finely  cracked  ice  or  snow 
with  1  part  of  sodium  chlorid  ;  this  is  placed  in  the  jar,  and  sufficient  water 
added  to  make  the  temperature  about  —  3°  C.     If  the  temperature  rises  in  the 

'  See  Cohen,  Vortrdge  uber  physlkalische  Chemie,  1901,  p.  10. 
^  Osmotischer  Druck  und  Jonenlehre,  1902. 


548  URINARY  EXAMINATION. 

course  of  the  experiment,  a  fresh  amount  of  ice  and  sodium  chlorid  in  the  given 
proportion  should  be  added.  The  fluid  to  be  examined  is  now  placed  in  the 
freezing-tube,  and  the  thermometer  and  the  platinum  stirrer  subsequently  intro- 
duced. Care  must  be  taken  that  the  mercury  reservoir  of  the  thermometer  is 
completely  surrounded  by  the  fluid,  so  that  it  is  entirely  submerged,  and  does 
not  come  in  contact  with  any  portion  of  the  freezing-tube.  The  freezing-tube  is 
then  inserted  into  the  reagent  glass  in  the  cover  of  the  battery  jar  so  that  it  is 
surrounded  by  a  uniform  layer  of  air.  The  fluid  in  the  freezing-tube  must  be 
kept  in  constant  motion  by  gentle,  but  interrupted,  movements  of  the  platinum 
stirrer  {Ji).  The  fluid  must  not  splash.  The  mercury  soon  commences  to  sink 
in  the  thermometer,  leaves  the  upper  expanded  j^ortion,  enters  the  capillary 
tube,  and  quickly  falls  to  a  point  more  or  less  below  the  freezing-point  (excessive 
cooling),  and  then  suddenly  rises  to  a  definite  point  at  which  it  remains  station- 
ary for  some  time.  This  point  is  the  freezing-point  of  the  fluid  examined,  and 
is  read  off".  At  this  time  needles  of  ice  commence  to  form  in  the  fluid,  and  it 
gradually  becomes  solidly  frozen.  "When  this  has  happened,  the  mercury  com- 
mences to  descend  again.  This  complete  freezing  should  not  be  waited  for,  how- 
ever, but  the  determination  should  be  repeated  immediately  after  the  mercury  has 
ceased  to  ascend,  by  taking  out  the  freezing-vessel,  holding  it  in  the  hand  and 
stirring  the  fluid  constantly  until  the  mercury  commences  to  ascend,  when  the 
freezing  vessel  is  again  introduced  into  the  reagent  glass  (d),  and  the  freezing- 
point  again  determined  as  before.  In  warming  the  freezing-vessel  for  the  pur- 
pose of  repeating  the  determination  all  of  the  crystals  should  not  be  melted — 
*.  e.,  the  temperature  must  not  reach  0°  (since  the  crystals  consist  of  pure  water) — 
because  errors  would  arise  if  the  fluid  were  subsequently  "inoculated"  with 
small  pieces  of  ice  (see  below).  When  three  determinations  have  been  made, 
one  immediately  after  the  other,  the  average  of  the  three  is  taken  as  the  final 
result. 

In  order  to  determine"  correctly  the  freezing-point  it  is  important  to  avoid 
excessive  cooling  (see  above),  since  large  masses  of  ice  will  form,  and  as  these 
consist  of  pure  water  a  more  concentrated  solution  remains,  which  gives  a  lower 
freezing-point,  corresponding  to  its  higher  osmotic  pressure.  The  error  of  excess- 
ive cooling  is  avoided,  first  of  all,  by  compounding  the  freezing-mixture  so  that 
its  temperature  is  not  too  low.  The  safest  way  would  be  to  compound  it  so  that 
its  temperature  would  be  but  a  few  tenths  of  a  degree  below  the  expected  freez- 
ing-point, which  could  be  approximately  determined  in  a  preliminary  experi- 
ment. This  takes  up  too  much  time,  however,  since  the  cooling  would  proceed 
so  slowly,  and  in  addition  it  makes  the  necessary  recognition  of  the  descent  and 
ascent  of  the  mercury  much  more  difficult.  If  the  temperature  of  the  freezing- 
mixture  be  —  3°  C,  instead  of  the  very  low  temperatures  so  commonly  employed 
previously,  the  chances  of  excessive  cooling  are  considerably  reduced.  An 
additional  means  of  avoiding  excessive  cooling  consists  of  the  introduction  of  a 
minute  piece  of  ice  into  the  fluid  through  the  lateral  prolongation  at  the  moment 
when  the  mercury  falls  below  the  zero-point.  In  physical  chemistry  this  is 
referred  to  as  "inoculation"  of  the  fluid  with  a  piece  of  ice.  This  accelerates 
the  formation  of  ice,  and  consequently  diminishes  the  danger  of  excessive  cool- 
ing. This  would  seem  to  dilute  the  solution,  and  consequently  lead  to  false 
results ;  but  this  is  not  the  case  when  the  manipulation  is  correctly  performed, 
because  the  piece  of  ice  cannot  melt  if  the  temperature  be  below  zero.  This 
would  be  possible,  however,  if  the  fluid  were  warmed  in  the  hand  to  the  zero 
point  in  making  the  second  and  third  determinations.  This  must  be  avoided, 
as  has  been  previously  pointed  out,  and  no  error  will  then  result  if  the  fluid 
be  repeatedly  "inoculated."  It  will  readily  be  understood  that  the  fluid  is 
useless  for  subsequent  determinations  after  it  has  become  thoroughly  melted. 
In  the  writer's  experience  he  has  found  that  "inoculation"  is  unnecessary  if 
the  temperature  of  the  freezing-mixture  be  not  more  than  3°  C.  below  the 
expected  freezing-point,  since  in  this  manner  the  excessive  cooling  is  avoided. 


QUANTITATIVE   URINARY  ANALYSIS.  549 

EMPLOYMENT    OF    CRYOSCOPY   FOR   THE    STUDY    OF   THE    RENAL 

FUNCTIONS. 

Since  the  determination  of  the  freezing-point  fiirnishes  us  with  a  simple  and 
clinically  applicable  method  of  estimating  the  osmotic  pressui-e,  and  consequently 
the  molecular  concentration  of  a  fluid,  this  method  of  examination  has  been 
applied  to  the  urine  and  to  the  study  of  the  functions  of  the  kidney.  By  this 
method  it  has  been  attempted  to  determine  not  only  the  total  amount  of  work 
done  by  both  kidneys,  but  also,  by  the  practice  of  ureteral  catheterization  or  by 
Luys'  method  of  separation  of  the  urines  (see  p.  458  et  seq.),  to  compare  the 
functions  of  the  two  kidneys.  Disregarding  the  excretion  of  water,  which  is 
doubtless  a  renal  function  and  not  to  be  regarded  simply  as  a  filtration,  it  is 
clear  that  the  greater  part  of  the  w^ork  of  the  kidney  consists  of  excreting  a  fluid 
of  high  osmotic  pressure  from  the  blood,  which  has  a  much  lower  molecular 
concentration.  An  expenditure  of  energy  is  necessary  for  this  purpose,  and  the 
production  of  a  urine  of  high  osmotic  pressure  is  consequently  to  be  regarded  as 
an  accumulation  of  potential  energy.  Should  we  assume,  as  is  frequently  done, 
that  this  production  of  a  fluid  of  higher  osmotic  pressure  fi-om  the  blood  repre- 
sents the  entire  work  of  the  kidney,  the  daily  amount  of  work  done  by  both 
kidneys  would  be  calculated  by  W=Q,  (A— f5),  in  which  Q  is  the  daily  excretion 
of  urine,  A  the  freezing-point  of  the  urine,  and  6  that  of  the  blood.  The  result 
may  be  designated  as  the  daily  osmotic  capability  of  the  kidney.  It  should  be 
remembered,  however,  that  this  measure  of  the  renal  functions  is  neither  complete 
nor  exact.  It  is  not  complete,  because  it  neglects  the  work  done  by  the  kidneys 
in  excreting  water,  and  also  because  it  is  evident  that  by  the  exci'etion  of  a 
diluted  urine,  which  has  a  lower  osmotic  pressure  than  that  of  the  blood,  and  in 
which  the  kidneys  create  no  osmotic  pressure  whatever,  the  kidneys  still  perform 
work  that  is  not  aj^parent  as  osmotic  pressure.^  It  is  not  exact,  since  we  do 
not  know  that  different  molecules  require  the  same  amount  of  energy  for  their 
excretion.  Although  the  difference  in  the  molecules  is  immaterial  for  the  cal- 
culation of  the  potential  energy  stored  up  in  the  urine,  it  is  not  only  plausible, 
but  also  possible,  that  the  excretion  of  a  molecule  of  sodium  chlorid  requires  a 
different  expenditure  of  energy  than  is  necessary  for  the  excretion  of  a  molecule 
of  urea.  The  difference  probably  exists  in  variations  in  the  amount  of  heat 
evolved,  and  is  not  at  all  apparent  in  the  osmotic  pressure  of  the  urine.     The 

^  Should  we  assume  that  the  production  of  an  osmotic  pressure  in  the  urine  exceed- 
ing that  of  the  blood  is  the  only  work  done  by  the  kidneys,  as  is  frequently  stated,  we 
should  arrive  at  the  paradoxic  and  ridiculous  conclusion  that  kidneys  which  furnish  a 
diluted  urine  perform  no  work  at  all,  or  even  a  negative  amount  of  work  (the  latter 
if  A  — (5  is  negative),  while,  on  account  of  the  markedly  increased  quantity  of  water  in 
the  urine  in  these  cases,  a  particularly  large  amount  of  work  is  perhaps  represented. 

The  writer's  opinion,  that  tlie  excretion  of  water  by  the  kidney  is  a  specific  function 
of  this  organ,  will  possibly  be  objected  to  on  the  ground  that  this  excretion  can  be 
accounted  for  by  assuming  that  the  secreting  membranes  of  the  kidney  are  extremely 
permeable  to  water,  and  that  it  is  not  at  all  necessary  for  the  kidney  to  supply  energy 
for  a  simple  filtration.  Such  a  permeability  to  water,  however,  must  lae  something  quite 
specific,  since  a  similar  permeability  is  found  nowhere  else  in  the  body.  We  also  have 
reason  to  believe  that  this  excretion  of  water  is  an  active  function,  since  under  physio- 
logic conditions  it  is  always  accurately  adapted  to  the  needs  of  the  organism.  A  further 
proof  of  the  activity  of  the  kidneys  in  excreting  water  is  furnished  by  the  hypertrophied 
kidneys  of  beer  drinkei-s,  which,  by  their  differences  from  the  kidneys  of  wine  drinkers, 
demonstrate  that  the  hypertrophy  is  due  to  the  effect  of  water  and  not  to  that  of 
alcohol.  The  same  tiling  is  still  more  strikingly  shown  by  the  renal  hypertrophy 
acquired  in  diabetes  insipidus.  If  the  activity  of  tlie  kidneys  were  not  increased  under 
these  conditions,  they  would  not  become  hypertrophic. 

Another  reason  for  the  writei-'s  opinion  that  the  so-called  osmotic  energy  of  the 
kidneys  is  no  accurate  measure  for  the  work  done  by  these  organs  is  the  fact  that  the 
ionization  of  the  urinary  constituents  varies  with  the  concentration  of  the  urine.  Since 
part  of  this  ionization  occui-s  after  passing  througli  the  renal  epithelium  (in  case  a  con- 
centrated urine  becomes  more  dilute),  this  portion  of  the  osmotic  pressure  dependent 
upon  ions,  or  at  least  some  of  it,  cannot  be  reckoned  as  work  done  by  the  kidney. 


550  URINARY  EXAMINATION. 

majority  of  the  works  upon  cryoscopy  of  the  urine  do  not  regard  this  point  at 
all,  and  consequently  deduce  far-reaching  conclusions  from  the  determination  of 
the  freezing-point  of  the  urine  which  are  by  no  means  justified. 

The  utilization  of  the  results  of  cryoscopy  for  the  determination  of  the 
functional  activity  of  the  kidneys  is  also  complicated  by  difficulties  which  are 
encountered  in  the  study  both  of  the  mixed  twenty-four-hour  urine  and  of 
the  separately  collected  urine  from  each  kidney.  It  is  difiicult  to  deduce  con- 
clusions from  the  freezing-point  of  the  mixed  twenty-four-hour  urine,  since 
this  freezing-point  is  subject  to  great  variations  under  normal  conditions.  It  is 
not  unusual  for  the  lowering  of  the  freezing-point  of  the  twenty-four-hour 
urine  to  exhibit  a  physiologic  variation  of  from  0.9  to  2.7°  C,  and  still  greater 
variations  may  be  encountered  under  perfectly  normal  conditions,  dependent  upon 
the  ingestion  of  food  and  water.  If  an  individual  drink  large  quantities  of 
water,  the  difference  between  the  freezing-point  of  the  urine  and  that  of  distilled 
water  may  amount  only  to  0.11°  C.  (Koj^pe).  In  nursing  infants,  the  osmotic 
pressure  of  the  urine  is  always  less  than  that  of  the  blood,  and  the  lowering  of  the 
freezing-iooint  may  vary  between  0.087  and  0. 455°  (Koppe).  In  any  individual  case 
the  freezing-point  may  vaiy  from  day  to  day.  Since  there  is  no  normal  freezing- 
point  for  normal  urine,  we  can  draw  conclusions  in  reference  to  the  renal  function 
in  pathologic  cases  only  when  repeated  examinations  have  shown  the  freezing- 
point  to  be  constantly  too  high  or  too  low,  and  when  this  extreme  variation 
cannot  be  accounted  for  by  anomalies  in  the  ingestion  of  food  or  water.  These 
difficulties  are  by  no  means  overcome  by  basing  the  calculation  upon  the  daily 
osmotic  energy  of  the  kidneys  determined  by  W  =  Q  (A — S)  instead  of  upon  the 
lowering  of  the  fi-eezing-point  (a)  or  by  employing  the  product  of  the  daUy  excre- 
tion and  the  freezing-point  of  the  urine  (Q  A).  The  formula  W  =  Q  (A — 6)  is 
more  exact  than  the  freezing-point  alone,  since  it  not  only  indicates  the  molecular 
concentration,  but  also  measures  the  osmotic  energy  expended  by  the  kidneys 
within  twenty-four  hours,  while  the  product  Q  A  is  a  measure  for  the  number  of 
molecules  excreted  in  a  similar  period  of  time.  The  previously  emphasized  objec- 
tions to  utilizing  the  freezing-point  also  exist  here,  since  under  normal  conditions 
the  number  of  excreted  molecules  and  the  product  Q  A  vary  just  as  much  as  does 
the  molecular  concentration  or  the  freezing-point.  These  results  may  conse- 
quently be  employed  for  diagnostic  purposes  only  when  they  are  extreme,  when 
they  extend  over  long  periods  of  time,  and  when  they  cannot  be  explained  by  an 
abnormal  diet. 

The  most  pronounced  pathologic  changes  in  the  molecular  concentration  of 
the  urine,  in  the  daily  osmotic  energy  of  the  kidneys,  and  in  the  product  Q  A  are 
encountered  in  nephritis,  and  particularly  in  the  uremia  which  frequently  results. 
In  these  cases  the  retention  of  urinary  solids  is  very  frequently  manifested  by  an 
abnormally  low  molecular  concentration  and  a  consequent  abnormally  low  daily 
excretion  of  molecules.  Eveiy  improvement  of  the  condition  is  indicated  by  an 
increase  of  both.  According  to  Strauss,  the  chronic  parenchymatous  nephritis  cases 
produce  a  more  marked  diminution  of  the  daily  excretion  of  molecules  than  do 
the  interstitial,  since  in  the  latter  cases  the  marked  lowering  of  the  freezing-point 
is  more  than  compensated  for  by  the  increased  quantity  of  urine  excreted.  In 
diabetes  mellitus  the  osmotic  pressure  of  the  urine  and  the  daily  excretion  of 
molecules  are,  of  course,  greatly  increased  by  the  amount  of  sugar  in  the  urine. 

The  utilization  of  cryoscopy  in  determining  the  functional  activity  of  a  single 
kidney,  the  urine  from  which  is  obtained  either  by  ureteral  catheterization  or  by 
Luys'  urinary  separator,  is  accompanied  by  difficulties  equally  as  great  as  those 
encountered  in  studying  the  mixed  twenty-four-hour  urine.  The  object  of  such 
examinations  is  to  determine  whether  one  kidney  is  functionating  normally,  and 
whether  it  will  be  able  to  do  all  the  work  after  the  removal  of  the  diseased 
kidney.  The  conclusions  drawn  from  the  separate  cryoscopic  examinations  of  the 
urines  of  both  kidneys  in  such  cases,  which  have  given  rise  to  a  large  amount  of 
literature  contain  a  great  many  sources  of  error,  only  the  most  important  of 
which  will  be  given.      First  of  all,  it  by  no  means  follows  that  the  kidney 


QUANTITATIVE   URINARY  ANALYSIS.  551 

Temaining  after  the  extirpation  will  do  the  same  amount  of  work  as  before. 
Rather,  if  the  diseased  kidney  still  functionated  to  a  certain  extent,  it  is  quite 
possible  that  the  remaining  kidney  will  respond  to  the  increased  excretory 
stimulus  and  compensate  for  the  defect,  even  if  it  apparently  did  too  little  work 
before  the  extirpation.  Upon  the  other  hand,  if  the  function  of  the  healthier 
kidney  be  impaired,  and  yet  sufficient  to  meet  the  needs  of  the  organism  when 
aided  by  the  diseased  kidney,  it  is  possible  that  it  may  be  insufficient  when  called 
upon  to  do  the  entire  amount  of  work.  These  possibilities  are  not  even  mentioned 
in  many  of  the  publications  upon  the  subject.  Another  frequent  error  is  the  false 
supposition  that  the  freezing-point  of  the  urine  is  the  only  measure  of  the  func- 
tional activity  of  the  kidney.  As  we  have  already  seen,  this  is  not  the  case,  and 
the  supposition  of  Kiimmel,  that  a  freezing-point  of  the  urine  below  — 1°  C.  in- 
dicates insufficiency  of  the  viscus,  is  purely  arbitrary.^  Again,  in  order  to  reach 
more  accurate  conclusions,  the  quantity  of  urine  excreted  must  also  be  considered. 
This  cannot  be  correctly  done,  however,  since  it  is  not  possible  to  collect  the 
twenty-four  hours'  urine  from  a  single  kidney.  Great  caution  is  also  necessary 
when  the  results  of  the  cryoscopic  examination  of  the  separate  urines  are  employed 
for  the  purpose  of  comparing  the  functions  of  the  two  kidneys.  This  examina- 
tion is  usually  made  by  catheterizing  first  one  and  then  the  other  ureter,  and  then 
comparing  the  freezing-points  of  the  two  urines.  Although  the  excretion  of  the 
urines  is  approximately  simultaneous,  it  is  not  exactly  so  ;  and,  since  the  excre- 
tion of  the  urine  is  subject  to  sudden  temporary  variations,  the  comparison  is  not 
accurate.  Even  if  the  two  urines  were  excreted  simultaneously,  as  is  the  case 
when  Luys'  separator  or  simultaneous  catheterization  of  the  ureters  is  employed, 
we  should  be  by  no  means  sure  of  obtaining  comparative  values,  since  experiments 
upon  animals  prove  that  the  excretions  of  the  two  kidneys  are  not  always  alike. 
It  is  therefore  justifiable  to  assume  a  difference  in  function  only  when  repeated 
examinations  always  demonstrate  similar  variations.  The  fact  that,  in  the  cus- 
tomary utilization  of  the  cryoscopic  findings,  the  surgery  of  the  kidney  is  usually 
correct,  in  spite  of  these  errors,  may  be  partly  due  to  the  fact  that  the  indication 
for  the  operation  is  not  based  exclusively  upon  these  results,  but  also  the  chemical 
and  microscopic  examination  of  the  separate  urines. 

In  view  of  the  objections  to  the  utilization  of  the  cryoscopic  findings,  we  are 
justified  in  raising  the  question  as  to  whether  this  new  method  of  urinary  exami- 
nation is  of  more  value  than  a  very  old  procedure  dealing  with  similar  questions 
— namely,  the  determination  of  the  specific  gravity.  It  is  quite  clear  that  the 
determination  of  the  osmotic  pressure  or  of  the  freezing-point  is  not  equiva- 
lent to  the  determination  of  the  specific  gravity.  The  determination  of  the 
freezing-point  furnishes  a  relative  idea  of  the  number  of  molecules  excreted, 
irrespective  of  their  quality,  and  the  result  of  such  a  determination  is  theoreti- 
cally independent  of  the  specific  gravity  of  the  urine,  since  molecules  of  low  and 
high  specific  gravity  exert  exactly  the  same  influence  upon  the  freezing-point. 
The  specific  gravity,  on  the  contrary,  is  dependent  not  only  upon  the  number  of 
molecules  dissolved  in  a  given  volume  of  urine,  but  also  upon  their  chemical 
composition  or  weight.  With  a  single  exception,  presently  to  be  mentioned, 
this  difference,  however,  is  more  theoretic  than  practical.  The  quality  of  the 
excreted  molecules  in  different  urines  is  subject  to  such  slight  variation  that  a 
marked  parallel  usually  exists  between  the  lowering  of  the  freezing-point  and 
the  specific  gravity  ;  and  if  the  specific  gravity  of  the  urine  of  a  patient  rises  or 
falls  we  may  rest  assured  that  the  lowering  of  the  freezing-point  or  the  osmotic 
pressure  has  undergone  a  similar  variation.  We  are,  consequently,  just  as  much 
justified  in  drawing  conclusions  in  reference  to  the  work  done  by  the  kidney 
from  the  specific  gravity  of  the  urine  as  from  the  height  of  the  osmotic  pressure. 
One  exception,  however,  must  be  borne  in  mind  :  If  the  urine  contain  proteid, 
this  substance  may  be  responsible  for  a  considerable  part  of  the  specific  gravity, 

^  Such  conclusions  would  be  more  Justifiable  if  all  fluids  were  interdicted  before  the 
examination  of  the  patient,  in  which  case  the  approximately  healthy  kidney  would 
always  excrete  a  concentrated  urine  with  a  marked  lowering  of  its  freezing-point. 


552  URINARY  EXAMINATION. 

since  it  is  heavier  than  water,  but  it  has  no  perceptible  influence  upon  the 
osmotic  pressure  or  the  freeezing-point.  Since  the  proteid  molecule  is  very  large 
and  heavy,  quite  a  small  number  of  such  molecules  may  cause  a  rise  in  the  specific 
gravity  without  appreciably  influencing  the  freezing-point.  With  an  albuminous 
urine  we  should  consequently  not  be  justified  in  attributing  a  high  specific  gravity 
to  increased  renal  activity,  particularly  since  the  proteid  is  not  secreted  by  the 
kidney,  but  is  an  indication  that  the  filtering  action  of  the  kidney  has  been  im- 
paired by  inflammation.  With  this  exception,  however,  the  writer  maintains  that 
the  determination  of  the  specific  gravity  gives  us  the  same  indication  of  the  work 
done  by  the  kidney  as  does  the  determination  of  the  freezing-point.  In  order  to 
draw  similar  conclusions  from  the  specific  gravity  of  albuminous  urine,  it  is 
necessary  simply  to  remove  the  albumin  and  then  utilize  the  specific  gravity  of 
the  remaining  fluid.  Just  as  in  the  estimation  of  the  total  work  done  by  the 
kidneys  from  the  determination  of  the  freezing-point,  the  urine  examined  must 
be  a  portion  of  the  mixed  twenty-four  hours'  elimination  if  correct  conclusions  are 
to  be  obtained.  In  doing  this  we  may  calculate  a  product  whose  significance  com- 
pletely corresponds  to  the  significance  of  the  cryoscopic  product  Q  A  (see  above), 
by  multiplying  the  last  two  figures  of  the  specific  gravity,  carried  to  the  third  deci- 
mal place,  by  the  amount  of  urine  secreted  in  twenty-four  hours.  The  number  so 
obtained  gives  a  relative  idea  of  the  amount  of  urinary  solids  secreted  in  twenty- 
four  hours.  We  may,  however,  easily  obtain  absolute  quantities,  as  stated  upon 
page  452,  by  multiplying  the  last  two  figures  of  the  specific  gravity  by  2.33,  and 
then  multiplying  this  product  by  the  daily  urinary  excretion  expressed  in  liters. 
The  resulting  figure  is  the  approximate  number  of  grams  of  urinary  solids  excreted 
in  twenty-four  hours.  The  writer  believes  that  this  number  is  just  as  good  an 
indication  of  renal  activity  as  is  the  number  of  molecules  excreted  daily,  provided 
that  any  proteid  present  be  removed  before  the  specific  gravity  is  determined. 
This  number  is,  of  course,  markedly  influenced  by  the  quantity  of  ingested  food 
and  water,  so  that  the  normal  is  hard  to  determine,  and  the  same  ditficulties  are 
encountered  in  drawing  accurate  conclusions  as  have  been  previously  mentioned 
in  reference  to  the  determination  of  the  number  of  excreted  molecules.  In  an 
entirely  analogous  manner  the  specific  gravity  of  the  urines  (after  the  removal  of 
proteid,  if  present)  obtained  by  ureteral  catheterization  or  Luys'  separator  (see  p. 
458  et  seq.)  may  be  utilized  in  place  of  the  osmotic  pressure  for  the  critical  study 
of  the  urine  of  each  kidney  ;  but,  owing  to  the  impossibility  of  obtaining  the  total 
t^venty-four  hours'  urine,  this  procedure  is  open  to  the  same  objection  previously 
mentioned  in  our  consideration  of  osmotic  pressure.  The  writer  must  also  take  this 
occasion  to  claim  that  cryoscopy  has  not  materially  aided  our  diagnostic  ability  in 
reference  to  the  critical  study  of  renal  activity,  since  all  of  the  facts  learned  by 
ureteral  catheterization  could  also  have  been  discovered  by  means  of  the  specific 
gravity.  Cryoscopy  accidentally  became  popular  just  at  that  time  and  was  given 
preference  over  the  older  method  from  an  exaggerated  idea  of  its  value,  just  as 
all  new  methods  are  usually  supposed  to  be  an  advance  over  those  formerly 
employed.  In  addition  to  the  fact  that  it  is  not  necessary  to  remove  proteid,  it 
must  nevertheless  be  admitted  that  cryoscopy  possesses  one  distinct  advantage, 
particularly  in  the  study  of  the  separate  urines,  in  that  it  requires  a  smaller  amount 
of  urine  than  is  necessary  for  the  determination  of  the  specific  gravity.  Never- 
theless, the  chief  advantage  of  the  introduction  of  the  new  method  has  been 
that  it  has  caused  us' to  study  these  questions  more  carefully  than  was  done  by 
means  of  the  specific  gravity,  since  the  latter  method  had  not  the  charm  of 
novelty.  We  shall  subsequently  learn  that  the  case  is  quite  different  with  refer- 
ence to  the  cryoscopy  of  the  blood,  which  is  of  special  significance  for  general 
pathology  and  diagnosis. 

How  closely  the  conclusions  obtained  by  means  of  the  determination  of  the 
freezing-point  of  the  urine  correspond  to  those  which  the  practical  physician  may 
deduce  much  more  readily  from  the  specific  gravity  is  best  shown  by  the  statement 
of  G.  FuchSji  that  in  a  urine  free  from  proteid  and   sugar  the  lowering  of  the 

^  Zeits.  f.  angewandie  Chemie,  1902,  p.  1072. 


SEDIMENTS  AND   TURBIDITY  OF  THE   URINE.  553 

freezing-point  may  be  empirically  calculated  by  multiplying  the  last  two  figures 
of  the  specific  gravity,  carried  to  the  third  decimal  place,  by  0.075°  C. 

The  far-reaching  calculations  and  conclusions  (based  upon  the  freezing-point 
of  the  urine)  which  Koranyi  ^  and  others  have  formulated  in  regard  to  the  freezing- 
point  of  the  blood,  as  well  as  to  the  amount  of  sodium  chlorid  contained  in  both 
fluids,  will  not  be  discussed,  since  the  writer  regards  their  fundamental  principles 
as  hypothetic,  and  in  many  respects  erroneous. 

SEDIMENTS  AND  TURBIDITY  OF    THE  URINE. 

EXAMINATION  OF  URINARY    SEDIMENTS;    SEDIMENTATION;    nL- 
TRATION;    CENTRIFUGATION ;   MICROCHEMICAL  REACTIONS. 

Both  urinary  sedimeuts  and  turbidity  may  be  frequently  enough 
recognized  and  characterized,  without  any  microscopic  examination,  by 
their  physical  and  chemical  behavior.  But  a  microscopic  examination 
is  necessary  in  most  cases,  especially  for  the  differentiation  of  organized 
sediment.  If  the  sediment  is  very  abundant,  a  drop  of  the  cloudy  urine 
under  the  microscope  will  be  sufficient ;  but  generally  the  sediment  is  so 
scant  that  it  is  advisable  to  isolate  and  collect  it  by  sedimentation,  filtra- 
tion, or  centrifugation. 

In  concentrated  urines  with  uratic  sediments  the  microscopic  exami- 
nation of  other  constituents,  and  particularly  of  the  organized  elements, 
is  frequently  rendered  very  difficult  by  the  presence  of  urates.  In  such 
cases  the  urates  should  be  dissolved  by  heating  the  urine  slightly  and 
adding  enough  water  to  hold  the  urates  in  solution  upon  cooling.  If 
this  cannot  be  accomplished,  which  may  be  the  case  if  uric  acid  has  also 
been  thrown  down,  both  substances  may  be  brought  into  solution  by 
rendering  the  urine  alkaline  by  the  addition  of  a  concentrated  solution 
of  soda.  A  borax  solution  may  also  be  employed  for  the  same  purpose 
(see  below).  Such  a  solution  of  the  precipitated  urates  and  uric  acid 
may  be  necessary  not  only  for  the  direct  microscopic  inspection  of  the 
remaining  deposits,  but  also  as  a  preliminary  to  sedimentation,  filtration, 
or  centrifugation.  In  certain  cases  sediment  of  phosphates  or  of  car- 
bonates may  similarly  interfere  with  the  microscopic  examination. 
These  sediments  may  be  readily  dissolved  by  acidulating  the  urine  with 
hydrochloric  acid.  A  reference  to  the  important  experiments  of  Moritz 
will  be  found  in  the  supplement  of  this  work. 

For  Sedimentation. — A  tall  pointed  glass  is  filled  with  the  urine,  and 
the  sediment  is  examined  under  the  microscope  just  as  soon  as  enough  has 
settled  to  be  plainly  visible  at  the  bottom  of  the  glass.  This  usually 
requires  a  few  hours.  The  sediment  is  picked  up  with  a  pipet  while  the 
upper  end  is  closed  with  the  finger.  By  slightly  decreasing  the  pressure 
of  the  finger  a  certain  amount  of  sediment  is  allowed  to  enter  the  pipet. 
It  is  then  closed  again,  removed,  and  carefully  dried,  while  the  finger 
pressure  is  kept  constant.  A  drop  of  its  contents  is  then  allowed  to 
flow  upon  a  glass  slide  by  slightly  releasing  the  finger. 

Strassburger  has  recently  recommended  diluting  the  urine  with  two  parts  of 
alcohol,  in  order  to  hasten  sedimentation  by  diminishing  the  specific  gravity  of 
the  fluid.     But  alcohol  will  precipitate  proteids,  so  that  this  procedure  can  be 

1  Zeits.  f.  klin.  Med.,  1897 


554 


UBINAR  Y  EXAMINA  TION. 


recommended  only  where  the  amount  of  these  bodies  is  very  slight  or  where  the 
presence  of  an  amorphous  precipitate  will  not  produce  confusion,  especially  for 
the  microscopic  demonstration  of  tubercle  bacilli  or  other  bacteria. 

The  urinary  sediment    changes  so  quickly  that  it  is  important    to 
examine  it  as  soon  after  settling  as  possible. 

The  various  constituents  of  a  sediment  differ  in  their  specific  gravi- 
ties ;  hence,  in  many  cases  it  is  advisable  to  select  specimens  for  exam- 
ination at  varying  depths  of  a  sediment.  With  practice  and  care  this 
selection  can  be  made  while  picking  up  one  specimen. 

To  prevent  bacterial  decomposition,  so  prone  to  occur  during  the 
summer   months,  it  is  a  good  plan  to   add   to  the  urine   one-fifth   its 

volume  of  chloroform  water  (1 :  200) 
or  a  small  piece  of  camphor,  and  to 
select  a  cool  place  for  the  sedimenta- 
tion. To  avoid  obscuring  the  exami- 
nation of  organized  sediments  by  the 
formation  of  heavy  urate  sediments  in 
very  concentrated  or  very  acid  urines, 
we  may  add  to  the  urine  one-fifth  to 
one-third  its  volume  of  a  saturated 
(1  :  17)  borax  solution.  This  solu- 
tion will  not  coagulate  proteids,  and 
at  the  same  time  will  act  antisep- 
tically.  If  the  sediment  is  very 
scanty  the  filtration  method  may  be 
employed.  As  large  an  amount  of 
the  urine  as  possible  is  filtered,  and 
the  residue  upon  the  filter  is  picked 
up  with  the  ordinary  pipet  while  only 
a  few  drops  of  the  urine  remain. 

The  centrifuge  ^  is  now  employed 
in  practically  all  laboratories  for 
obtaining  the  sediment.  With  it  the  sediment  may  be  obtained  for 
examination  within  a  few  minutes  and  from  very  small  specimens  of 
perfectly  fresh  urine.  [Fig.  185  represents  a  very  satisfactory  form  of 
electrical  centrifuge,  to  be  connected  to  the  ordinary  street  current  avail- 
able in  all  large  towns.  There  are  numerous  other  electrical  centrifuges 
upon  the  market,  some  of  which  are  thoroughly  trustworthy,  others 
unreliable.  Where  there  is  no  street  current  available,  practitioners 
may  find  the  ordinary  hand  or  water  centrifuge  a  very  convenient  addi- 
tion to  their  laboratory  equipment.  They  are  both  less  expensive. — Ed.] 
Many  chemical  reactions  which  reveal  the  nature  of  certain  sediments 
can  be  performed  macroscopically  and  also  observed  under  the  micro- 
scope. In  the  latter  case — e.  g.,  to  determine  the  nature  of  unfamiliar 
crystals — a  drop  or  two  of  the  agent  is  allowed  to  run  under  one  edge 
of  the  cover-glass,  or  perhaps  sucked  under  with  the  help  of  a  piece  of 
filter  paper  at  the  other  edge. 

1  Stenbeck,  Zeits.f.  klin.  Med.,  vol.  xx..,  457, 1892.  Litten,  Dent.^ch.  med.  Woch.,  1891,  p.  23. 


Fig.  185. — Electrical  centrifuge. 


SEDIMENTS  AND   TURBIDITY  OF  THE   URINE.  555 

The  amount  of  the  sediment  is  best  estimated  by  v.  Posner's  method 
■of  estimating  the  amount  of  pus  present  (p.  568).  (See  p.  564  et  seq. 
in  regard  to  the  preservation  of  organized  sediment.) 

NON-ORGANIC  CRYSTALLINE,  AND  AMORPHOUS  SEDIMENTS  AND 

MIXTURES. 

THE   URATES. 

When  the  urine  cools,  urates  may  settle  to  the  bottom,  especially  if 
the  sample  is  concentrated,  scanty,  or  strongly  acid — e.  g.,  the  urine  of 
congestion  and  of  fever,  less  often  the  urine  of  nephritis.  The  sediment 
will  then  present  a  fairly  characteristic  appearance,  clay-colored,  reddish 
yellow,  brick  red,  or  rose  red  (sedimentum  lateritium).  Sometimes  it 
adheres  to  the  wall  of  the  urine  glass  as  a  thin  coating.  Unlike  all 
other  sediments,  it  dissolves  extremely  readily  even  with  very  gentle 
heating,  and  so  can  be  accurately  recognized.  The  addition  of  acid  will 
also  dissolve  urate  sediments  with  a  gradual  separation  of  uric  acid 
crystals.  The  addition  of  alkalies  also  dissolves  the  precipitate  particu- 
larly easily,  and  often  with  the  separation  of  phosphates.  The  ordinary 
urate  sediments  consist  of  a  mixture  of  sodium,  potassium,  calcium, 
magnesium,  and  ammonium  urates.  Sodium  urate  predominates.  With 
the  exception  of  ammonium  urates,  the  urates  appear  only  in  acid  urine. 
They  are  formed  by  a  double  rearrangement  between  acid  sodium  phos- 
phate and  the  neutral  urates  held  in  solution,  from  which  acid  urates  are 
formed,  which  are  not  very  soluble  and  become  precipitated.  Aside 
from  these  chemical  processes,  the  cooling  of  the  urine  favors  the  separa- 
tion of  urates.  That  the  mere  cooling  of  the  urine  alone  will  not,  how- 
ever, produce  the  separation  is  shown  by  the  fact  that  the  sediment 
forms  sometimes  only  a  considerable  time  after  the  cooling,  and  also  by 
the  fact  that  a  urate  sediment  usually  does  not  entirely  dissolve  until  the 
urine  is  heated  to  a  temperature  above  that  of  the  body. 

Urate  sediments  often  contain  crystals  of  pure  uric  acid,  which  also 
arise  from  the  double  rearrangement  mentioned  above. 

The  peculiar  pronounced  brick-  or  rose-red  color  of  some  urate  sedi- 
ments arises  from  uroerythrin,  a  pigment  as  yet  little  understood  (com- 
pare p.  478).  It  seems  to  be  formed  to  excess  in  certain  febrile  affec- 
tions (acute  rheumatism,  pneumonia). 

If  a  urine  with  a  urate  sediment  is  decomposed  by  ammoniacal  fer- 
mentation, the  sediment  will  be  partly  changed  to  acid  ammonium  urate. 
The  latter  is  the  only  urate  sediment  which  occurs  in  alkaline  urine 
(compare  p.  558). 

Under  the  microscope  urate  sediment  appears  as  fine  amorphous 
granules.  If  acetic  acid  is  added,  characteristic  crystals  of  uric  acid  may 
be  seen  to  shoot  out  from  these  granules  (Fig.  186).  Ammonium  urate 
presents  characteristically  shaped  crystals  (Figs.  189,  6).  Uratic  sedi- 
ments respond  to  the  murexid  test.     (See  p.  556,  under  Uric  Acid.)  ^ 

As  already  mentioned,  the  concentration  of  the  urine  and  its  acidity 
are  particularly  important  in  the  formation  of  urate  sediments.  If, 
therefore,  despite  a  normal  specific  gravity,  a  urine  very  readily  deposits 


556  URINARY  EXAMINATION. 

a  sediment  of  amorphous  urates,  it  does  not  signify,  as  was  formerly 
supposed,  an  increased  production  of  uric  acid,  but  usually  merely  an 
increase  in  the  acidity  of  the  urine — /.  e.,  an  increased  amount  of  the 
acid  sodium  phosphates. 

URIC  ACID   IN  THE  SEDIMENT. 

Crystals  of  uric  acid  occur  in  the  urine  at  the  same  time  with  amor- 
phous urate  sediments,  and  sometimes  without  any  separation  of  urates, 
mostly  as  a  fine  crystalline  precipitate,  often  adherent  to  the  walls  of  the 
vessels  (Fig.  186).  The  beautifully  shaped,  sparkling,  shining  crystals 
of  red-brown  color  can  often  be  recognized  by  the  naked  eye.  Their 
appearance  is  usually  very  characteristic.  In  case  of  doubt  the  mnrexid 
test  may  be  performed  with  a  few  small  crystals.  The  latter  are  heated 
with  dilute  nitric  acid  upon  a  porcelain  plate  or  dish.  Solution  takes 
place  with  effervescence.  After  evaporation  there  remains  a  reddish 
residue,  which  turns  a  beautiful  purple  red  upon  the  addition  of  a  little 
diluted    ammonia,    due     to  the    formation    of   ammonium    purpurate 


Fig.  186.— The  more  common  forms  of  uric  acid  crystals  (after  Bizzozero  and  Scheube). 

(murexid).  The  addition  of  potassium  hydroxid  will  change  the  color 
to  violet.  The  urates  also  react  to  the  murexid  test.  The  most  frequent 
shapes  which  the  uric  acid  crystals  present  under  the  microscope  are 
depicted  in  Fig.  186. 

If  uric  acid  crystals  are  observed  in  the  sediment  at  the  same  time 
as  amorphous  urates,  they  have  the  same  significance  as  the  latter. 
They  may  be  found  in  any  concentrated  urine.  Eapid  precipitation  of 
purely  crystalline  uric  acid  without  any  amorphous  urate  in  a  compara- 
tively abundant  urine  shows  that  it  is  strongly  acid.  Such  a  condition 
has  nothing  to  do  with  the  so-called  uric  acid  diathesis  (gout  and  uric 
acid  calculns).  Moritz  has  demonstrated  that  every  individual  crystal 
of  uric  acid  has  an  albuminous  ground-substance. 

CALCIUM    OXALATE    IN  THE    SEDIMENT. 

These  crystals  occur  both  in  pathologic  and  in  normal  urine.  The 
sediment  is  usually  scant,  and  recognized  only  when  examined  micro- 
scopically. An  abundant  oxalate  sediment  is  often  noticed  after  the 
ingestion  of   foodstuffs  rich  in  oxalic  acid   (fruit,  especially  tomatoes, 


SEDIMENTS  AND   TURBIDITY  OF  THE   URINE.  557 

etc.),  sometimes  in  diabetes  mellitus,  and  finally  in  oxaluria.  The  last- 
named  disorder  occurs  chiefly  in  dyspepsia  and  nervous  disorders.  It  is 
questionable  if  it  is  an  independent  anomaly  of  metabolism  (Fig.  187). 

The  formation  of  oxalate  calculi  will,  of' course,  be  favored  by  such 
a  condition. 

According  to  Fiirbringer,  calcium  oxalate  is  in  all  probability  a 
normal  urinary  constituent,  held  in  solution  in  the  urine  by  the  acid 
sodium  phosphate.  If  for  any  reason  the  acid  reaction  is  reduced  so 
that  the  acid  phosphate  becomes  converted  to  a  neutral  salt,  calcium 
oxalate  becomes  precipitated.  Ordinarily  the  double  change  between 
neutral  urate  and  acid  phosphate  mentioned  in  connection  with  the  urate 
sediments  is  the  cause  of  the  reduction  of  the  acid  reaction  ;  and  then, 
besides  the  urates,  calcium  oxalate  precipitates.  The  separation  of  the 
oxalate  usually  takes  place  very  slowly, 
and  it  therefore  generally  occurs  as  well- 
formed  crystals  (Fig.  187).  They  usu- 
ally present  a  very  characteristic  octa- 
hedral type  (envelopes) ;  but  other 
varieties  also  occur  (see  Fig.  187,  note 
to  Fig.  188),  which  cannot,  however, 
be  recognized  immediately  from  their 
shape. 

From   the    way   in    which    calcium         ^     ,0.,    ^     .  ,     ^    ,  • 

''  .       .  ,    .  Fig.  187.— Crystals  of  calcium  oxalate: 

oxalate  crystals  separate,  it  is  plain  a,  So-called  envelopes ;  h  and  c,  rarer 
,1     ,    ..  "^  •       f>  •    ,1  -I     •  forms  (after  Scheube). 

that  they  may  occur  m  laintly  acid,  in 

neutral,  and  in  faintly  alkaline  urine.  Calcium  oxalate  crystals  are 
characterized  not  only  by  their  shape  and  insolubility  in  acetic  acid,  but 
by  the  fact  that  they  are  soluble  in  hydrochloric  acid. 

The  foregoing  explanation  of  the  separation  of  calcium  oxalate 
crystals  makes  it  evident  that  their  appearance  in  the  sediment  does  not 
justify  the  assum})tion  of  oxalic  acid  any  more  than  urate  sediment 
necessarily  implies  increased  uric  acid.  "  Oxaluria  "  is  often  diagnosed 
without  sufficient  reasons.  An  increase  of  the  oxalic  acid  elimina- 
tion can  be  determined  only  by  a  quantitative  urinalysis. 

SEDIMENTS  OF  THE  EARTHY   PHOSPHATES  AND    CARBONATES  AND    OF 
AMMONIUM    URATE. 

They  are  usually  light  in  color,  because  they  are  less  inclined  than 
the  urates  to  absorb  the  urinary  pigments,  and  because  their  separation 
does  not  depend  so  much  upon  the  degree  of  concentration  as  upon  the 
reaction  of  the  urine. 

1.  Amorphous  ^Earthy  Phosphates  and  Carbonates. — 
Normal  and  basic  phosphate  and  carbonate  of  calcium  and  magesium 
occur  as  granular  amorphous  masses,  and  may  be  present  in  every  alka- 
line urine,  particularly  if  the  alkalinity  is  due  to  a  fixed  alkali.  These 
salts  are  also  precipitated  if  the  urine  is  artificially  rendered  alkaline, 
or  if  a  faintly  acid,  neutral,  or  faintly  alkaline  urine  is  boiled,  the  acid 
combinations  in  which  calcium  and  magnesium  phosphate  and  carbonate 


558 


URINARY  EXAMINATION. 


are  dissolved  in  the  urine  being  changed  to  basic  combinations  by  boiling. 
Their  precipitation  produces  a  turbidity  which,  unlike  the  precipitate  of 
proteid  from  heating,  is  soluble  in  dilute  acids.  The  carbonates  when 
dissolved  by  dilute  acids  give  off  COg,  a  peculiarity  which  will  dis- 
tinguish them  from  the  phosphates. 

Amorphous  phosphates  and  carbonates  compose  the  chief  part  of  the 
urinary  sediment  after  the  diminution  of  acidity  following  gastric  lavage 
or  vomiting.  Sometimes  they  are  separate  even  in  the  bladder.  Hyper- 
secretion of  the  acid  gastric  juice  with  delayed  gastric  motility  causes 
sometimes  a  permanent  turbidity,  and  sometimes  a  turbidity  only  after 
meals.  In  either  case  it  is  due  to  a  precipitation  of  the  phosphates  and 
carbonates,  probably  because  the  secreted  hydrochloric  acid  is  not 
completely  or,  at  least,  not  quickly  enough  reabsorbed  and  the  urmary 
acidity  is  proportionately  diminished.  This  is  an  explanation  of  the 
so-called  phosphaturia  in  nervous 
individuals.     The   name   is  incor-  \.-rc^ 

rectly     applied,     of    course,    and 
should  be  limited  strictly  to  those 
cases    where    the    elimination    of 
phosphates     is    quantitatively 
creased.     In    very    mild    cases 


m- 
of 


C3 


2? 


^\ 


•^^ 


Fig.  188.— Indistinct  crystalline  sediment 
(dumbbell  crystals)  of  calcium  carbonate. 
Similar  crystals  are  formed  by  calcium  oxa- 
late and  calcium  sulpliate  (after  Funke). 


Fig.  189.— (I,  Crystals  of  ammoniomagnesium. 
phosphate  (triple  phosphate)  ;  h,  crystals  of 
ammonium  urate  (after  Neubauer  and  Vogel). 


such  hyperchlorhydria,  turbidity  appears  only  after  the  urine  has  been 
boiled. 

A  crystalline  precipitate  of  calcium  carbonate  sometimes  appears  as  a 
sandy  powder  mixed  with  the  amorphous  phosphate  sediments.  Micro- 
scopically, it  consists  of  spheric  or  dumbbell-shaped  formations  (Fig.  188), 
which  dissolve  in  acetic  acid  with  the  evolution  of  gas,  and  so  can  be 
distinguished  from  similar  formations  of  calcium  oxalate  (see  p.  557). 

2.  Ammoniomagnesium  Phospliate  (Triple  Phosphate) 
and  Ammonium  Urate. — These  are  combined  with  the  amorphous 
phosphate  and  carbonate  sediment  if  the  alkaline  reaction  of  the  urine  is 
entirely  or  partially  due  to  the  formation  of  ammonium  carbonate  within 
the  urinary  passages  from  the  urea,  or,  after  voiding  the  urine,  from  bac- 
teriologic  fermentation.  In  such  a  condition  triple  phosphate  will  compose 
the  major  part  of  the  sediment.  The  large  characteristically  shaped 
prisms,  the  so-called  "coffin  lids"  (Fig.  189,  a),  are  readily  recognized 
under  the  microscope.    The  ammonium  urate  which  so  frequently  accom- 


SEDIMENTS  AND   TURBIDITY  OF  THE   URINE. 


559 


panics  the  triple  phosphate  crystals  (Fig.  189,  b)  is  the  only  urate  pre- 
cipitated in  an  alkaline  urine.  This  salt  forms  dark-colored  spheres  with 
projecting  spines,  "morning-star  or  thorn-apple  balls."  Crystals  of  am- 
monium urate  dissolve  in  acetic  acid  with  a  gradual  formation  of  uric 
acid.  Ammoniomagnesium  phosphate  crystals  are  also  readily  soluble 
in  acetic  acid.  Although  both  these  crystalline  forms  occur  chiefly  in 
ammoniacal  urine,  they  also  appear  in  faintly  acid  or  amphoteric 
urine  if  an  ammoniacal  fermentation  has  commenced. 


Fig.  190.— other  forms  of  triple  phosphate  crystals  (after  Peyer). 

3.  Dicalcium  phosphate  (neutral  or  simple  acid  calcium  phos- 
phate) is  a  rather  rare  sediment  formed  in  faintly  acid  or  amphoteric  urine 
as  microscopic  prismatic  or  wedge-shaped  prisms  grouped  as  rosets 
(Fig.  191).  These  crystals  are  soluble  in  acetic  acid.  The  rosets  are 
frequently  only  indistinctly  developed. 

4.  CrystaUine  Trimagnesium  Phosphate. — In  very  rare  cases  there  have 
been  observed  in  alkaline  urine  large,  flat,  strongly  refractive  masses  which  consist 
of  elongated  rhombic  plates  with  angles  of  60°  and  120°  (chiefly  when  the  alkalinity 
of  the  urine  is  due  to  removal  of  the  gastric  contents).  These  are  trimagnesium 
phosphate  (normal  magnesium  phosphate). 

OTHER  INORGANIC  SEDIMENTS  OR  TURBIDITIES   (RARE). 

Gypsum  (calcium  sulphate)  occurs  very  rarely,  and  only  in  the  sediment  of 
strongly  acid  urine.     Its  crystals  are  represented  in  Fig.  192  (compare  Fig.  188). 


560 


URINARY  EXAMINATION. 


They  are  insoluble  in  ammonia,  alcohol,  and  acetic  acid;  slightly  soluble  in 
hydrochloric  acid,  nitric  acid,  and  hot  water.  Their  aqueous  solutions  may  be 
'  precipitated  with  barium  chlorid,  and  the  resulting  precipitate  is  insoluble  in 
hydrochloric  or  nitric  acid.  Ammonium  oxalate  also  removes  them  from  their 
aqueous  solutions,  and  the  resulting  precipitate  is  insoluble  in  acetic  acid,  but 
soluble  in  nitric  and  hydrochloric  acids. 

Cystin. — Cystin  occurs  in  the  urine  only  very  rarely  (so-called  cystinuria).i 


Fig.  191.— Crystals  of  dicalcium  phosphate  from  amphoteric  urine  (after  Neuhauer-Vogel  and 

Ultzmann-Hofmann). 

This  is  a  peculiar  metabolic  anomaly  which  leads  to  the  formation  of  cystin  and 
diamins.  According  to  recent  investigation,  it  is  probably  due  to  some  peculiar 
intestinal  mycosis,  because  these  substances  are  also  found  in  the  intestinal  con- 
tents. Cystin  usually  separates  from  an  acid  urine  within  the  urinary  passages  in 
characteristic  hexagonal  plate-like,  colorless  crystals  (Fig.  193)  (cause  of  cystin 
calculi). 

Uric   acid   also   separates  in  similar  crystals,   although   quite  exceptionally; 


Fig.  192.— Crystals  of  gypsum  (after  Neubauer  and  Vogel). 

hence  cystin  and  uric  acid  may  be  confounded.  The  crystals  of  cystin  are,  how- 
ever, perfectly  colorless.  To  differentiate  doubtful  crystals  chemically,  ammonium 
hydroxid  is  added  to  the  sediment.     Cystin  will  be  dissolved.     The  filtrate  is 

^  See   Stadthagen   and  Brieger,  Berlin,  klin.    Woch.,  vol.   xxvi.,  p.  344,   1889,  and 
Udransky  and  Bauraann,  Zeiis.f.  physiol.  Chemie,  1890. 


SEDIMENTS  AND   TURBIDITY  OF  THE   URINE. 


561 


then  acidulated  with  acetic  acid  or,  better  still  (Salkowski,  Drechsel),  allowed  to 
stand  exposed  to  the  air  for  some  time  until  the  ammonia  has  escajjed.  Cystin 
will  then  be  again  i^recipitated  in  hexagonal  disks.  Uric  acid  is  only  very 
slightly  soluble  in  ammonia,  and  also  differs  from  cystin  in  being  only  slightly 
soluble  in  hydrochloric  acid. 

Tyrosin  and  Leucin. — Tyrosin  very  rarely  appears  as  a  sediment.  It  is 
recognized  by  its  characteristic  crystals  (compare  p.  498  and  Fig.  173,  b). 

Leucin  is  a  still  rarer  sediment  than  tyrosin,  and  is  then  always  associated 
with  the  latter  (compare  p.  498  and  Fig.  173,  a). 

Xanthin,  although  a  normal  urinary  constituent,  is  very  rarely  obsen-ed  as  a 
sediment,  and  then  under  entirely  unknown  conditions.  It  forms  whetstone- 
shaped  crystals,  which  are  differentiated  from  those  of  uric  acid  by  being  readily 
soluble  in  ammonia.  Further,  if  xanthin  crj'stals  are  evaporated  with  moderately 
•concentrated  nitric  acid  over  a  water-bath,  they  leave  a  yellowish  white  residue, 
which  turns  to  an  intense  yellow  after  carefiil  heating  over  a  small  flame  ;  then 
the  addition  of  potassium  hydroxid  will  change  the  color  to  a  yellowish  red, 
which  will  become  more  deeply  colored  when  freshly  heated,  and  which  will 
finally  turn  to  a  violet  red  when  the  potassium  hydroxid  is  evaporated  (Strecker). 
This  test  must  not  be  confused  with  the  murexid  reaction  (p.  556). 

Cholesterin. — Cholesterin  crystals  have  been  found  occasionally,  and  some- 
times in  considerable  quantity  (cholesterinuria),  in  the  urine  in  diseases  of  the 


'^ 


Fig.  193.— Crystals  of  cystin  (after  Neubauer 
and  Vogel). 


Fig.  194.— a,  Xanthin  crystals  ;  b,  crys- 
tals from  the  solution  of  xanthin  in  hydro- 
chloric acid  (after  Neubauer  and  Vogel). 


urinary  passages  (inflammation  of  the  bladder,  pyelitis,  echinococci,  chyluria,  and 
nei^hritis).  This  occurrence  is,  however,  extremely  rare.^  Cholesterin  is  sup- 
jjosed  to  be  derived  from  the  epithelium  (Fig.  211,  b). 

Hematoidin  Crystals  (Bilirubin,  compare  Fig.  211,  d.'^). — Hematoidin  crys- 
tals occur,  although  very  rarely,  in  the  urine  of  hemorrhagic  nephritis.  Bili- 
rubin, crystals,  on  the  contrary,  are  not  infrequently  precipitated  in  sediment  of 
markedly  icteric  urine  when  cool,  particularly  if  it  is  strongly  acid  or  artificially 
acidulated.  They  can  be  easily  recognized  by  their  yellowish-red  color,  by  their 
solubility  in  alkalies  and  chloroform,  and  by  their  reaction  to  Gmelin's  test 
(p.  472  et  seq.),  under  the  microscope. 

Indigo. — If  the  indican  is  increased  in  the  urine,  indigo  may  separate  as 
pointed  or  rhombic  crystals.  These  may  either  be  found  in  the  sediment  or  form 
a  scum  on  the  surface.  They  dissolve  readily  with  a  blue  color  in  chloroform 
(pp.  454  and  475). 

Melanin. — Melanin  separates  in  rare  cases  as  fine  amorphous  granules.  It 
usually  remains,  however,  in  solution  (p.  477). 

Hemoglobin. — This  may  be  precipitated,  while  hemoglobin  is  still  in  solu- 
tion, as  a  sediment  of  amorphous  cakes  or  cvlinders  in  hemoglobinuria  (compare 
pp.  453  and  469). 

Fat. — A  large  amount  of  fat  in   the, urine  almost  always  signifies  c/i?//«ria 


1  Cf.  ITir.schlaff,  D.  Arch.f.  kUn.  Med.,  vol.  Ixii.,  p.  531. 

^  Hematoidin  and  bilirubin  are  usually  considered  identical. 


36 


562  URINARY  EXAMINATION. 

(lipuria).  The  urine  is  then  albuminous,  of  a  milk-white  to  a  cloudy-yellow 
appearance,  sometimes  even  slightly  blood-tinged,  neutral  or  faintly  acid,  forms 
a  cream-like  layer,  and  often  contains  small  coagula.  The  latter  may  form  withia 
the  body  as  well  as  after  the  urine  is  voided.  (Fibrin  and  Fibrinogen  Contained 
in  the  Urine,  see  p.  464.)  A  microscopic  examination  shows  that  the  fat  is  sub- 
divided much  more  freely  in  the  urine  than  in  the  milk.  Xo  distinct  fat-drops 
can  be  seen,  but  extremely  finely  divided,  almost  invisible,  fat-granules.  These 
granules  furnish  the  cloudiness  and  the  cream-like  layers.  The  other  character- 
istics of  this  fatt^"  admixture  are  the  same  as  those  that  will  be  described 
later  on  (see  p.  709  in  reference  to  the  chylous  fluids  sometimes  found  in  the 
serous  cavities.  Chylous  urine  does  not  contain  sugar,  since  this  substance  is  not 
removed  from  the  intestine  by  the  lacteals,  but  by  the  A'eins.  Chyluria  is  well 
knowTi  to  be  a  tropic  disease  caused  by  a  threadworm,  Filaria  sanguinis,  which 
inhabits  the  blood.  The  urine  occasionally  contains  the  embryos  of  the  filariae 
(see  Fig.    205). 

The  occurrence  of  tropic  chyluria  is  due  to  the  presence  of  adult  filarise  in 
the  thoracic  duct,  producing  a  stasis  of  the  chyle,  which  extends  not  only  to  the 
lymphatics  of  the  intestines,  but  also  to  those  of  the  urinary  apparatus.  In  such 
cases  chyle  may  become  admixed  with  the  urine  by  drapedesis  or  by  rupture  of 
those  lymphatics  which  do  not  ordinarily  contain  chyle.  In  one  case  Havelburg 
succeeded  in  definitely  proving  that  the  escajse  of  chyle  into  the  urine  took  place 
in  the  bladder.  The  frequent  simultaneous  admixture  of  blood  is  to  be  explained, 
according  to  Scheube,  partly  by  the  coincident  rupture  of  blood-vessels  and  vari- 
cose lymphatics,  and  partly  by  the  disappearance  of  the  tissue  between  the  ve- 
nous and  lymphatic  vessels,  due  to  the  lymph  stasis,  whereby  the  contents  of  the 
lymphatics  become  mixed  with  blood.  A  similar  stasis  of  chyle,  produced  in 
diflferent  ways  in  individual  cases,  may  probably  be  the  cause  of  the  rare  chyluria 
observed  in  this  climate. 

If  the  amount  of  fat  contained  in  the  blood  is  abnormal  (lipemia),  the  urine 
also  contains  an  abnormal  amount  (bone  fractures,  fat-embolism,  diabetes  mellitus, 
alcoholism,  and  acute  phosphorus-poisoning).      (See  Examination  of  the  Blood.) 

A  small  amount  of  fat  is  also  found  in  the  urine  in  Bright' s  disease  when  the 
kidney  elements  (casts  and  epithelium)  are  eliminated  in  a  fatty  degenerated  con- 
dition. The  fat  is  then  ordinarily  enclosed  within  cells  or  casts,  but  exception- 
ally it  may  appear  as  fat-drops  floating  upon  the  surface,  as  a  result  of  the  degen- 
eration of  the  cells  or  casts.  Crystalline  needles  of  fat  have  in  a  few'  cases  been 
found  in  the  urine.  Such  crystals  are  sometimes  formed  within  the  body,  some- 
times only  outside  from  the  fluid  fat.      (Fig.  211,  «). 

The  examiner  must,  of  course,  be  careful  not  to  confound  contamination 
from  dirty  vessels  or  catheter  grease  with  lipuria. 

If  the  macro-  or  microscopic  appearance  of  the  urine  does  not  suffice  for  the 
demonstration  of  fat,  then  the  urine  should  be  extracted  with  ether.  After  evapo- 
rating the  ether  the  physical  characteristics  of  the  fat  are  more  easily  recognized 
(grease  spots),  or  an  odor  of  acrolein  (like  smoking  tallow  candles)  can  be  demon- 
strated if  the  residue  is  heated  on  a  platinum  foil,  or,  if  the  fat  contains  oleic  acid 
the  addition  of  a  1  per  cent,  solution  of  osmic  acid  will  turn  the  residue  black. 

According  to  Spath,  lipvric  acid  has  been  obser\'ed  in  urine,  in  rare  cases,  in 
the  shape  of  prisms  or  needles.  The  factors  governing  its  occurrence  are  not  yet 
definitely  known,  although  it  seems  to  have  been  more  frequently  observed  after 
the  administration  of  salicylic  acid. 

MUCOUS  SEDIMENTS. 

If  the  urine  contains  considerable  nucleo-albumin  (compare  p.  468 
et  seq.),  it  will  separate  spontaneously  as  a  sediment  of  mucus-like  con- 
sistence. Such  a  sediment  consists  microscopically  of  a  cloud  of  clotted, 
transparent,  indistinct  masses.  The  addition  of  acetic  acid  will  make 
their  contours  more  distinct.     They  sometimes  enclose  various  morpho- 


SEDIMENTS  AND   TURBIDITY  OF  THE   URINE.  563 

logic  elements,  white  blood-corpuscles,  epithelium,  crystals,  etc.  Epithe- 
lial elements  and  white  blood-corpuscles  are  almost  always  found  in 
mucous  sediments,  because  the  increased  nucleo-albumin  is  the  product 
of  a  catarrhal  disintegration  of  the  mucous  membrane. 

ANALYTIC  SCHEME   OF  THE  PRINCIPAL  INORGANIC  URINE  SEDIMENTS. 

Readily  soluble  upon  heating  :  Urates. 
Insoluble  or  soluble  only  with  difficulty  upon  heating. 
''  Phosphates,  no  eifervescence. 
Soluble    in  J    Calcium  carbonate  with  development  of  carbonic  acid, 
acetic  acid  1    Ammonium  urate  with  microscopic  precipitation  of  uric 
acid. 

^    Soluble     in     hydro- 
Calcium  oxalate.  I        chloric    acid,    the 
Insoluble  in  J   Leucin,  tyrosin,  xanthin,  cystin.  f       last   three  soluble 
acetic  acid.  |                                                           J        i"  ammonia. 

Uric  acid.  1   Insoluble    in  hydro- 

Gypsum,  j       chloric  acid. 

APPENDIX    TO    DISCUSSION    OF   INORGANIC    SEDIMENTS.     URINARY 

CALCULI. 

Many  of  the  substances  enumerated  as  inorganic  sediments  are  under  cer- 
tain conditions  eliminated  in  the  urine  in  the  shape  of  concretions  or  urinary- 
calculi. 

Only  the  most  imijortant  points  in  recognizing  the  various  forms  of  urinary 
calculi  will  be  mentioned  here.  The  earthy  phosphatic  calculi  are  distinguished 
by  their  friability.  The  commonest  calculi,  those  of  uric  acid  and  urates  (urate 
calculi),  are  far  more  firm.  The  hardest  of  all  are  the  calculi  of  calcium  oxalate 
(so-called  oxalate  calculi). 

The  rare  cystin  calculi  are  usually  yellow,  smooth,  small,  and  soft  as  wax  ; 
the  still  rarer  xanthin  calculi  are  clearer,  rather  hard,  and  when  rubbed  exhibit  a 
wax-like  polish.  Calculi  of  cholesterin  are  also  very  rare  and  resemble  the  cystin 
concretions.  The  concrements,  consisting  of  fat  and  of  fatty  soaps  of  the  alka- 
line earths  and  designated  as  urostealiths,  are  extremely  rare  ;  they  are  charac- 
terized by  their  light  color,  soft  consistence,  and  hardness  when  dried.  Mention 
should  also  be  made  of  a  single  recorded  instance  of  a  calculus  consisting  of 
indigo,  w'hich  was  sufficiently  characterized  by  its  color.  Urinary  calculi  fre- 
quently consist  of  different  substances  arranged  in  layers,  each  of  which  may  be 
more  or  less  distinctly  recognized  by  the  previously  mentioned  characteristics. 

For  qualitative  analysis  a  finely  powdered  specimen  of  the  stone  is  first  heated 
upon  platinum  foil.  If  the  specimen  burns  up  entirely  or  nearly  so,  it  is  com- 
posed of  uric  acid,  xanthin,  or  cystin.  Cystin  and  xanthin  dissolve  in  dilute 
hydrochloric  acid  ;  uric  acid  does  not.  Uric  acid  may  also  be  recognized  by  the 
murexid  test  (p.  556).  Xanthin  can  be  distinguished  from  cystin,  as  shown  on 
page  561.  To  identifs'  cystin,  Salkowski  digested  the  powder  with  ammonium 
hydroxid,  filtered,  and  evaporated  the  filtrate  in  a  watch  glass.  Cystin  crystallized 
out  in  its  characteristic  hexagonal  plates  (Fig.  561).  Cholesterin  is  characterized 
by  its  solubility  in  ether  and  by  the  beautiful  rhombic  plates  which  are  formed 
by  evajjorating  this  ethereal  solution. 

If  the  powdered  calculus  does  not  burn  up  entirely  ui)on  the  platinum  foil, 
it  must  consist  either  of  lime  or  magnesia.  If  in  such  a  case  the  ])Owdered  speci- 
men completely  dissolves  in  dilute  hydrochloric  acid,  it  contains  no  uric  acid  along 
with  the  alkaline  earths.  What  dissolves  must  consist  of  phosjihates,  carbonates, 
or  calcium  oxalate.     Carbonates  can  be  recognized  by  the  development  of  gas. 


564  URINARY  EXAMINATION. 

Calcium  oxalate  can  be  recognized  by  the  fact  that  (by  acetic  acid)  it  is  jM-ecipitated 
gradually,  as  a  flaky  cloudiness,  from  the  dilute  HCl  solution  neutralized  with 
clear  ammonium  hydroxid.  If  any  residue  remain  after  the  treatment  with  dilute 
hydrochloric  acid,  it  generally  consists  of  uric  acid,  which  can  easily  be  identified 
by  means  of  the  murexid  test  Qx  556). 

ORGANIC   ADMIXTURES  AND   SEDIMENTS   OF  URINE 

As  to  the  method  of  isolating  these,  see  page  553  et  seq.,  at  which  place  will 
be  found  the  necessary  information  in  reference  to  the  elimination  of  interfering 
sediments  composed  of  urates,  phosphates,  or  carbonates. 

PRESERVATION  OF  THE  ORGANIC  SEDIMENT. 
If  it  is  impossible  to  examine  an  organic  sediment  immediately  after  settling 
or  after  centriftiging,  it  may  be  preserved  by  washing  several  times  with  a  normal 
salt  solution  and  then  kept  in  1  per  cent,  osmic  acid.  The  fat-drops  of  the  cel- 
lular elements  will  be  colored  black  if  they  contain  any  oleic  acid.  Instead  of 
this  procedure  i  the  sediment,  which  has  been  washed  with  physiologic  salt  solu- 
tion, may  be  hardened  in  a  1  :  20  sublimate  solution  for  five  minutes  and  then 
preserved  in  a  2  to  10  per  cent,  formalin  solution.  Formalin  will  destroy  the 
red  blood-corpuscles  if  they  have  not  been  previously  hardened  in  the  sublimate 
solution  ;  hence  the  hardening  by  sublimate  may  be  omitted  if  there  are  no  red 
cells.  May  ^  calls  attention  to  the  fact  that  even  in  a  case  of  this  sort  the  urinary 
sediment  must  be  first  washed,  otherwise  considerable  sediment  of  spheric  crystals 
of  diformaldehyd  urea  readily  forms. 

STAINING    OF    THE    ORGANIC    SEDIMENT. 

There  is  no  perfectly  satisfactory  method  for  staining  a  urine  sediment.  Most 
pigments  jsroduce  precipitates  after  being  added  to  the  urine,  so  that  the  sediment 
is  disfigured  by  granular  masses.  Dry  specimens  are  unsatisfactory,  because  urme 
with  an  organic  sediment  is  always  more  or  less  albuminous,  and  dried  proteid 
stains  strongly  ;  hence  the  dry  preparations  are  never  neat.  These  disadvantages 
may  be  partially  obviated,  although  in  a  rather  cumbersome  way,  by  washing  the 
sediment  repeatedly  with  normal  salt  solution,  repeating  the  sedimentation,  then 
drawing  off  the  fluid  repeatedly  with  a  pipet,  thus  separating  it  from  the  urinary 
constituents  which  are  held  in  solution,  especially  from  albumin,  and  then  finally 
adding  the  staining  .pigment.  A  cover-glass  preparation  may  then  be  made  in 
the  same  manner  as  with  sputum  (see  pp.  593  and  596).  The  sediment  must 
not  be  washed  for  too  long  a  time,  however,  or  sufficient  material  will  not  be 
obtained  for  the  cover-glass.  The  same  rules  apply  to  the  staining  of  the  diy 
preparation  as  obtain  in  the  examination  of  the  sputum.  If  the  attempt  to  make 
a  dry  preijaration  be  unsuccessful,  the  moist  sediment  may  be  best  stained  accord- 
ing to  the  method  of  T.  Liebmann :  ^  The  urine  is  centrifiiged,  the  supernatant 
fluid  poured  off,  and  the  sediment  treated  with  2  to  4  drops  of  a  solution  of  2  gm. 
of  methylene-blue  (Merck)  in  100  c.c.  of  a  10  per  cent,  solution  of  formalin. 
The  sediment  and  the  staining  solution  are  then  well  shaken  in  the  centrifuge  tube 
and  allowed  to  stand  for  several  minutes.  The  tube  is  then  filled  with  water  to 
remove  the  salts  and  the  excess  of  stain,  the  solution  is  again  centrifuged,  and  the 
sediment  placed  beneath  the  microscope.  Hyaline  casts  are  stained  light  blue, 
waxy  casts  dark  blue,  nuclei  and  bacteri  dark  blue,  and  red  blood-corpuscles  gray- 
ish blue.     This  method  may  also  be  employed  for  specimens  preserved  with  formol. 

If  it  be  desired  to  demonstrate  the  fatty  elements,  a  good  method  of  staining 
the  urinary  sediment  is  that  of  Cohn  *  :  The  dry  slide  is  hardened  in  a  10  per 
cent,   solution  of  formalin  for  about  ten  minutes,  then  washed  with  water,  and 

1  Gumprecht,  Centralhl.  f.  inn.  Med.,  1896,  No.  30. 
^  Arch.f.  klin.  Med.,  vol.  Ixviii.,  p.  425. 
^  3Iiinch.  med.  Woch.,  1904,  vol.  xlix.,  p.  1768. 

*  Zeits.  f.  klin.  Med.,  vol.  xxxviii.,  1899,  parts  1,  2,  and  3.  This  article  also  contains 
good  illustrations  of  urinary  sediments  stained  by  this  method. 


SEDIMENTS  AND   TURBIDITY  OF  THE   URINE.  565 

placed  for  ten  minutes  in  a  concentrated  solution  of  Sudan  stain  in  70  per  cent, 
alcohol.  1  Hematoxylin  is  used  as  a  counterstain,  and  the  specimen  mounted  in 
glycerin.     Fat  is  stained  red  and  the  nuclei  violet. 

Posner  recommends  hardening  the  dry  preparation  with  osmic  acid.  He 
proceeds  as  follows :  '^  Several  crystals  of  osmic  acid  are  placed  in  a  wide-mouthed 
dark-glass  bottle  provided  with  an  accurately  ground  glass  stopper.  The  moist, 
smeared  cover-glass  is  now  placed  over  the  mouth  of  the  open  bottle,  with  the 
smeared  side  down.  This  is  accomplished  by  making  the  clean  side  of  the  cover- 
glass  adhere  to  a  slide  by  means  of  a  drop  of  water.  The  slide  is  then  held  in 
position  by  the  dark-colored  stopper  so  that  light  is  excluded.  Fixation  is  com- 
pleted in  forty  seconds.  The  cover-glass  is  then  dried  in  the  air,  and  stained 
without  previous  washing.  Posner  found  that  this  treatment  adapted  the  prepa- 
ration for  all  the  finer  staining  methods,  and  that  it  was  also  applicable  for  blood- 
preparations. 

EPITHELIUM. 

Scattered  epithelium  cells  may  be  found  even  in  normal  urine.  The 
desquamation  of  epithelium  is  a  normal  physiologic  process.  If  they 
are  present  in  large  numbers,  however,  they  point  to  inflammatory  and 
destructive  changes  of  the  urinary  apparatus.  The  following  kinds  may 
be  distinguished  : 

Renal  Kpithelium. — They  are  generally  spheric  or  cubic,  a  little 
larger  than  white  blood-corpuscles,  often  distinguishable  from  the  latter 
only  by  their  larger  size  and  by  their  large 
single  nucleus.  The  nucleus  is  readily  seen, 
and  looks  like  a  bubble,  especially  when 
stained  (compare  p.  567).  They  may  show 
any  degree  of  fatty  degeneration,  and  may 
eventually  become  disintegrated  to  form  a 
conglomeration  of  fat-drops.  These  cells 
are  very  uncommon  in  normal  urine,  but  in 
some  forms  of  nephritis  are  very  plentiful 
(Fig.  195). 

epithelium  of  the  Urinary  Tract. 

—These  present  extremely  varied  forms.  from'neJhriUc^TineTj'w 
The  cells  of  the  upper  layers  are  generally     iJedrai  renai  epithelium  in  ne- 

111  /»ii  phniis  of  scarlet  fever:  6  and  c, 

flat,  round,  or  polygonal  ;  those  of  the  deeper  different  grades  of  fatty  degen- 
,  1,1  1  -ii-.i  eration    in    renal   epithelium   in 

layers  are  elongated  and  provided  Avith  proc-  chronic  nephritis  (x  400)  (after 
esses.      Fig.    196    illustrates   a  number  of 

these  cells.  A  considerable  quantity  of  the  epithelium  of  the  urinary 
passages  is  thrown  off  in  all  inflammatory  processes.  It  was  formerly 
believed  that  all  cells  provided  with  prolongations  always  came  from 
the  pelvis  of  the  kidney.  Unfortunately  for  the  differential  diagnosis 
of  pyelitis  and  cystitis,  this  old  idea  is  not  true.  No  absolute  point  of 
differentiation  between  epithelium  of  the  pelvis  of  the  kidney  and  that 
of  the  bladder  has  yet  been  found.  Nevertheless  a  very  great  predomi- 
nance of  caudate  epithelium,  as  compared  with  the  permanent  variety, 
suggests  pyelitis  rather  than  cystitis.  Fig.  197  represents  the  sediment 
taken  directly  from  the  pelvis  of  the  kidney  in  a  case  of  pyelitis. 

^  The  solution  is  prepared  by  Dr.  Griibler,  Leipzig,  Bayrischestrasse  63. 
^  Berlin,  klin.  Woch.,  1903,  vol.  xxxii. 


566 


URINARY  EXAMINATION. 


Vaginal  and  preputial  epithelia  are  typical  large  pavement 
cells.  Their  shape  should  be  familiar,  because  their  accidental  occur- 
rence in  the  urinary  sediment  may  lead  to  the  erroneous  presumption  of 


Fig.  196.— Epithelium  of  urinary  passages  :  a,  6,  c,  d.  Profile  of  cells  in  their  normal  position: 
a,  cell  of  deep  layer;  b,  long  ceil  of  second  layer  ;  c.  simple-  and  double-caudate  cells ;  d,  flat  sur- 
face cell ;  e,  surface  appearance  of  superficial  flat  cell  with  three  nuclei ;  /,  surface  appearance  of 
superficial  flat  cell  with  one  nucleus  and  4  impressions  (Xischeni :  o,  surface  appearance  of  super- 
ficial flat  cell  with  many  nuclei  and  many  impressions ;  h,  i,  k,  epithelium  of  bladder  modified 
by  action  of  urine ;  h,  from  alkaline  urine,  one  cell  swollen,  the  other  two  with  vacuoles  ;  i,  sur- 
face cells  ;  k,  caudate  cells  ;  ?.  bladder  epithelium,  granular  and  stained  yellow  by  blood-pigment, 
from  a  case  of  cystitis  and  nephritis  ;  m,  cylindric  epithelium  of  male  urethra  (x  37U  to  100)  (after 
Bizzozero). 


desquamative  affections  of  the  urinary  tract, 
men  is  examined,  no  such  mistake  is  possible. 


If  a  catheterized  speci- 


PUS    CELLS. 

Pus  cells  may  also  appear  in  the  urine  in  all  inflammatory  processes 
of  the  urinary  tract  or  kidneys  or  when  an  abscess  breaks  into  the  uri- 


'<55*"r' 


Pt-IH  <K?^5^S^is-.  ^^*^  ^^  e^  / 


Fig.  197.— Sediment  from  a  case  of  pyelitis,  taken  directly  from  the  pelvis  of  the  kidney  in  post- 
mortem examination. 

nary  tract.     Their  number  may  vary  greatly.     Sometimes  they  form  the 
chief  part  of  an  abundant  sediment,  and  sometimes  they  are  only  found 


SEDIMENTS  AND  TURBIDITY  OF  THE   URINE. 


567 


scattered.  When  the  urinary  tract  is  diseased  the  amount  of  pus  in 
the  urine  may  be  great,  but  in  disease  of  the  renal  parenchyma  proper 
the  pus  cells  are  usually  very  few.  The  origin  of  the  pus  cells  can  be 
determined  with  some  degree  of  certainty  only  when  the  presence  of 
other  morphologic  elements  (epithelium,  casts)  serves  as  an  indicator. 
The  sudden  appearance  of  a  pus  sediment  in  the  urine  suggests  the  rupt- 
ure of  an  abscess  into  the  urinary  tract,  provided  that  the  other  clinical 
signs  correspond  with  this  assumption.  The  occurrence  of  thread-like 
formations  is  very  characteristic  of  gonorrhea  and  gonorrheal  sediment 
(gonorrheal  threads,  compare  p.  573).  They  consist  of  pus  cells  glued 
together  with  mucus. 

In  females  the  pus  sediment  may  come  from  the  vagina.  To  exclude 
such  a  possibility,  either  the  vagina  must  be  thoroughly  irrigated  before 
the  urine  is  voided  or  the  urine  must  be  drawn  with  a  catheter. 

With  alkaline  fermentation  a  pus  sediment  is  oftentimes  converted 


A  ^<;^^ 


^  ^S^v'-'^ily^'^^ 


Fig.  198.— Sediment  in  alkaline  inflammation  of  the  bladder  :  Pus,  epithelium,  and  triple 
phosphate  crystals  (after  Peyer). 

into  a  ropy,  gelatinous  mass  by  the  swelling  of  the  pus  corpuscles.  Puru- 
lent urinary  sediments  ai'e  often  of  a  slimy  consistence,  even  if  the  urine 
is  not  alkaline,  because  the  urine  in  inflammatory  affections  usually  con- 
tains nucleo-albumin  (compare  p.  468). 

The  pus  corpuscles  voided  in  the  urine  vary  in  their  microscopic 
appearance,  which  depends  partly  upon  the  length  of  time  since  their 
escape  from  the  blood-current,  and  partly  upon  the  consistence  of  the 
urine,  or  upon  the  nature  of  the  affection  in  question.  Sometimes  they 
are  very  cloudy  and  shrunken,  so  that  the  nuclei  can  be  seen  only 
after  the  addition  of  acetic  acid  (usually  polynuclear  or  with  nuclei 
irregularly  crumpled) ;  sometimes  in  an  alkaline  urine  they  are  much 
swollen  and  glossy,  and  in  this  case  also  the  nuclei  are  not  easily  seen. 
In  faintly  alkaline,  neutral,  or  faintly  acid  urine,  on  the  contrary,  the 
pus  corpuscles  are  often  well  preserved  and  sometimes  even  show  active 
ameboid  movements,  especially  when  the  slide  is  slightly  warmed.  The 
most  important  point  of  differentiation   between   pus   corpuscles  and 


568 


URINARY  EXAMINATION. 


epithelium,  especially  renal  epithelium,  is  the  shape  or  number  of  the 
nuclei.  In  the  pus  cells  the  nuclei  are  usually  multiple  or  very  irregu- 
larly shaped,  never  bubble-shaped.  This  can  be  best  recognized  in  a 
stained  specimen  (p.  565).  The  size  must  also  be  considered.  The 
pus  corpuscles  are  usually  of  a  diameter  of  7  to  10  n,  corresponding  to 
the  poly  nuclear  leukocytes  from  which  they  arise,  whereas  the  epithelium 
cells  are  usually  much  larger.  Figs.  198  and  199  represent  the  puru- 
lent sediment  of  alkaline  and  acid  inflammation  of  the  bladder  or  of 
pyelitis. 

Of  course,  pus-containing  urine  always  contains  proteid  in  solution. 
It  is  a  part  of  the  quantitative  estimation  (see  below)  to  decide  whether 
the  albuminuria,  when  pus  is  present,  can  be  explained  by  the  admixture 
of  pus  plasma  only,  or  whether  we  must  assume  the  simultaneous  occur- 
rence of  a  true  renal  albuminuria.  In  the  latter  case  the  amount  of 
proteid  is  much  greater.     According  to  Posner,  100,000  pus  corpuscles 


Fig.  199.— Sediment  in  acid  inflammation  of  the  bladder :  Pus,  red  blood-corpuscles,  and 
epithelium  (after  Peyer). 

in  a  cubic  centimeter  correspond  to  about  1  per  cent,  of  proteid.  Mor- 
phologic elements  characteristic  of  true  albuminuria  (casts,  renal  epithe- 
lium) will,  if  present,  decide  this  question.  Filtration  does  not  remove 
the  proteid  of  pus  plasma,  although  this  erroneous  view  has  so  often 
been  maintained. 

Posner  formerly  suggested  that  the  amount  of  pus  present  in  the 
urine  could  be  estimated  by  counting  the  number  of  pus  corpuscles  in 
the  centrifugalized  twenty-four-hour  amount  of  urine  (analogous  to 
counting  the  red  blood-corpuscles)  by  means  of  the  Thoma-Zeiss  count- 
ing apparatus.  This  process  is  too  complicated  for  practical  purposes, 
so  Posner,  in  a  later  communication,^  announced  another  method  of  esti- 
mating the  amount  of  pus  mixed  with  the  urine,  or  of  the  amount  of 
sediment  in  general.  The  procedure  is  as  follows  :  The  transparency 
of  the  urine  (the  specimen  must,  of  course,  be  taken  from^  the  mixed 
twenty-four-hour  urine)  is  determined  by  placing  a  beaker  with  flat  bot- 
1  Deutsch.  med.  Woch.,  1897,  No.  40. 


SEDIMENTS  AND   TURBIDITY  OF  THE   URINE.  569 

torn  upon  a  piece  of  paper  with  ordinary-sized  print,  and  estimating  the 
height  in  centimeters  to  which  it  is  necessary  to  fill  the  beaker  so  that 
in  good  daylight  the  print  can  no  longer  be  read.  The  degree  of  trans- 
parency is  indicated  by  the  thickness  of  the  layer  in  centimeters.  Pos- 
ner  found  that  a  transparency  of  |^  to  1  cm.  corresponded  to  40,000  pus 
corpuscles  per  centimeter,  and  a  transparency  of  6  cm.  to  about  1000 
pus  corpuscles.  Eight  centimeters'  thickness  and  above  he  assumed  to 
indicate  normal  conditions.  Such  a  quantitative  estimation  of  the 
amount  of  pus  present  is  important  for  estimating  the  effect  of  thera- 
peutic interference  in  cystitis  and  pyelitis. 

BLOOD. 

Red  corpuscles  are  found  in  the  urine  in  hemorrhagic  inflammation 
and  tumors  of  the  urinary  tract  and  of  the  kidneys,  in  traumatic  hem- 
orrhage, in  calculi,  in  hemorrhage  from  congestion,  and  in  hemorrhagic 
diathesis.  The  blood-corpuscles  appear  in  the  urine  partly  intact,  and 
partly  changed  in  various  ways  by  the  action  of  the  urine.  They  are 
most  frequently  both  swollen  and  minus  their  pigment,  exhibiting  only 
the  pale  shadow-like  stromata,  sometimes  as  pale  disks  and  sometimes 
as  peculiar,  almost  invisible  circles.  Sometimes  the  blood-corpuscles 
break  up  into  small  masses  of  substance  containing  hemoglobin. 

In  determining  the  diagnostic  significance  of  blood-cells  in  the  urine, 
we  meet  with  the  same  difficulty  as  in  determining  the  significance  of 
pus  corpuscles — the  difficulty  of  being  sure  of  their  source.  In  this 
connection  also  we  must  determine  whether  the  amount  of  proteid  pres- 
ent in  the  urine  may  be  explained  by  the  admixture  of  blood  alone,  or 
whether  it  depends  upon  a  renal  albuminuria  as  well.  In  the  latter  case 
the  hemorrhage  probably  comes  from  the  kidneys.  If  casts  with  blood- 
corpuscles  adherent  or  blood-casts  also  occur  in  the  sediment,  the  source 
is  certainly  a  renal  hemorrhage.  Hemorrhage  which  leads  to  the  elimi- 
nation of  larger  blood-coagula  in  the  urine  usually  arises  not  in  the 
kidney  parenchyma,  but  in  some  part  of  the  urinary  tract  lower  down, 
either  the  pelvis  of  the  kidney  or  the  bladder.  It  should  be  remem- 
bered, however,  that  in  cases  of  hemorrhage  from  the  renal  parenchyma 
due  to  nephritis,  blood-clots  of  considerable  size  may  sometimes  be 
found  in  the  urine.  A  characteristic  shape  of  the  coagulum  may  point 
to  its  source  from  the  pelvis  of  the  kidney  or  the  ureter.  A  consider- 
able amount  of  blood  at  the  end  of  micturition  probably  indicates  blad- 
der hemorrhage. 

Gumprecht^  claims  that  if  most  of  the  blood-corpuscles  are  fragments — i.  e., 
disintegrated  to  small  masses — the  kidney  is  generally  the  seat  of  the  blood- 
extravasation.  '  In  hemorrhage  of  the  bladder,  on  the  contrary,  but  few  frag- 
mented blood-corpuscles  will  be  found.  As  concentrated  solutions  of  urea  (as  low 
as  8  per  cent.)  cause  fragmentation  of  the  red  blood-corpuscles,  Gumprecht  main- 
tains that  the  above-mentioned  difference  is  due  to  the  influence  of  the  urea  con- 
tained in  the  renal  epithelium  upon  the  extravasated  blood.  The  amount  of  urea 
in  the  urine  itself  is  said  to  be  insufficient  to  produce  the  change.  An  objection 
to  this  supposition  is  that  it  is  probable  that  the  blood-corpuscles  never  come  in 

^  Deutsch.  Arch.f.  klin.  Med.,  vol.  liii.,  1894. 


570 


URINARY  EXAMINATION. 


contact  with  solutions  of  urea  of  the  above-mentioned  concentration  in  the  kidney. 
In  the  opinion  of  the  aiithor,  it  is  more  likely  that  the  fragmentation  is  caused 
mechanically  by  the  contusion  of  the  blood-corpuscles  in  the  urinary  tubules. 


CASTS. 


Urinary  casts  are  characteristic  microscopic  formations  of  cylindric 
form  (Fig.  200),  which  originate  in  the  kidney  tubnles.  They  are  elimi- 
nated in  the  urine  in  nearly  all  cases  of  renal  albuminuria;  and  infre- 
quently even  without  albuminuria.      Albuminuria   may  occur  without 


Fig.  200.— CJasts  in  nephritis  :  a,  Epithelial ;  h  and  b' ,  granular ;  c,  waxy  ;  d,  hyaline ;  e,  blood- 
cast;  /,  cast  of  white  blood-corpuscles:  g,  hyaline  cast  with  epithelium  and  white  blood-corpus- 
cles adherent ;  /(,  waxy  cast  with  epithelium  and  red  blood-corpuscles  adherent  {h  and  6',  after 
Bizzozero). 

casts  ;  but,  generally  speaking,  elimination  of  casts  and  albuminuria  go 
together.  Casts  occur  most  commonly  in  the  various  kinds  of  nephritis  ; 
but  they  may  be  present  in  the  albuminuria  of  passive  congestion  as  well 
as  in  other  types  of  renal  albuminuria.  Nevertheless,  casts  may  be  absent 
in  all  of  these  cases.  If  the  renal  albuminuria  does  not  depend  upon 
nephritis  proper,  this  is  much  more  apt  to  be  the  case.  In  nephritis  the 
degree  of  albuminuria  and  the  number  of  casts  eliminated  are  usually 
quantitatively  proportional  one  to  the  other.     Exceptionally,  however, 


SEDIMENTS  AND   TURBIDITY  OF  THE   URINE.  571 

and  then  only  for  a  short  time,  casts  may  be  absent  even  with  a  con- 
siderable amount  of  renal  albuminuria.  The  occurrence  of  casts  with- 
out albuminuria  (a  rare  condition)  has  been  observed  in  very  chronic 
cases  of  nephritis,  in  contracted  kidney,  and  in  jaundice. 

The  principal  varieties  of  casts  are  the  following  (Fig.  200)  : 

(1)  Epithelial  casts  (a),  composed  of  epithelium. 

(2)  Granular  casts  {h  and  e),  granules  partly  soluble  in  acetic  acid 
and  partly  consisting  of  fat. 

(3)  AVaxy  casts  (c),  strongly  refractive,  sharply  outlined,  often  of  a 
slightly  yellow  color. 

(4)  Hyaline  casts  {d),  pale,  indistinctly  outlined,  seen  readily  only 
with  a  slanting  light. 

(5)  Blood-casts  (e),  composed  of  red  blood-corpuscles  or  casts  with 
red  cells  adherent,  yellowish  red  to  brownish,  sometimes  decolorized. 

(6)  Casts  of  white  blood-corpuscles  (/). 

Besides  these  there  are  many  intervening  varieties^^.  g.,  hyaline  or 
waxy  casts  with  red  or  white  blood-corpuscles  or  epithelium  adherent 
(^  and  A). 

Fatty  casts  are  casts  which  contain  fat  in  such  large  quantities  that  the 
ground-substance  of  the  cast  is  entirely  obscured.  Casts  may  be  composed  of 
pus  bacteria.  Such  occur  in  infections — pyelonephritis  and  in  the  kidney  of 
pyemia.  Other  casts  may  become  filled  with  bacteria  in  infectious  conditions 
of  the  urinary  apparatus,  in  the  kidney  itself  or  in  the  urinary  tract,  and  even 
outside  the  body  in  urine  containing  bacteria.  In  uric  acid  infarct  of  the  new- 
born so-called  uric  acid  casts  are  found,  consisting  of  spheres  of  sodium  urate. 
Casts  of  any  variety  may  become  incrusted  with  urates  in  a  concentrated  urine 
after  standing  ;  they  then  present  a  peculiar  dark  granular  appearance.  They 
are  differentiated  from  true  granular  casts  by  their  uneven  margins.  The  urate 
granulation  disappears  as  soon  as  the  urine  is  warmed  or  rendered  alkaline. 

The  length  and  thickness  of  casts  varies  greatly.  It  is  impossible 
to  draw  any  conclusions  as  to  the  source  of  the  casts  in  the  kidney 
tubules  from  their  diameter,  because  the  diameters  of  the  renal  tubules 
are  changed  in  pathologic  aifections  of  the  kidney  parenchyma.  Some- 
times the  casts  present  peculiar  screw-like  twists,  but  such  a  peculiarity 
does  not  mean  that  they  originate  in  the  convoluted  tubules.  We  require 
a  microscope  to  see  casts  properly  unless  they  are  very  thick  and  long. 

The  epithelial  casts  evidently  consist  of  desquamated  epithelial  cells 
which  are  eliminated  adhering  to  each  other.  These  casts  sometimes 
possess  a  lumen,  and  are  then  spoken  of  as  epithelial  ''  tubules."  In  a 
similar  way  extravasated  red  corpuscles  form  the  so-called  blood-casts, 
and  the  leukocytes  the  white-corpuscle  casts.  Any  of  these  conglom- 
erations of  cellular  elements  may  be  so  tightly  compressed  or  disin- 
tegrated that -the  cell  borders  become  more  and  more  obliterated.  Such 
changes,  the  nature  of  which  we  do  not  well  understand,  may  take 
place  in  the  kidney  tubules  themselves  or  in  the  urine  after  voiding. 
All  grades  of  intermediate  forms  which  still  have  the  stamp  of  their 
origin  merge  without  any  sharp  division  into  granular  and  waxy  casts, 
in  which  no  nuclei  or  cell-walls  are  to  be  distinguished.  The  existence 
of  such  transitional  forms  makes  it  probable  that  the  granular  and  waxy 


572  URINARY  EXAMINATION. 

casts  originate  as  cell  conglomerations.  In  these  the  epithelium  and 
leukocytes  appear  to  play  the  chief  part,  the  red  corpuscles  a  much 
smaller  one.  This  view  as  to  the  genesis  of  the  waxy  and  granular 
casts  is  supported  by  many  investigations  upon  the  diseased  kidney 
itself.  Formerly  the  casts  which  contained  no  cells,  the  granular  and 
waxy  as  well  as  the  hyaline,  were  considered  to  be  coagulated.  Whether 
this  genesis  can  still  be  considered,  in  view  of  what  has  already  been 
mentioned,  has  not  yet  been  certainly  decided,  but  it  is  not  improbable 
that  the  hyaline  casts  are  really  formed  by  exudation.  It  is  as  yet  still 
unknown  by  what  process  the  hemoglobin  which  separates  from  the 
blood  in  solution  in  hemoglobinuria  assumes  in  the  kidney  tubules  the 
form  of  solid  casts,  the  so-called  hemoglobin  casts.  It  can,  however, 
be  easily  conceived  that  these  casts  do  not  consist  solely  of  hemoglobin, 
but  only  represent  hyaline  and  waxy  casts  infiltrated  with  hemoglobin. 

We  have  but  little  accurate  knowledge  of  the  chemical  nature  of 
casts.  Once  in  a  while  some  cast  (especially  a  waxy  one)  will  give  an 
amyloid  reaction — i.  e.,  stain  red  with  gentian  violet  and  brown  with 
iodin — although  such  a  reaction  does  not  indicate  any  amyloid  degener- 
ation of  the  kidney  itself,  for,  as  a  matter  of  fact,  in  amyloid  disease 
such  a  reaction  of  the  casts  is  hardly  ever  observed. 

The  importance  of  finding  casts  in  the  urine  is  due  to  the  fact  that 
they  always  indicate  some  pathologic  condition  in  the  kidney,  and,  if 
accompanied  by  albuminuria,  make  it  practically  certain  that  the  kidney 
itself  is  involved.  But  the  change  in  the  kidney  need  by  no  means  be 
of  a  severe  anatomic  nature.  Even  slight  disorders  which  produce  but 
a  temporary  albuminuria  may  be  accompanied  by  casts,  although  in 
small  numbers. 

For  the  distinction  between  nephritic  albuminuria,  on  the  one  hand, 
and  febrile  or  congestive  albuminuria,  on  the  other,  we  may  lay  down 
the  rule  that,  if  casts  do  occur  in  the  latter,  this  is  the  exception.  They 
are  almost  always  merely  hyaline.  But  both  the  febrile  and  congestive 
albuminuria  may  change  to  a  nephritis  without  any  very  sharp  border  line. 

Little  can  be  claimed  for  the  diagnostic  importance  of  the  different 
varieties  of  casts.  Granular  and  waxy  casts  (as  opposed  to  hyaline  and 
epithelial)  were  formerly  supposed  to  indicate  a  chronic  process ;  but 
the  idea  was  wrong.  Any  and  all  varieties  of  casts  may  be  found  in 
every  type  of  nephritis,  and  even  an  amyloid  kidney  does  not  produce 
any  distinctive  type  of  casts  (see  above).  Generally  speaking,  granular 
and  waxy  casts  probably  owe  their  peculiar  characteristics  to  the  fact 
that  they  have  remained  in  the  kidney  tubules  for  some  time.  But 
that  does  not  necessarily  mean  a  case  of  chronic  nephritis.  As  a  matter 
of  fact,  it  would  probably  mean  acute  nephritis  or  the  acute  exacerbations 
of  chronic  nephritis,  as  in  such  cases  the  casts  remain  especially  long 
in  the  kidneys  because  the  excretion  of  urine  is  most  interfered  with. 

MUCOUS   CASTS   (Cylindroids). 

These  are  peculiar  formations  which  an  inexperienced  observer  may  mistake 
for  true  casts.     They  are,  however,  less  distinctly  outlined,  shaped  more  irregu- 


SEDIMENTS  AND   TURBIDITY  OF  THE    URINE. 


573 


larly,  sometimes  flat  and  tape-like,  of  smaller  diameter,  and  frequently  branch- 
ing. They  probably  consist  of  mucus — i.  e.,  of  the  undissolved  portion  of 
nucleoproteid  contained  in  the  urine.      They  are,  generally  speaking,  pale  and 


Fig.  201.— Cylindroids  (after  Peyer). 

hyaline,  but  may  be  covered  with  urates,  and  then  appear  granular  (compare  p. 
671).     They  are  of  no  especial  diagnostic  importance. 

TESTICLE  CASTS. 

In  spermatorrhea  certain  formations  are  sometimes  found  in  the  urine  which 
by  themselves  can  hardly  be  distinguished  from  hyaline  casts.  The  chemically 
normal  condition  of  the  urine,  and  the  fact  that  this  type  of  cast  appears  only 
in  that  portion  of  the  urine  leaving  the  urethra  first  and  is  usually  accompanied 
by  spermatozoa,  will  generally  sutfice  to  differentiate  them  from  true  renal  casts. 

GONORRHEAL  THREADS  (Shreds). 

In  the  late  stages  of  acute  gonorrhea,  when  the  secretion  becomes  more  of  a 
mucous  consistence,  and  in  chronic  gonorrhea  even  when  it  gives  rise  to  no  other 
distinct  symptoms,  peculiar  thread-like  formations  are  found  floating  in  the  urine. 
They  are  up  to  1  cm.  in  length,  visible  to  the  naked  eye,  generally  pointed  at 
the  end,  and  of  a  yellowish  to  whitish  color.  Under  the  microscope  we  can  see 
that  they  have  a  mucoid  ground-substance,  probably  consisting  of  nucleo-albumin, 
in  which  piis  corpuscles  and  epithelium  are  embedded.  ^  They  are  probably  caused 
by  accumulation  of  secretion  in  the  longitudinal  folds  of  the  urethra,  whence 
they  are  torn  away  by  the  stream  of  urine. 

SPERMATOZOA. 

Spermatozoa  occur  in  the  urine  after  coitus,  nocturnal  emissions  and  onanism, 
in  spermatorrhea,  and  after  epileptic  and  other  convulsive  attacks. 


FRAGMENTS  OF  NEW  GROWTHS  AND  ELASTIC  FIBERS. 

We  may  find  in  the  sediment  bits  of  tissue  which  have  become  sepa- 
rated from  papillomata  and  carcinomata  of  the  urinary  tract  or,  more 
especially,  of  the  bladder.      Similar  bits  may  be  caught  in  the  catheter 

^  Plate  to  be  found  in  Peyer,  Atlas  der  Milcros/cojne  am  Krankenbeite,  1887,  Plates  62 
and  63. 


574  URINARY  EXAMINATION. 

when  irrigating  the  bladder.  If  such  fragments  are  large  enough  to 
be  sectioned  and  stained,  the  microscope  will  quickly  determine  their 
nature. 

The  demonstration  of  elastic  fibers  is  sometimes  quite  important  in 
the  diagnosis  of  ulcerative  processes  of  the  urinary  tract  (Fig.  210). 
(See  Examination  of  the  Sputum.)  The  urine  is  first  acidulated  to 
prevent  the  formation  of  a  phosphate  precipitate,  and  then  centrifu- 
galized  or  allowed  to  settle.  The  liquid  is  then  poured  off  from  the 
sediment,  and  the  latter  gently  heated  with  an  equal  quantity  of  diluted 
(10  per  cent.)  potassium  hydroxid.  This  will  destroy  most  of  the  mor- 
phologic constituents  except  the  elastic  fibers.  The  mixture  is  then 
diluted  with  water  and  centrifugalized  again.  If  the  urine  contains  a 
great  number  of  elastic  fibers,  they  may  be  recognized  microscopically 
witliout  further  preparation.  Elastic  fibers  must  not  be  confused  with 
vegetable  fibers,  which  may  gain  access  to  the  urine  from  the  walls  of 
a  dirty  vessel.  The  differentiation  is  discussed  at  p.  589 — Examina- 
tion of  the  Sputum. 

MICRO-ORGANISMS. 

Urine  which  has  been  allowed  to  stand  soon  furnishes  a  very  favor- 
able medium  for  the  growth  of  all  kinds  of  bacteria,  particularly  if  the 
surrounding  temperature  is  raised.  The  development  of  these  organisms 
will  decompose  the  urine  in  various  ways.  The  chemical  changes  which 
take  place  in  the  urine  may  lead  to  the  decomposition  of  any  organized 
admixture  and  also  to  deception  as  to  its  composition.  It  is  therefore 
important  to  preserve  the  urine  in  a  cool  place,  and  to  undertake  the 
qualitative  examination  as  quickly  as  possible  after  voiding.  For  this 
purpose  a  twenty-four-hour  specimen  is  not  necessary.  The  decompo- 
sition of  the  urine  may  be  checked  by  adding  chemically  indifferent 
antiseptic  substances — e.  g.,  several  cubic  centimeters  of  coarsely  pow- 
dered camphor  or  one-fifth  its  volume  of  chloroform  water  or  the  same 
amount  of  0.1  per  cent,  solution  of  thymol.  For  the  same  reason  urine 
glasses  must  be  kept  as  aseptic  as  possible.  This  is  best  accomplished 
by  washing  them  well  with  water  and  then  with  a  0.1  per  cent,  sublimate 
solution  or  a  2  per  cent,  warm  soda  solution  every  time  after  they  have 
been  emptied,  and  then  keeping  them  covered,  so  that  they  are  not  con- 
taminated by  the  bacteria  in  the  dust  of  the  air. 

As  we  have  seen,  bacteria  are  very  frequently  found  in  the  urine. 
The  microscope  will  quickly  settle  the  question  of  their  presence  in  the 
sediment.  A  diffuse  contamination  by  bacteria  alone  may  be  responsi- 
ble for  a  very  pronounced  turbidity.  Such  a  cloudiness  may  be  distin- 
guished from  one  caused  by  unorganized  material,  as  it  is  affected  neither 
by  heat  nor  by  the  addition  of  acids  or  alkalies.  It  differs  from  sedi- 
ment composed  of  pus,  epithelial  cells,  or  casts  in  that  the  latter  sedi- 
ment (1)  quickly  settles  and  so  clears  the  upper  layers  of  urine,  and  (2) 
is  practically  always  associated  with  the  presence  of  proteid.  Shaking 
a  urine  extensively  contaminated  with  bacteria  often  produces  a  peculiar 
opalescent,  wave-like  movement  of  the  cloudiness.     Also  the  opalescent 


SEDIMENTS  AND   TURBIDITY  OF  THE    URINE.  575 

film  which  appears  upon  the  surface  of  a  urine  which  has  been  kept  for 
some  time  usually  consists  of  bacteria. 

The  demonstration  of  bacteria  in  the  urine  is  diagnostically  impor- 
tant only  when  they  occur  in  freshly  voided  urine  or  in  a  specimen 
obtained  by  catheterization.  Then  they  consist  either  of  great  numbers 
of  saprophytic  bacteria,  which  are  readily  seen  under  the  microscope 
without  staining,  and  which  produce  abnormal  decomposition  of  the 
urine  within  the  urinary  tract  when  the  latter  is  diseased  (bacteria  of 
ammoniacal  fermentation  and  bacteriuria),  or  else  of  true  patho- 
genic bacteria,  which  can  be  recognized  microscopically  or  cultivated 
upon  appropriate  media.  The  latter  are  found  partly  in  local  diseases 
of  the  urinary  tract,  as  in  certain  cases  of  cystitis  and  especially  in 
types  of  acute  nephritis,  and  partly  in  general  infections.  They  include 
such  organisms  as  colon  bacilli  and  staphylococci  (Fig.  219),  streptococci 
(Fig.  218),  gonococci  (Fig.  203),  pneumococci  (Fig.  214),  typhoid 
bacilli,  and  tubercle  bacilli  (Fig.  213).  In  general  infections  in  which 
bacteria  (staphylococci,  streptococci,  pneumococci)  are  eliminated  in  the 
urine,  it  is  still  debatable  whether  the  kidneys  and  urinary  passages  are 
unaffected  or  whether  such  elimination  is  always  combined  with  a  lesion 
of  these  organs.  The  microscopic  demonstration  of  these  bacteria  is 
really  far  more  important  than  the  culture  method  of  demonstration, 
because  the  former  excludes  the  source  of  error  of  any  incidental  con- 
tamination, and  because  it  gives  more  accurate  information  than  the 
latter  as  to  the  quantitative  importance  of  individual  species  in  mixed 
infections.  With  a  culture  it  may  happen  that  bacteria  of  little  or  no 
pathologic  importance  develop  inordinately. 

The  microscopic  examination  is  performed  just  as  with  dry-sputum 
examinations — i.  e.,  dry  preparations  are  prepared  by  spreading  the  sed- 
iment on  cover-glasses  (pp.  593  and  596  d  seq.).  If  a  specimen  of 
urine  is  swarming  with  bacteria,  a  drop  of  the  urine  can  be  dried  and 
examined  like  an  ordinary  dry  preparation.  If,  on  the  contrary,  the 
specimen  of  urine  contains  but  few  bacteria,  it  is  better  to  examine  a 
freshly  and  cleanly  prepared  sediment  obtained  by  means  of  the  centri- 
fuge. Bacterial  suspensions  are  so  difficult  to  centrifugalize,  that  if 
other  morphologic  elements  are  wanting  the  examination  will  be  simpli- 
fied by  first  diluting  the  urine  with  alcohol.  If  the  urine  contains  pro- 
teid  or  albumoses,  the  precipitate  which  results  from  the  addition  of  the 
alcohol  aids  in  isolating  the  bacteria  by  helping  to  carry  them  down  in 
centrifugalizing.  Of  course,  such  a  precipitate  should  be  merely  flaky, 
otherwise  it  would  interfere  with  making  a  good  dry  preparation. 
Should  the  alcohol  precipitate  large  flakes,  the  urine  must  first  be  diluted. 
Dry  preparations  are  prepared  by  spreading  the  sediment  thinly  upon  a 
cover-glass  (just  as  in  sputum)  and  fixing  over  a  flame.  Fixation  is, 
of  course,  sometimes  difficult,  because  urea  is  hygroscopic.  Hence  it  is 
often  necessary  first  to  wash  the  sediment  several  times  with  distilled 
water,  centrifugalizing  after  each  washing,  or,  if  necessary,  heating  for 
a  longer  time  over  the  flame,  so  as  to  convert  the  urea  into  ammonium 
carbonate.      Staining   can    be   accomplished    exactly  as  with    sputum 


576 


URINAR  Y  EXAMINA  TION. 


preparations  (pp.  593  et  seq.  and  596  et  seq.).  The  bacteria  may  also 
be  stained  by  the  previously  described  method  of  Liebmann  (see 
p.   564). 

For  cultures  we  must  naturally  employ  perfectly  fresh  urine,  with- 
drawn by  means  of  a  sterilized  catheter  into  sterilized  vessels  after 
careful  disinfection  of  the  urinary  opening.  The  first  urine  drawn  in 
this  manner  must  be  thrown  away,  since  it  may  contain  bacteria  which 
have  been  scraped  from  the  walls  of  the  urethra  by  the  eye  of  the 
catheter.  Even  after  observing  this  precaution  the  urine  may  become 
contaminated,  so  that  positive  conclusions  should  not  be  drawn  unless 
there  are  a  large  number  of  colonies. 

The  demonstration  of  tubercle  bacilli  in  the  urine  is  important  for  the 
diagnosis  of  tuberculosis  of  the  urinary  tract  (Fig.  213).  Dry  prepa- 
rations of  the  sediment  are  employed  in  the  same  way  as  with  the 
examination  of  sputum  (p.  593).  In  difficult  cases  the  search  for  the 
tubercle  bacilli  may  be  facilitated  by  treating  the  sediment  with  sodium 


Fig.  202.— Smegma  bacilli  (X  about  800)  (after 
Frankel). 


Fig.  203.— Gonoeoceus  (X  about  800)  (after 
Frankel). 


hydroxid  (see  p.  596),  or  tuberculosis  may  be  proved  to  be  present  by 
inoculation  experiments  upon  guinea-pigs  (see  p.  596).  A  difficulty  in 
such  a  method  is  that  other  pathologic  bacteria  which  occur  in  the  urine 
may  multiply  and  kill  the  animal  before  the  tuberculosis  can  develop. 
By  washing  the  sediment  before  inoculation,  the  danger  of  such  infec- 
tion is  lessened  by  the  removal  of  toxic  urinary  substances.  The  reader 
should  refer  to  p.  596  and  to  bacteriologic  text-books  for  the  details  of 
performing  an  inoculation  and  for  the  conditions  found  in  the  inoculated 
animals. 

The  so-called  smegma  bacillus  (Fig.  202  et  seq.)  has  been  so  frequently  con- 
fused with  tubercle  bacilli  as  often  to  lead  to  an  erroneous  diagnosis  of  uro- 
genital tuberculosis.  The  smegma  bacillus,  as  described  by  Alvarez  and  Tavel, 
occurs  very  frequently  in  the  preputial  fold  of  the  male  and  in  the  folds  above  the 
female  clitoris.  In  the  specific  staining  for  tubercle  bacilli  they  also  are  stained 
(p.  595).     From  their  location  they  can  easily  contaminate  the  urine  and  multiply 


SEDIMENTS  AND  TURBIDITY  OF  THE   URINE. 


577 


in  it  outside  of  the  body  (?).     These  parts  should  therefore  be  washed  very  care- 
ftilly  before  the  urine  is  passed  or  before  catheterization.^ 

The  smegma  bacilli  differ  from  the  tubercle  bacilli  in  being  more  slender  and 
not  granular,  and  not  exhibiting  the  characteristic  groupings  of  the  tubercle  bacilli 
(see  Figs.  202  and  213).  Finally,  when  the  stained  preparations  are  afterward 
treated  with  HCl  alcohol  for  from  five  to  ten  minutes,  the  smegma  bacilli  become 
decolorized,  but  not  the  tubercle  bacilli.  Grette  recommended  combining  the 
counterstaining   effect   of    methylene-blue   with   the    decolorized    action   of   the 


1  2  3 

Fig.  204. — Echinococcus  elements  :  1,  Free  scoliees  ;  a,  rostellum  projected ;  6,  rostellum  with- 
drawn; 2,  hooklets;  3,  membrane  (X  cross-section)  (after  Heller). 

alcohol.^  He  stains  as  ordinarily  with  carbol  fuchsin,  and  after  washing  with 
wat«r  he  treats  the  specimen  with  a  concentrated  alcoholic  solution  of  methylene- 
blue  (without  acid).  With  this  method  the  tubercle  bacilli  remain  red,  whereas 
all  the  rest  of  the  preparation,  including  the  smegma  bacilli,  is  stained  blue. 
Another  difference  between  them  is  that  Gram's  stain  decolorizes  the  smegma  but 
not  the  tubercle  bacillus.  Finally,  the  tubercle  but  not  the  smegma  bacilli  are 
changed  to  formations  like  strings  of  pearls,  resembling  streptococci,  by  excessively 
heating  the  dry  preparation — i.  e.,  by  passing  it  perhaps  ten  times  through  the 


Fig.  205.— Embryos  of  Filaria  sanguinis: 
Length,  0.0075  to  0.21  mm. ;  thickness,  0.004  to 
0.36  mm.  (after  Scheube). 


Fig.  206.— Eggs  of  Distomum  hEematobium 
(Bilharzia  hsematobia):  Length,  0.12  mm.; 
breadth,  0.05  mm.  (after  Bilharz). 


flame.  Compare  also  the  staining  method  recommended  by  Pappenheim  for  dis- 
tinguishing tubercle  bacilli  from  smegma  bacilli  in  the  sputum.  The  employ- 
ment of  Ebner's  decolorizing  fluid  will  also  prevent  the  confusion  of  these  bacilli 
(see  p.  595).  The  presence  of  gonococci  in  the  urine  sediment  is  also  of  diagnostic 
interest. 

'  Runge  and  Trautenroth  have  shown  that  the  urine  obtained  by  catheterization 
after  carefully  cleansing  the  external  orificium  urethrte  is  always  free  from  smegma 
bacilli.  ^  Fortschr.  d.  Med.,  1896,  No.  9. 

37 


578  URINARY  EXAMINATION. 

The  bladder  catarrh  and  pyelitis  which  may  complicate  gonorrhea 
never  depend  upon  a  pure  gonorrheal  infection,  but  upon  secondary 
infections  of  the  urinary  tract  with  other  organisms.  At  the  same  time, 
in  such  cases,  if  the  disease  has  not  been  entirely  cured,  pus  corpuscles 
which  contain  gonococci  are  sometimes  found  in  the  sediment.  They 
have  probably  become  mixed  with  the  urine  from  the  urethra.  Fig.  203 
shows  the  characteristic  arrangement  of  the  gonococci  in  the  interior  of 
the  pus  cells.  A  diagnosis  of  gonorrhea  is  permissible  only  when  this 
characteristic  intercellular  arrangement  has  been  recognized,  because 
the  same  biscuit-like  grouping  so  characteristic  of  diplococci  is  also  seen 
with  the  ordinary  staphylococci.  Another  characteristic  of  gonococci 
is  that  they  do  not  grow  upon  ordinary  culture  media. 

Braatz  ^  found  actinomycosis  granules  in  a  case  of  actinomycosis  of 
the  urinary  tract  (Figs.  224  and  225). 

In  diabetic  urine  a  rapid  yeast  growth  is  sometimes  produced  by  the 
presence  of  yeast  fungi.  The  sugar  becomes  fermented,  carbon  dioxid 
bubbles  are  formed,  and  yeast  spores  settle  in  the  sediment.  Hence, 
the  demonstration  of  yeast  fungi  in  the  urine  may  suggest  the  diagnosis 
of  diabetes ;  but  even  non-saccharine  urine  may  exhibit  yeast-like 
fungi. 

ANIMAL   PARASITES. 

EehinococcilS  of  the  urinary  tract  and  of  the  kidneys  may  cause  fragments 
of  echinococcus  cysts  and  hooklets  or  whole  daughter  cysts  to  be  voided  in  the 
urine  (Fig.  204). 

Embryos  of  Filaria  sanguinis  (Fig.  205)  are  found  in  the  urine  in  the  tropic 
hematochyluria,  and  the  eggs  of  Distomum  haematobium  (Bilharzia  hsematobia, 
Fig.  206)  in  the  Egyptian  hematuria.^  It  remains  to  be  mentioned,  finally,  that 
in  rare  cases  the  trichomonas  is  found  in  the  urine  in  disease  of  the  urinary  tract. 
This  species  is  probably  identical  with  that  occurring  in  the  intestine  (Trich- 
omonas intestinalis  ;  compare  p.  449  and  Fig.  151). 


EXAMINATION   OF  THE  SPUTUM. 

Expectoration,  or  sputum,  is  what  is  voided  by  coughing  or 
cleariug  the  throat.  It  is  composed  of  the  secretion  or  exudate  from 
the  respiratory  mucous  membrane  of  the  nose,  pharynx,  and  trachea 
down  to  the  finest  bronchi  and  alveoli ;  of  material  which  has  reached 
the  respiratory  tract  from  neighboring  regions  (pus  of  abscesses  and 
empyema)  ;  of  blood  derived  from  somewhere  along  the  respiratory 
tract ;  and,  finally,  of  material  from  the  buccal  cavity  or  from  any  part 
of  the  digestive  tract.  Macro-  and  microscopic  foreign  bodies  which 
have  entered  the  respiratory  system  from  without  are  usually  voided  in 
the  expectoration. 

On  account  of  its  numerous  sources  of  origin,  the  composition  of 
the  sputum  is  very  complex  and  of  great  symptomatologic  importance. 

1  Petersburg,  med.  WoeL,  1888,  No.  13. 

^  Riittimeyer,  Mittheilungen  aus  kliniken  und  medicinischen  Instituten  der  Schweiz,  1894, 
vol.  i. 


COLOR  AND   TRANSPARENCY  OF  THE  SPUTUM.  579 

The  sputum  is  not  always  expectorated.  Small  children,  and  occasion- 
ally adults,  in  consequence  of  bad  habits,  insufficient  practice,  or  im- 
paired consciousness,  swallow  their  sputum.  In  such  case  its  help  in 
diagnosis  is  lost.  Some  of  these  adults  and  most  older  children  can  be 
taught  to  expectorate.  For  diagnostic  purposes,  the  expectoration  for 
twenty-four  hours  is  collected  most  conveniently  in  a  transparent  spu- 
tum cup. 

AMOUNT    OF   SPUTUM* 

The  amount  of  sputum  may  vary  greatly,  depending  upon  what 
process  produces  it.  Some  pulmonary  patients,  in  spite  of  violent 
coughing,  expectorate  only  a  small  quantity,  and  that  usually  very 
tenacious  (dry  bronchitis,  incipient  phthisis).  Others  may  expectorate 
large  quantities  during  the  day,  or  even  at  one  time  (in  certain  types  of 
chronic  bronchitis  sometimes  called  bronchorrhea,  in  advanced  pulmo- 
nary tuberculosis,  in  bronchiectasis,  in  pulmonary  edema,  in  pulmonary 
hemorrhages,  and  in  perforation  of  abscesses  or  an  empyema  into  the  air 
passages).  The  special  characters  of  these  various  types  of  sputum 
will  be  discussed  later  on. 

CONSISTENCE    OF   THE    SPUTUM. 

The  consistence  of  the  sputum  bears  a  certain  relation  to  its  amount. 
If  very  abundant,  a  sputum  is  usually  less  tenacious  than  if  scant}*. 
Ordinary  sputum  is  "  slimy  "  ;  it  may,  however,  be  either  serous,  puru- 
lent, or  bloody.  The  peculiar  slimy  consistence  of  sputum  depends 
largely  upon  the  amount  of  mucus  it  contains,  since  the  mucin-like  sub- 
stances excreted  from  tlie  respiratory  mucous  membrane  form  a  consid- 
erable portion  of  the  expectoration. "^  The  stickiness  of  the  sputum  also 
is  partly  due  to  mucus  and  partly,  in  some  cases,  to  proteid,  especially 
the  sputum  of  croupous  pneumonia,  the  stickiness  of  which  is  supposed 
to  be  largely  due  to  the  amount  of  nuclein  contained. 

REACTION    OF   THE    SPUTUM. 

The  reaction  of  fresh  sputum  is  generally  alkaline.  It  may  become 
acid,  after  standing  for  some  time,  from  decomposition  of  the  sputum 
by  bacterial  growth. 

COLOR   AND    TRANSPARENCY    OF   THE   SPUTUM. 

The  color  of  the  sputum  varies  decidedly.  Pure  mucoid  or  glassy 
sputum  may  be  perfectly  colorless,  and  so  viscid  that  it  might  easily  be 
mistaken  for  saliva.  Admixture  of  blood -corpuscles  makes  this  slimy 
secretion  more  and  more  yellow  or  greenish,  and  also  cloudy  and  opaque. 
It  is  not  clear  why  the  color  in  one  case  is  more  yellow,  and  in  another 
more  greenish,  any  more  than  in  the  case  of  pus.     But  as  the  more 

^  The  mucus  of  the  respiratory  apparatus  appears  to  be  composed  mostly  of  true 
mucin  (Cohnheim,  Chemie  der  Eiweiss/cijrper,  Braunschweig,  Viewig,  1900;  F.  Miiller, 
"Beitrage  zur  Kenntnis  des  Mucins,"  etc.,  Zeits.f.  Biol.,  vol.  xlii.). 


580  EXAMINATION  OF  THE  SPUTUM. 

intense  inflammations  are  usually  associated  with  the  transudation  of  red 
blood-corpuscles,  it  seems  fair  to  assume  that  the  green  derivatives  of 
blood-pigment  usually  produce  the  greenish  pus  color.  (See  later  with 
reference  to  other  causes  of  green  discoloration  of  the  sputum.) 

A  mucopu7'ulent  sputum  consists  of  an  admixture  of  masses  of  pure 
mucus  with  masses  of  pus,  or  of  a  moderate  but  uniform  admixture  of 
the  two  elements,  the  whole  appearing  but  slightly  clouded.  Purulent 
sputum  is  the  next  step  in  such  admixtures.  Its  consistence  is  still 
mucoid  unless  composed  of  pure  pus  (either  thick  or  thin)  derived  from 
an  abscess  or  from  an  empyema,  and  expectorated  as  such  without  any 
mucus. 

Serous  sputum  is  another  type  of  colorless  expectoration.  It  differs 
from  the  pure  mucoid  or  glassy  sputum  in  its  very  liquid  consistence 
and  foamy  appearance.  It  occurs  in  pulmonary  edema,  and  rarely  from 
the  perforation  of  serous  pleural  exudates  into  the  lung.  Serous  sputum 
is  frequently  slightly  tinged  with  blood. 

Sputum  has  a  slightly  reddish  color  whenever  mixed  with  blood. 
In  some  cases  the  sputum  consists  of  pure  blood ;  in  other  cases  it  con- 
tains only  a  slight  admixture,  producing  a  salmon  color.  Between 
these  two  extremes  all  sorts  of  transitional  forms  occur.  Hemorrhagic 
sputum  is  observed  in  traumatic  and  tuberculous  hemorrhages  from  the 
lungs,  in  hemorrhagic  infarctions  of  the  lungs,  in  pneumonia  (especially 
in  croupous  pneumonia),  in  gangrene  of  the  lung,  in  tumors  of  the 
lung,  and  finally  in  congestion  of  the  pulmonary  circulation. 

Certain  derivatives  of  blood-pigment  produce  in  the  sputum  very 
similar  shades  to  that  of  bloody  sputum  proper.  Rusty  sputum,  the 
most  common  type  in  pneumonia,  is  an  instance.  The  coloring  matter 
is  here  partly  unchanged  blood,  partly,  however,  a  yellowish-red  deriv- 
ative of  the  blood-pigment,  about  which  little  is  as  yet  known.  Pecu- 
liar lemon-colored  and  grass-green  shades  are  infrequently  observed  in 
pneumonia  sputum.  They  are  due  to  further  chemical  alterations  of 
the  blood-pigment.  All  these  variations  are  analogous  to  the  changes 
of  blood-pigment  observed  in  subcutaneous  ecchymoses.  Such  sputa 
respond  to  Gmelin's  test  for  bile  pigment  (see  p.  472  et  seq.).  Lemon- 
yellow  and  greenish  sputa  in  pneumonia  are  frequently  regarded  as 
icteric.  This  supposition  is,  however,  justifiable  only  when  there  is  gen- 
eral jaundice  or,  at  least,  some  icteric  discoloration  of  the  eonjunctivse, 
or  when  bile  pigment  is  contained  in  the  urine.  In  the  remaining  cases 
we  cannot  speak  of  icteric  sputum,  although  it  must  be  admitted  either 
that  the  contained  coloring  matter  is  related  to  bile  pigment,  because  it 
is  derived  from  hemoglobin,  or  that  it  is  identical  with  bile  pigment 
when  a  distinct  Gmelin  reaction  is  obtained.  A  peculiar  light-brown 
shade  characterizes  sputum  which  contains  abundant  cells  of  heart  dis- 
ease (see  Plate  8,  Fig.  3).  Here,  especially  in  mitral  disease,  amor- 
phous blood-pigment  is  found  encapsulated  in  the  pulmonary  lung 
epithelium.  The  brownish  or  ochre-like  color  of  the  sputum  which  is 
occasionally  observed  in  destructive  processes  of  the  lung,  especially  in 
pulmonary  abscesses,  or  in  a  liver  abscess  which  has  perforated  into  the 


COLOR  AND   TRANSPARENCY  OF  THE  SPUTUM.  581 

lung,  is  due  to  hematoidin  or  bilirubin  crystals.  In  the  expectoration 
from  a  liver  abscess  the  hematoidin  or  bilirubin  crystals  are  derived  not 
from  the  blood,  but  from  the  admixture  of  bile  with  the  pus.  The  bit- 
ter taste  noticed  by  patients  when  expectorating  such  sputum  depends 
upon  the  presence  of  biliary  salts.  Gmelin's  reaction  for  bile  pigment 
will  not  diiferentiate  the  source  of  the  hematoidin  or  bilirubin,  as  they 
react  in  the  same  way,  whether  derived  from  blood  or  from  bile. 

True  icteric  sputa,  such  as  has  been  observed  in  certain  cases  of 
pneumonia  or  with  any  other  pulmonary  aifections  with  jaundice  (com- 
pare p.  42  et  seq.),  may  present  various  shades  of  color,  due  to  the 
oxidizing  of  bilirubin.  Yellow  and  then  dirty-green  shades  are  the 
most  common. 

A  rather  diiferent  type  of  green  sputum  has  been  observed  in  lung 
tumors  ;  but  the  nature  of  the  pigment  in  question  is  as  yet  unknown. 
Certain  pulmonary  tumors  (chloroma)  which  belong  to  the  sarcomata  or 
to  the  lymphadenomata  are  greenish  in  color.  Hence  a  greenish  spu- 
tum in  a  tumor  of  the  lung  would  suggest  a  chloroma ;  but  green  spu- 
tum has  been  observed  in  cases  of  carcinoma.  The  pigment  of  chloroma 
dissolves  in  alcohol.  Too  much  attention  has  probably  been  devoted  to 
the  green  sputum  in  tumors  of  the  lung,  because,  as  we  shall  see,  bac- 
teria which  may  produce  pigment  may  cause  a  greenish  discoloration  of 
sputum  outside  of  the  body. 

Other  noticeable  pigmentation  in  sputum  has  been  observed  from  the 
admixture  of  inhaled  dust  particles.  Black  sputum  belongs  to  this 
class.  Its  pigment  is  due  to  inhaled  coal  dust  or  soot,  of  which,  as  is 
well  known,  normal  lung  pigment  consists.  A  small  portion  of  the 
carbon  is  free  in  the  sputum  ;  the  larger  part  is  contained  in  the  interior 
of  round  or  oval  epithelium  and  white  blood-cells  (compare  p.  209). 
Under  the  microscope  we  can  frequently  recognize  the  vegetable  struct- 
ure of  the  larger  particles  of  carbon.  These  are  usually  not  contained 
in  the  cells,  but  are  found  free.  The  gray  or  blackish  discoloration  of 
such  sputa,  as  well  as  the  degree  of  lung  pigmentation,  depends  chiefly 
upon  the  individual's  occupation.  The  sputa  of  coal  miners  are  fre- 
quently intensely  black  (anthracosis  of  the  lung).  Other  pneumoconioses 
— i.  e.,  changes  in  the  lung  produced  by  the  inhalation  of  dust — are 
associated  with  peculiar  discoloration  of  the  sputum.  Workmen — e.  g., 
in  polishing  mirrors — who  breathe  the  dust  of  oxid  of  iron  (English- 
red,  caput  mortuum),  and  who  have  thereby  acquired  siderosis  of  the 
lung,  may  expectorate  an  ochre-colored  sputum.  The  reddish  particles 
are  for  the  most  part  enclosed  within  the  cells.  To  demonstrate  side- 
rosis from  the  sputum,  add  hydrochloric  acid  and  a  solution  of  ferrocy- 
anid  of  potash  ;  Berlin  blue  will  then  be  formed.  Blue  sputum  has 
been  observed  in  men  working  in  ultramarine. 

These  discoloration s  of  the  sputum  are  not  due  to  the  pigment  which  has 
impregnated  the  lung,  for  whatever  pigment  particles  are  deposited  in  the  lung 
probably  never  leave  it ;  they  should  rather  be  considered  as  coefFects  of  the  same 
cause — viz.,  inhalation  of  dust.  Only  the  dust  which  has  been  recently  inhaled, 
and  which  has  not  penetrated  the  interior  of  the  pulmonary  tissue,  is  expectorated. 


582  EXAMINATION  OF  THE  SPUTUM. 

Consequently  the  characteristic  discoloration  of  the  sputum  will  disappear  soon 
after  the  patient  gives  up  the  occupation  that  jDroduced  it,  although  the  pneumo- 
coniosis will  persist.  Discolored  sputum  should  be  considered  rather  as  a  sign  of 
the  inhalation  of  dust  than  of  pneumoconiosis.  Where  the  characteristic  dis- 
coloration of  the  sputum  continues  or  reappears  after  the  individual  has  been 
removed  for  some  length  of  time  from  the  specific  dust  atmosphere,  it  generally 
means  that  some  destructive  process,  usually  tuberculosis,  is  added  to  the  pneumo- 
coniosis. 

The  ' '  gluing "  or  "  smearing ' '  of  the  respiratory  passages,  described  by 
Gerhardt  and  Lublinski,^  which  occurs  in  bakers  and  millers  should  be  mentioned. 
Here  paste-like  masses  are  expectorated.      It  is  due  to  the  inhalation  of  flour. 

Hair  and  teeth  are  sometimes  found  in  the  sputum  following  the  perforation 
of  a  dermoid  cyst  of  the  mediastinum  into  the  bronchi. 

The  manifold  discolorations  of  the  sputum  due  to  admixtures  from 
without,  and  not  from  the  air  passages,  should  be  mentioned — e.  g., 
when  patients  take  milk,  eggs,  claret,  coffee,  chocolate,  or  some  colored 
medicine  before  expectorating,  the  sputum  is  apt  to  become  discolored 
in  the  mouth.  A  green  discoloration  of  the  sputum  is  sometimes  due 
to  the  growth  of  certain  chromogenic  bacteria,  especially  the  Bacillus 
virescens,^  Yellow,  bluish,  and  reddish  sputa  of  probable  bacteriologic 
origin  have  also  been  observed.  The  parasite  of  "  blue  pus  "  (Bacillus 
pyocyaneus)  probably  grows  in  sputum.^ 

AIR    CONTENT   OF   THE    SPUTUM. 

Sputum  is  often  more  or  less  distinctly  foamy  or  frothy,  due  to  the 
presence  of  air.  Other  things  being  equal,  the  amount  of  air  contained 
in  sputum  is  greater  the  finer  the  bronchi  from  which  it  is  derived. 
This  is  because  air  is  most  easily  incorporated  with  tiny  masses  of  spu- 
tum, as  they  are  being  collected  into  large  masses,  while  passing  from 
the  smaller  to  the  larger  bronchi.  The  consistence  of  the  sputum  is 
also  of  importance.  Thin  sputum  is  usually  very  frothy.  Thick, 
tough  sputum  is  less  so.  The  amount  of  air  contained  in  the  sputum 
can  be  readily  recognized  by  its  specific  gravity.  Air-containing  sputum 
will  float  on  the  water  in  a  sputum  cup  ;  airless  sputum  will  sink.  The 
sinking  of  sputum  (sputa  fundum  petentia)  has  been  considered  a  proof 
of  its  derivation  from  a  cavity  of  the  lungs.  Evidently,  sputum  de- 
rived from  the  pus  of  pulmonary  cavities  will  ordinarily  contain  but  a 
slight  amount  of  air ;  but  so  may  purely  catarrhal  secretion  from  the 
larger  bronchi,  so  that  this  test  is  of  slight  diagnostic  value,  and  then 
only  in  connection  with  other  signs. 

SPUTUM   STRATA. 

Sputa  which  settle  in  layers  in  the  cup  are  observed  chiefly  in  bron- 
chorrhea  (chronic  bronchitis  with  abundant  secretion),  in  bronchiectasis, 

1  Gerhardt,  Centralbl.  f.  inn.  Med.,  1896,  No.  20;  Lublinski,  Ibid.,  1896,  No.  28. 

^  See  Frick,  Virchow's  Archiv,  vol.  cxvi.,  1889,  p.  226. 

^  [A  bacillus  which  could  not  be  differentiated  from  the  Bacillus  pyocyaneus  was 
isolated  from  the  sputum  of  a  case  of  chronic  bronchitis.  This  sputum  when  first  ex- 
pectorated was  colorless,  but  developed  an  intense  greenish  color  upon  standing  less  than 
three  hours.     The  literature  contains  a  number  of  similar  instances. — C.  N.] 


CHARACTERISTIC  GROSS  APPEARANCES  OF  THE  SPUTUM.  583 

in  putrid  bronchitis,  and  in  gangrene  of  the  lung.  There  are  usually 
three  layers — an  uppermost,  aerated  portion  ;  a  middle  or  serous  layer, 
consisting  chiefly  of  pus,  serum  or  mucoid  fluid ;  and  a  third  layer,  the 
sediment,  which  consists  of  pus  corpuscles,  gangrenous  shreds  of  lung 
tissue,  and  molecular  lung  detritus. 

ODOR   OF   THE   SPUTUM. 

Fresh  sputum  rarely  has  any  particular  odor ;  but  upon  standing  it 
may  acquire  a  disagreeable  odor,  due  to  the  action  of  bacteria.  Freshly 
expectorated  sputum  has  a  very  strong  odor  in  purulent  bronchitis,  in 
some  cases  of  pulmonary  tuberculosis,  in  bronchiectasis  and  pulmonary 
gangrene,  and  very  frequently  in  pulmonary  abscess  and  in  empyema  of 
the  lung.  The  disagreeable  odor  in  these  cases  arises  from  the  growth 
of  putrefactive  bacteria  even  before  the  expectoration  of  the  sputum. 
Stagnation  of  the  secretion  in  cavities  favors  the  processes  of  decompo- 
sition. The  foul  odor  of  the  contents  of  the  lung  is  usually  imparted 
to  the  exhaled  breath,  where  it  may  even  be  more  distinct  than  in  the 
sputum  itself.  This  is  frequently  noticed  in  consumptives.  The  pecu- 
liar carrion-like  odor  of  the  breath  so  characteristic  of  this  disease  will 
sometimes  point  to  pulmonary  tuberculosis  before  even  any  definite  path- 
ologic signs  have  appeared  in  the  chest,  and  while  the  sputum  may  be 
remarkably  free  from  odor.  We  should  then  naturally  suspect  that  the 
foul  odor  came  from  the  mouth,  which  is  not  by  any  means  always  the 
€ase.  This  paradoxical  condition  is  very  likely  due  to  the  fact  that  the 
warm  air  in  the  lung  takes  up  odors  more  readily  than  the  air  at  room 
temperature.  Besides,  sputum  may  very  rapidly  lose  its  odor  upon 
standing.  The  same  is  true  of  the  fecal  vomitus  in  intestinal  obstruc- 
tion. It  seems  to  the  writer  probable,  and  his  idea  is  confirmed  by 
others,  that  consumptives  with  this  characteristic  odor  usually  have  cav- 
ities (even  if  quite  small)  in  which  the  secretion  stagnates. 

The  sputum  may  have  a  peculiar  odor  after  the  administration  of 
myrrh,  oil  of  turpentine,  ether,  alcoholic  drinks,  paraldehyd,  etc.  It 
has  been  assumed  that  these  substances  are  partly  eliminated  by  the 
lungs  ;  but  it  has  been  proved  recently  that  no  appreciable  quantity  of 
alcohol  is  expired,  and  that,  except  for  the  slight  trace  of  alcohol  which, 
of  course,  adheres  to  the  mucous  membrane  of  the  mouth,  the  odor  of 
the  expired  air  after  drinking  alcoholic  beverages  is  due  principally  to 
the  esters  which  all  liquors  contain.  At  all  events,  the  odor  comes 
largely  from  the  lungs,  for  deodorizing  mouth  washes,  such  as  perman- 
ganate of  potash,  produce  no  effect. 

CHARACTERISTIC   GROSS    APPEARANCES   OF   THE 

SPUTUM. 

Many  sputa  appear  to  the  eye  perfectly  homogeneous — pure  mucous, 
pure  purulent,  pure  bloody,  etc.  But  sometimes  not  only  may  the  sputa 
from  one  patient  vary,  but  differences  can  be  distinguished  in  each  ex- 
pectoration.     Particularly  in  mucopurulent  sputum  the    particles  of 


584 


EXAMINATION  OF  THE  SPUTUM. 


mucus  and  pus  may  alternate.  From  the  quantity  of  these  individual 
constituents  we  can  judge  more  or  less  correctly  whether  the  sputum 
arises  from  a  larger  or  a  smaller  bronchus. 

A  peculiar  fine,  flocculent  appearance  of  purulent  sputum  is  very 
characteristic  of  the  slow  emptying  of  a  pleural  empyema  or  of  a  pul- 
monary abscess.  The  flocculi  can  be  best  seen  if  the  sputum  is  sus- 
pended in  water.  They  are  probably  due  to  the  fact  that  the  pus  is 
pressed  into  the  shape  of  shreds  or  strands  in  being  squeezed  through 
the  seat  of  perforation.  These  shreds  become  surrounded  by  mucus, 
and  are  then  no  longer  confluent. 

To  detect  other  admixtures  which  exhibit  a  microscopic  difference 
from  the  main  bulk  of  the  sputum,  it  is  advisable  to  examine  a  small 
portion  of  the  sputum  upon  a  plate  one-half  of  which  has  been  painted 
with  black  enamel  paint,  so  that  the  background  may  be  either  black  or 


III. 

Fig.  207.— Curschmann's  spirals :  I.,  Natural  size  ;  II.  and  III.,  enlarged :  a,  central  fiber  (after 

Curschmann). 

white,  as  desired.  In  this  way  it  is  easy  to  select  ropy,  fibrous,  gener- 
ally dirty  dark  particles  or  larger  grayish-black  shreds  characteristic  of 
necrotic  lung  tissue.  If  elastic  fibers  (Fig.  210)  are  detected  by  the 
microscope,  the  diagnosis  is  confirmed.  These,  however,  may  be  absent 
in  gangrene  of  the  lungs  (p.  590).  Bits  of  necrotic  cartilage  in  ulcer- 
ative processes  of  the  bronchi,  trachea,  or  larynx,  and  tumor  fragments 
may  be  detected  in  the  same  way. 

"  Dittrich's  plugs,"  yellowish-white  bits  the  size  of  a  mustard  seed, 
are  very  conspicuous  when  looked  for  over  a  dark  background.  They 
come  from  the  smaller  bronchi  in  putrid  diseases  of  the  lungs,  especially 
in  putrid  bronchitis  and  in  pulmonary  gangrene.  Microscopically, 
they  consist  of  clumps  of  bacteria  and  crystals  of  fatty  acids  (compare 
Fig.  211,  a).     They  have  a  very  intense  and  disagreeable  odor. 

Similar  plugs  may  be  seen  mixed  in  the  sputum  in  follicular  tonsil- 
litis, or  may  even  be  extruded  from  the  crypts  of  a  normal  tonsil. 


CHARACTERISTIC  GROSS  APPEARANCES  OF  THE  SPUTUM.  585 

"  Dittrich's  plugs  "  should  not  be  confused  with  the  spiral  formations 
described  by  and  named  after  Curschmann.  These  are  represented  in 
Fig.  207  ;  I.,  natural  size ;  II.  and  III.,  slightly  magnified.  They 
consist  of  worm-like  formations  1  and  2  cm.  long  and  about  1  mm. 
thick,  more  or  less  opaque,  and  usually  suspended  in  a  glassy  men- 
struum. They  are  shiny,  viscid  in  consistence,  are  visible  to  the 
naked  eye,  and  are  composed  of  shreds  twisted  into  a  spiral.  They 
are  only  rarely  branched.  Some  of  them  exhibit  a  central,  more 
strongly  refractive  fiber  (Fig.  207,  II.,  a  and  III.,  a).  Other 
formations  which  resemble  these  central  fibers  occur  in  sputum,  but 
they  are  isolated  and  not  surrounded  by  spirals.  A.  Schmidt  showed 
that  Curschmann's  spirals  and  the  central  fibers  consist  of  a  mucin- 
like  substance  and  not  of  fibrin,  as  was  formerly  supposed.'^  They 
are  not  so  dense  as  the  shreds  of  fibrin  which  occur  in  the  sputum. 
These  spirals  of  Curschmann  are  portions  of  the  secretion  or  exudate 
which  forms  in  the  finest  bronchi  as  the  product  of  a  so-called  bronchio- 
litis exudativa.  This  affection  is  frequently  the  cause  of  or  secondary  to 
bronchial  asthma.  Hence  Curschmann's  spirals  are  more  or  less  charac- 
teristic of  asthmatic  sputum.  After  the  end  of  a  typical  attack  they 
are  sometimes  found  in  extraordinary  numbers.  We  must  not,  how- 
ever, suppose  that  Curschmann's  spirals  are  pathognomonic  of  asthma, 
for  not  only  do  cases  of  asthma  occur  without  spirals,  but  spirals  may  be 
found  in  the  sputum  of  a  bronchitis  without  asthma.  They  are  some- 
times found  in  croupous  pneumonia,  in  which  case  there  is  a  very  good 
opportunity  to  distinguish  them  from  bits  of  fibrin.  When  strongly 
magnified  the  spirals  will  frequently  be  found  to  contain  white  blood- 
corpuscles  and  Charcot's  crystals  (Fig.  211,  e).  These  leukocytes,  par- 
ticularly in  cases  of  bronchial  asthma,  are  strikingly  white,  mostly 
mononuclear,  and  contain  eosinophilic  granules  (see  p.  591  et  seq.y 

Curschmann's  spirals  can  be  preserved  in  glycerin.  Their  mode  of  origin  is 
by  no  means  definitely  known.  Doubtless  their  shape  is  due  to  the  screw-like 
movement  of  the  mucus  while  passing  through  the  bronchi.  Personally  the 
author  prefers  to  consider  that  this  spiral  motion  is  caused  by  the  lashing  move- 
ment of  the  cilia  of  the  bronchial  epithelium,  although  we  do  not  yet  know  whether 
the  direction  of  the  motion  of  the  cilia  is  spiral  or  not.  Senator  believes  that  the 
screw-like  shape  of  these  structures  is  brought  about  by  physical  means,  and  that 
it  is  analogous  to  the  spiral-like  mass  of  a  salve  which  is  forced  out  of  a  com- 
pressible tube  by  pressure. 

Formations  consisting  of  fibrin  may  be  found  in  the  sputum  under 
various  conditions.  They  are  easily  recognized  by  their  white  color,  by 
their  tenacious  consistence,  and  sometimes  by  their  shape.  In  diph- 
theria of  the  pharynx,  larynx,  and  trachea,  the  expectorated  fibrinous 
pseudomembranes  consist  of  uniform  masses  or  casts  of  these  organs. 
Diphtheria  not  infrequently  reaches  as  far  as  the  bronchi,  and  branching 
bronchial  casts  may  be  expectorated.  They  are  readily  recognized  and 
are  important  in  diagnosing  the  extension  of  the  disease  to  the  lungs, 
and  so  determining  the  prognosis.  Similar  branching  bronchial  casts 
are  observed  quite  as  frequently  in  croupous  pneumonia,  because  the 
1  Zeita.f.  klin.  Med.,  vol.  xx.,  p.  476,  1892. 


586 


EXAMINATION  OF  THE  SPUTUM. 


bronchial  mucous  membrane  usually  participates  in  the  fibrinous  inflam- 
matory process.  Fig.  208  represents  a  cast  of  this  sort.  Large  num- 
bers of  such  casts  are  often  contained  in  the  sputum  of  pneumonia. 
They  look  like  white  strauds  or  shreds.  To  investigate  their  nature 
more  accurately,  they  should  be  isolated  by  shaking  the  portion  of 
sputum  which  contains  them  in  a  test  tube  with  water.  All  other 
formations  lose  their  shape,  whereas  these  casts  float  about  in  the  water. 

These  tree-like  formations  may  be 
solid  or  hollow.  Similar  forma- 
tions are  found  in  the  sputum  of 
patients  with  fibrinous  or  croupous 
bronchitis.  The  etiology  of  this 
disease  has  not  been  investigated 
carefully.  Its  course  is  usually 
chronic,  very  rarely  acute.  The 
sputum  is  more  or  less  blood- 
tinged,  and  not  infrequently  con- 
tains beautiful  branching  casts  of 
very  large  bronchi.  Under  the 
microscope  these  fibrinous  casts 
show  the  ordinary  coarse  structure 
of  fibrin  and  the  same  power  of  re- 
fracting light.  Like  Curschmann's 
spirals,  they  often  contain  Charcot's 
crystals  (Fig.  211,  e).  Fibrin  co- 
agula  can  be  distinguished  both 
macroscopically  and  microscopically  from  mucous  constituents  of  the 
sputum  by  their  swelling  and  becoming  more  translucent  after  the 
addition  of  acetic  acid.  If  fresh  fibrin  is  submerged  in  peroxid  of 
hydrogen,  gas  will  develop  much  more  quickly  than  in  the  case  of 
mucus  (catalytic  action). 

Foreign  bodies  are  sometimes  aspirated.  They  may  even  remain  in 
a  bronchus  for  years  without  causing  any  symptoms,  and  finally  be 
expectorated.  There  are  cases  reported  where  foreign  bodies,  such  as 
teeth,  cherry  stones,  etc.,  have  been  expectorated  after  having  been  ten 
and  even  nineteen  years  in  the  lungs. 

Calcareous  concretions  are  sometimes,  but  very  rarely,  formed  in  the 
lungs  during  chronic  infections.  They  may  be  finally  coughed  up 
(lung  stones). 

Very  rarely  daughter  cysts  of  pulmonary  or  hepatic  echinococcus 
reach  the  bronchi,  and  so  appear  in  the  sputum  (Fig.  204). 


Tig.  20S.— Fibrinous  bronchial  casts. 


MICROSCOPIC   EXAMINATION    OF    THE    SPUTUM. 

In  many  cases  this  purpose  can  be  satisfactorily  accomplished  by 
placing  a  small  particle  of  the  sputum  upon  a  slide  and  then  pressing 
down  with  a  cover-glass.  To  recognize  some  of  the  constituents,  the 
specimen  must   first  be   treated  with  reagents   and  stains    (see   later). 


MICROSCOPIC  EXAMINATION  OF  THE  SPUTUM. 


587 


The  sputum  should,  however,  first  be  examined  just  as  expectorated. 
This  process  is  frequently  neglected.  The  presence  of  fungi  or  of  crys- 
tals in  the  sputum,  the  nature  of  many  cellular  elements,  etc.,  can  be 
recognized  only  in  such  a  fresh  preparation,  or,  at  least,  much  more 
easily  recognized  there. 

Most  sputa  consist  microscopically  of  a  groundwork  of  mucoid 
material  of  indefinite  structure  in  which  pus  corpuscles  are  embedded. 
The  number  of  the  latter  determine  the  more  or  less  purulent  nature  of 
the  sputum.  The  character  of  these  corpuscles  varies  considerably. 
Their  size  is  from  7  to  10  [i.  They  are  more  or  less  granular.  The 
granules  consist  partly  of  proteid  material  (neutrophilic  granules,  com- 
pare Examination  of  the  Blood,  Leukocytes),  partly  of  fat,  partly  of 
extraneous  debris  identical  with  that  of  so-called  lung  epithelium  (see 


Fig.  209.— DiflFerent  morphologic  elements  of  the  sputum :  a,  b,  c,  Pulmonary  or  alveolar  epi- 
thelium :  o,  with  normal  lung  pigment  (carbon) ;  6,  with  fat-globules;  c,  with  myelin  granules  or 
drop;  d,  particles  of  pus  ;  e,  red  blood-corpuscles  ;  /,  cylindric  beaker-shaped  bronchial  ei)ithelial 
cells ;  g,  free  myelin  granules ;  h,  ciliated  epithelium  of  different  kinds  from  the  nose,  altered  by 
coryza;  i,  stratified  epithelium  from  the  pharynx  (after  Bizzozero). 

below).  Like  polymorphous  leukocytes,  these  pus  corpuscles  usually 
possess  one  irregular  nucleus  or  several  nuclei.  In  stained  preparations 
(hematoxylin)  the  nuclear  substance  never  appears  as  a  vesicle,  but  is 
compact.     (For  the  presence  of  eosinophilic  cells  see  p.  591  et  seq.) 

Epithelial  cells  are  also  found  in  sputum.  They  differ  from  pus 
corpuscles  in  exhibiting  a  single  rather  large  vesicular  nucleus.  Various 
types  of  epithelium  are  found  in  the  sputum.  Their  demonstration  and 
recognition  is  of  especial  importance  for  determining  the  origin  of  a 
catarrhal  expectoration.  First  of  all,  there  is  squamous  epithelium, 
derived  from  the  mouth,  the  pharynx,  and  a  portion  of  the  larynx, 
especially  the  true  vocal  cords  (Fig.  209,  i).  There  is  cylindric  epi- 
thelium (Fig.  209,  /,  A),  derived  from  the  deep-seated  bronchi  or 
from  the  nose,  and  represented  by  beaker-shaped  and  ciliated  cells, 
although,  of  course,  many  of  the  latter  have  lost  their  cilia.     They  are 


588  EXAMINATION  OF  THE  SPUTUM. 

rarely  very  numerous  except  perhaps  in  a  fresh  bronchial  catarrh.  In 
the  latter  stages  of  catarrh  they  are  almost  completely  supplanted  by 
leukocytes. 

Besides  epithelium  derived  from  the  upper  portion  of  the  respiratory 
tract,  there  is  the  so-called  jmlmonary  or  alveolar  epithelium  (Fig.  209, 
a,  b,  c).  These  are  oval  cells  20  to  50  ju  in  diameter,  with  one  or  several 
nuclei  and  various  inclusions.  The  latter  consist  of :  (a)  normal  lung  pig- 
ment— i.  e.,  carbon  (Fig.  209,  o)  ;  (6)  fat ;  (c)  so-called  myelin  granules 
or  drops,  which  are  pale,  irregular  bodies  of  considerable  size,  showing 
concentric  layers,  and  resembling  the  myelin  globules  of  the  central 
nervous  system  (see  below  as  to  their  origin) ;  (d)  granules  or  scales  of 
brown  pigment,  in  all  probability  derived  from  blood-pigment  (heart 
cells  ;  Plate  8,  Fig.  3) ;  (e)  hematoidin  crystals.  The  same  cell  may 
enclose  a  variety  of  inclusions.  We  do  not  know  whether  these  cells, 
as  claimed  by  Bizzozero,  are  derived  exclusively  from  the  epithelium  of 
the  pulmonary  alveoli,  or  whether  some  of  them  may  not  be  cells  from 
the  epithelium  of  the  upper  air  passages,  or  phagocytic  leukocytes. 

The  character  of  the  epithelial  cells  found  in  the  sputum  makes  it 
possible  to  locate  the  portion  of  the  respiratory  tract  from  which  the 
microscopic  specimen  was  obtained. 

The  myelin  drops  or  granules  above  mentioned  are  often  found  free  in  tlie 
sputum.  According  to  the  investigations  of  A.  Schmidt,  they  should  be  consid- 
ered a  product  of  normal  secretion  of  the  mucous  membrane  of  the  respiratory 
system.  They  make  up  the  larger  part  of  the  morning  sputum,  which  is  swal- 
lowed by  the  majority  of  people.  Chemical  examinations  by  A.  Schmidt  and 
F.  Miiller  have  shown  that  the  myelin  of  sputum  consists  largely  of  protagon, 
with  which  is  mixed  a  small  amount  of  cholesterin  and  lecithin. 

"When  "  heart  cells  "  occur  in  large  numbers  in  the  sputum,  we  are 
justified  in  assuming  definite  anatomic  changes  in  the  lung.  These 
cells  are  filled  with  yellowish-brown  pigment  granules.  They  have 
been  called  the  "  cells  of  heart  disease,"  because  they  are  found  in  the 
sputum  in  brown  induration  of  the  lung  from  cardiac  failure,  especially 
with  mitral  lesions.  If  found  in  considerable  numbers  for  a  consider- 
able length  of  time  without  the  existence  of  an  infarction,  they  are  of 
real  diagnostic  importance.  These  cells  are  also  found  in  the  sputum 
of  pulmonary  infarctions  and  after  hemoptysis.  Their  characteristic 
pigmentation  is  probably  derived  from  the  pigment  of  red  blood-glob- 
ules which  they  have  ingested.  Sputum  containing  many  of  these  car- 
diac cells  may  sometimes  appear  slightly  reddish  brown. 

Whenever  the  bloody  character  of  a  sputum  is  doubtful,  a  micro- 
scopic examination  will  usually  determine  the  presence  of  the  red  cor- 
puscles. They  may  have  preserved  their  normal  appearance,  or  they 
may  be  altered  in  various  ways.  They  may  disintegrate  into  distinct 
and  separate  accumulations  of  hemoglobin  and,  later  on,  become  amor- 
phous or  crystalline  hematoidin,  or  sometimes  the  coloring  matter  may 
be  entirely  dissolved. 

Wherever  lung  tissue  is  considerably  destroyed  by  any  pathologic 
process,  elastic  fibers  are  apt  to  be  found  in  the  sputum.     They  form 


MICROSCOPIC  EXAMINATION  OF  THE  SPUTUM.  589 

the  residual  portion  of  the  pulmonary  parenchyma  (Fig.  210).  Their 
presence  in  the  sputum  proves  beyond  a  doubt  tlie  occurrence  of  some 
destructive  process  in  the  lungs ;  hence  their  importance  in  the  diag- 
nosis of  tuberculosis  of  the  lungs  before  the  tubercle  bacillus  was  dis- 
covered. Even  now  the  presence  of  elastic  fibers  may  decide  the 
diagnosis  if  we  are  unsuccessful  in  our  search  for  tubercle  bacilli. 
Elastic  fibers  are  also  found  in  pulmonary  abscess  and  gangrene  in 
greater  or  less  number  according  to  the  rate  of  disintegration. 

The  fibers  can  usually  be  detected  if  a  thin  layer  of  the  sputum  is 
examined  microscopically.  If  they  are  so  scarce  that  they  cannot  be 
found  in  this  way,  the  following  procedure  is  recommended  :  About  10 
c.c.  of  sputum  are  boiled  in  a  small  porcelain  dish  with  an  equal  quan- 
tity of  10  per  cent.  KOH.  The  mixture  should  be  well  stirred  during 
the  boiling.  When  it  becomes  homogeneous  it  is  diluted  with  about 
four  times  as  much  water,  well  shaken,  and  then  ceutrifugated  or  allowed 


Fig.  210.— Elastic  fibers  from  the  sputum  (after  Bizzozero). 

to  stand  in  a  pointed  glass.  From  the  sediment  any  elastic  fibers  which 
may  be  present  may  be  picked  up  with  a  pipet  and  then  examined  under 
the  microscope.  After  subjecting  elastic  fibers  to  KOH,  they  are  usually 
somewhat  less  sharply  outlined  and  slightly  swollen. 

When  present  in  considerable  quantity  they  are  easily  recognized  by 
their  alveolar  arrangement  (Fig.  210,  h).  Beginners  are  liable  to  con- 
fuse isolated  elastic  with  vegetable  fibers,  but  most  of  the  latter  have  a 
large  diameter^  and  are  much  less  plainly  wavy. 

R.  May  recently  described  a  very  convenient  method  of  staining  elastic  fibers 
with  orcin.  The  method  is  useful  in  doubtful  cases.  The  technic  will  be  found 
in  May's  original  article.^ 

Weigert  has  also  given  an  excellent  method  for  staining  elastic  fibers  in  sec- 
tions by  means  of  fuchsin.  The  author  does  not  know  whether  it  has  been  em- 
ployed for  the  demonstration  of  elastic  fibers  in  the  sputum,  but  it  would  seem 

^  Deutsch.  Arch.  f.  klin.  Med.,  vol.  Ixviii.,  parts  5  and  6,  p.  427. 


590 


EXAMINATION   OF  THE  SPUTUM. 


that  it  could  be  made  use  of,  provided  that  the  cover-glass  smear  were  dried,  and 
then  fixed  with  absolute  alcohol  or  formalin.  A  few  minutes  will  suffice  for 
fixation  if  alcohol  be  employed.  If  formalin  is  used,  the  specimen  should  be 
left  in  a  4  per  cent,  aqueous  solution  of  formaldehyd,  and  then  washed  off  with 
absolute  alcohol.  The  staining  fluid  is  prepared  as  follows :  Two  hundred  cubic 
centimeters  of  an  aqueous  solution  of  fuchsin  (1  per  cent.)  and  resorcin  (2  per 
cent.)  are  brought  to  the  boiling-point  in  a  porcelain  dish  ;  20  c.  c.  of  liquor 
ferri  sesquichlorati  are  then  added,  and  the  mixture  constantly  stirred  and  boiled 
for  three  to  five  minutes,  when  a  muddy  precipitate  will  form.  The  mixture  is 
then  cooled  and  filtered.  The  filter  and  the  contained  precipitate  are  dried,  and 
again  placed  in  the  same  porcelain  dish,  which  will  also  contain  some  of  the  pre- 
cipitate. Two  hundred  cubic  centimeters  of  94  per  cent,  alcohol  should  then  be 
added,  and  the  mixture  boiled  over  a  water  bath  and  constantly  stirred.     During 


Fig.  211.— Crystals  in  the  sputum :  a,  Fat;  b,  cholesterin ;  c,  leucin  (balls)  and  tyrosin  (needles) ; 
d,  hematoidiu  (bilirubin)  in  rhomboids  and  needles  ;  e,  Charcot-Leyden  crystals. 

this  procedure  great  care  must  be  exercised  to  avoid  ignition  of  the  vapor.  The 
fluid  is  cooled,  and  enough  alcohol  is  added  to  bring  the  amount  up  to  200  c.c, 
after  which  4  c.c.  of  hydrochloric  acid  are  added.  The  cover-glasses  should 
remain  in  this  fluid  from  twenty  minutes  to  an  hour,  after  which  they  are  washed 
with  alcohol,  cleared  in  xylol,  and  finally  examined  in  Canada  balsam. 

Some  cases  of  incipient  phthisis  which  can  hardly  be  recognized  may- 
show  the  presence  of  elastic  fibers. 

It  is  a  peculiar  fact  that  in  some  cases  of  gangrene  of  the  lung,  but 
not  in  all,  elastic  fibers  of  the  lung  are  absent  in  necrotic  pieces  of  lung 
tissue  recognized  microscopically  as  such.  In  such  cases  the  elastic 
fibers  have  been  destroyed  by  a  trypsin-like  ferment  formed  by  bacteria 
which  grow  in  the  gangrenous  tissue. 


MICROSCOPIC  EXAMINATION  OF  THE  SPUTUM.  591 

Fragments  of  neoplasms  of  the  lung  which  are  sometimes  seen  in  the 
sputum  (p.  584)  are  best  recognized  in  microscopic  sections. 

Crystals  Observed  in  the  Sputum  (Fig.  211). — They  occur 
in  the  sputum  almost  exclusively  when  the  latter  has  remained  in  the 
body  for  a  considerable  length  of  time.  .  Crystals  of  fat  or  of  fatty  acids 
are  most  frequently  found.  They  form  long  needles  («),  sometimes  free 
and  sometimes  grouped  together  in  resets.  They  may  be  distinctly  bent, 
and  so  perhaps  may  be  mistaken  for  elastic  fibers  ;  but  may  be  readily 
distinguished  by  the  fact  that  they  dissolve  in  potassium  hydrate  or 
ether.  Crystals  of  cholesterin  (6),  of  leucin  and  tyrosin  (c)  are  very 
rarely  observed.  They  are  formed  chiefly  in  stagnating,  putrid  sputum. 
Crystals  of  triple  phosphate  (see  Figs.  189  and  190)  may  be  found  in 
the  sputum  under  similar  conditions.  Hematoidin  crystals  (Fig.  211,  d) 
are  found  chiefly  in  the  sputum  of  abscess  and  of  perforating  empyema. 
The  blood-pigment  in  pulmonary  hemorrhages  is  mostly  changed  in  the 
interior  of  the  cells  to  amorphous  pigment  (see  Heart-failure  Cells),  and 
but  very  rarely  forms  hematoidin  crystals.  Charcot-Leyden  crystals 
(e)  sometimes  occur  in  the  sputum.  They  are  colorless,  elongated, 
double  pyramids,  and  vary  considerably  in  size.  They  also  occur  else- 
where in  the  body  during  life  and  post  mortem  (in  tumors,  in  stools,  in 
leukemic  blood,  in  bone  marrow,  and  in  the  spleen). 

Fr.  Miiller  and  Gollasch  not  long  ago  discovered  a  peculiar  relationship  be- 
tween Charcot's  crystals  and  the  presence  of  eosinophilic  leukocytes  in  the 
sputum.  According  to  Miiller,  60  per  cent,  of  the  leukocytes  in  asthmatic  sputum 
are  sometimes  eosinophiles.  It  therefore  seems  rational  to  assume  that  Charcot's 
crystals  are  products  of  the  crystallization  of  eosinophilic  cells.  This  assumption 
is  supported  by  the  fact  that  the  crystals  readily  stain  with  eosin,  and  that  they 
occur  in  leukemic  blood  (see  p.  667).  Nothing  definite  is  yet  known  regarding 
the  chemistry  of  Charcot's  crystals.  Schreiner  demonstrated  that  the  so-called 
"Bottcher's  sperm  crystals"  could  be  obtained  by  drying  spermatic  fluid.  They 
resemble  Charcot's  crystals  in  appearance,  and  are  the  phosphate  of  an  organic 
base  (spermin  Pohl).  Schreiner's  idea  is  pretty  generally  accepted  that  they  are 
identical  with  Charcot's  crystals.  But  Cohn  ^  claims  that  these  crystals  differ 
considerably  crystallographically,  and  that  they  belong  to  a  different  system. 
Charcot's  crystals,  as  shown  by  their  transverse  surfaces,  belong  to  the  hexagonal 
system.  They  are  doubly  refracting,  like  Bottcher's  crystals,  but,  unlike  the 
latter,  have  a  hexagonal  transverse  section. 

These  crystals  are  chiefly  but  not  exclusively  found  in  the  sputum  in  bronchial 
asthma,  so  that  for  some  time  they  were  regarded  as  the  exciting  cause  of  such  an 
attack.  The  bronchial  nerves  were  supposed  to  be  irritated  by  the  pointed  crys- 
tals. The  relation,  however,  is  not  constant  enough  to  justify  any  such  con- 
clusion. Asthma  fi-equently  occurs  without  crystals,  and  crystals  are  often  foixnd 
in  the  sputum  without  asthma.  It  seems  much  more  rational  to  assume  that  the 
crystals  are  formed  during  the  attack  of  asthma  from  eosinophilic  cells,  owing  to 
the  stagnation  of  the  secretion  products  of  the  bronchial  mucous  membrane. 
Curschmann's  spirals  are  to  be  included  among  these  same  products.  The  fact 
that  Charcot's  crystals  are  found  in  asthmatic  sputum  chiefly  after  the  expecto- 
ration has  been  interrupted  for  a  considerable  length  of  time  would  seem  to  favor 
this  theory.  When  expectoration  is  free  and  abundant,  the  crystals  are  usually 
absent.  Furthermore,  Charcot's  crystals  are  found  very  abundantly  in  the 
interior  of  Curschmann's  spirals  ;  and,  when  the  latter  are  preserved  in  a  moist 
chamber,  crystals  may  form  in  spirals  which  were  previously  free  from  them. 

1  Deutsch.  Arch.  f.  klin.  Med.,  vol.  liv.,  p.  514, 1895. 


592  EXAMINATION  OF  THE  SPUTUM. 

Animal  parasites  or  fragments  of  them  are  very  rarely  found  in 
the  sputum.  Infusoria  are  very  uncommon  in  the  sputa,  and  of  little 
importance  clinically.  Hooks,  scolices,  and  bits  of  membrane  of  echino- 
coccus  may  be  found  in  the  sputum  in  the  rare  cases  where  echinococci 
cysts  of  the  lung  or  liver  perforate  the  bronchi.  There  is  a  disease  in 
eastern  Asia  which  usually  manifests  itself  by  the  occurrence  of  hem- 
optysis. It  is  due  to  the  presence  of  a  worm  (Distomum  pulmonale)  in 
the  lungs.  Its  eggs  (Fig.  212)  can  always  be  demonstrated  in  the 
expectoration.  They  are  oval,  of  a  brownish-red 
color,  0.08  mm.  long  and  0.056  mm.  broad,  and 
are  surrounded  by  a  cuticle.  They  are  easily  iden- 
tified under  the  microscope. 

Vegetable  parasites  are  of  greater  interest 
and  importance,  especially  the  bacteria ;  the  fungi 
play  a  more  subordinate  part.  In  examining  the 
sputum  for  vegetable  organisms,  we  should  always 

.  Fig.  212.— Distomum       i  •  •     i    j.i     x   i        r       j.1.  •      'j. 

pulmonale  with  embryo  bear  m  miud  that  by  tar  the  majority  are  sapro- 
hama-Leuckart).  ^^^^'  phytic  in  nature — i.  e.,  they  develop  in  the  sputum 
either  outside  of  the  body  or,  if  within  the  air 
passages,  only  in  the  secretion,  and  exist  there  in  a  more  or  less  harm- 
less way.  To  determine  whether  vegetable  organisms  in  doubtful  cases 
are  expectorated  as  such,  or  are  due  to  contamination  of  the  sputum 
outside  the  body,  we  should  examine  the  sputum  immediately  after  it 
has  been  expectorated.  There  are,  however,  a  number  of  bacteria 
which  can  be  distinguished  with  so  much  certainty  from  accidental  con- 
taminations that  their  presence,  even  in  an  old  sputum,  is  of  diagnostic 
importance.  This  is  especially  true  of  tubercle  bacilli  and  pneumococci. 
In  obtaining  sputum  for  bacteriologic  examination  a  number  of 
precautions  must  be  observed.  Since  it  is  usually  desired  to  examine 
the  secretion  originating  in  the  deeper  parts  of  the  respiratory  tract 
rather  than  that  coming  from  the  mouth,  the  mucopurulent  masses 
should  be  selected  instead  of  the  thin  secretion,  which  largely  consists 
of  saliva.  It  is  well  to  examine  only  such  clumps  as  are  expectorated 
in  the  presence  of  the  physician.  If  this  be  done,  it  is  easy  to  deter- 
mine from  the  character  of  the  expectoration  whether  the  mass  has 
originated  in  the  bronchi,  in  the  larynx,  in  the  pharynx,  or  in  the  nose. 
In  order  to  reduce  bacterial  contamination  from  the  mouth  to  a  minimum, 
the  oral  cavity  should  be  thoroughly  washed  with  water  just  before 
the  expectoration.  The  sputum  obtained  after  this  precaution  is 
received  in  a  clean  glass  ;  if  cultures  are  to  be  made  the  glass  receptacle 
should  be  sterile  and  provided  with  a  lid,  so  that  the  sputum  may  be 
immediately  covered. 

DETERMINATION  OF  TUBERCXE  BACILLI  IN  THE  SPUTUM. 

Tubercle  bacilli  are  often  so  numerous  in  the  sputum  that  they 
may  be  found  with  ease  in  any  particle  examined  (Fig.  213) ;  but  in 
cases  which  are  doubtful  clinically  and  where  the  diagnosis  depends 
upon  the  examination  of  the  sputum,  tubercle  bacilli  may  be  found  only 


MICROSCOPW  EXAMINATION  OF  THE  SPUTUM.  593 

after  prolonged  search.  If  the  sputum  is  absolutely  homogeneous,  we 
must  prepare  a  large  number  of  slides  without  any  particular  selection. 
If  mucopurulent,  we  can  save  time  by  spreading  the  expectoration  upon 
a  black  background,  and  then  selecting  for  examination  the  larger  puru- 
lent clumps  and  any  very  cloudy,  friable,  cheesy-looking  particles. 
Tubercle  bacilli  may  be  found  in  the  initial  hemoptysis,  although  the 
patient  seemed  perfectly  healthy  beforehand.  It  is,  of  course,  advisa- 
ble in  such  a  case  to  select  particles  which  are  not  pure  blood,  but 
which  have  a  certain  amount  of  mucus  and  purulent  material  admixed. 
In  a  fresh  hemorrhage  from  the  lung,  the  more  profuse  the  bleeding  the 
less  chance  of  finding  bacilli. 

The  recognition  of  the  tubercle  bacillus  depends  upon  a  special  pro- 
cedure by  which  they  alone  are  stained.  If  unstained,  they  cannot  be 
distinguished  from  other  bacteria.  The  ordinary  methods  of  staining 
bacteria  are  not  suitable.  A  speci- 
men is  prepared  by  teasing  a  por- 
tion of  the  sputum  to  be  examined, 
placing  a  small  fragment  of  it  or 
of  the  sediment  (provided  centri- 
fugalization  has  been  performed, 
see  p.  596)  upon  a  cover-slip,  and 
then  carefully  spreading  it.  To 
•obtain  a  uniform  distribution,  a 
second  cover-slip  is  placed  over 
the  first,  and  the  two  then  drawn 
apart  with  the  fingers  or  forceps. 
Unless  too  much  material  has 
been  used,  a  thin  layer  will  be  left 

upon  each  cover-slip,  and  this  may       Fig.  213.— Tubercle  bacilli  (after  a  photograph 

be  dried  over  an  alcohol  or  gas  by  ounther)  (x  500). 

flame  with  a  moderate  amount  of  heat.  It  must  then  be  fixed  so  that 
it  will  not  wash  off  in  the  staining  fluid.  This  is  done  by  passing  the 
slip  rapidly  through  a  flame  three  times.  The  principle  of  the  special 
stain  for  tubercle  bacilli  depends  upon  the  fact  that  these  bacteria  do 
not  stain  readily  with  the  ordinary  anilin  colors,  but  that  when  they  are 
once  stained  they  do  not  readily  decolorize.  An  anilin  dye  which  acts 
very  intensely  is  selected  ;  and  for  this  purpose  the  ordinary  basic  anilin 
colors  are  the  best,  such  as  fuchsin  or  gentian  violet,  mixed  with  car- 
bolic acid  or  with  anilin.  The  directions  for  preparing  this  stain  are 
given  below  (see  p.  594).  A  few  drops  of  the  stain  are  dropped  upon 
the  cover-glass,  and  the  latter  held  over  the  flame  with  a  pair  of  forceps 
till  the  fluid  steams.  This  process  will  stain  the  tubercle  bacilli  and  all 
other  organisms  present. 

The  next  step  is  to  decolorize  all  the  other  organisms  and  any  other 
morphologic  constituents  of  the  preparation.  This  is  easily  accom- 
plished, because  the  tubercle  bacilli  holds  the  anilin  colors  with  great 
tenacity.  Some  mineral  acid  is  generally  employed  for  decolorizing, 
most  frequently   nitric  acid    in  some  dilution  or  other,  as  mentioned 

38 


594  EXAMINATION  OF  THE  SPUTUM. 

below.  The  acid  is  allowed  to  work  until  the  specimen  appears  entirely 
decolorized.  This  occupies  a  few  seconds  to  a  minute,  according  to  the 
thickness  of  the  preparation.  If  parts  of  specimens  are  too  thick,  we 
select  only  the  thin  places  for  examination. 

After  decolorizing,  the  preparation  is  washed  in  water.  If  any  color 
remains  the  acid  must  be  renewed.  It  is  sometimes  necessary  to  alter- 
nate these  two  processes  several  times.  The  specimen  is  then  mounted 
upon  a  slide  with  water  or  balsam,  and  examined  with  an  oil-immersion 
lens.  A  much  larger  specimen  can  be  prepared  and  examined  directly 
with  the  oil-immersion  lens  by  dropping  some  cedar  oil  upon  the  slide. 
Although  this  method  is  a  very  good  one,  it  is  not  to  be  recommended^ 
on  account  of  the  danger  of  scratching  the  objective  by  particles  of 
mineral  matter  contained  m  the  sputum.  Such  a  dry  preparation  may 
be  made  upon  the  slide,  but  it  should  be  covered  by  one  large  or  several 
cover-glasses  of  the  usual  dimensions. 

A  counterstain  after  decolorizing  aids  in  recognizing  other  micro- 
organisms or  tissues  in  the  specimen,  and  makes  them  form  a  contrast 
to  the  tubercle  bacilli.  Methylene-blue  is  well  adapted  for  this  purpose 
if  the  tubercle  bacilli  have  been  stained  red.  If  gentian  violet  has  been 
employed,  Bismarck-brown  or  fuchsin  are  suitable  counterstains.  This 
second  staining  may  be  accomplished  without  heating.  The  counterstaia 
should  not  be  intense  enough  to  obscure  the  tubercle  bacilli. 

Details  in  reference  to  the  counting  of  tubercle  bacilli  ■will  not  be  given^ 
since  the  author  can  impute  neither  a  diagnostic  nor  a  prognostic  value  to  such 
a  procedure.  The  number  of  tubercle  bacilli  in  a  single  preparation  is  dependent 
upon  chance  in  the  selection  of  the  particle  examined  ;  and  even  when  such 
chance  is  eliminated  by  the  study  of  a  large  number  of  specimens,  the  prog- 
nosis and  the  gravity  of  the  case  are  entirely  independent  of  the  number  of 
tubercle  bacilli  in  the  sputum.  For  this  reason  he  regards  Gaffky's  scale  for  the 
quantitative  designation  of  the  bacilli  as  valueless,  and  employs  simply  the  terms- 
"a  few,"  "many,"  or  "very  many"  tubercle  bacilli. 

Solutions  for  Staining  Tubercle  Bacilli. — 1.  A  solution 
of  fuchsin  or  gentian  violet  in  saturated  anilin  vrater  (Ehrlich).  This- 
is  best  prepared  fresh  for  each  examination  by  pouring  2  c.c.  of  anilin 
oil  into  a  test  tube,  filling  with  distilled  water,  and  shaking.  The  mixt- 
ure is  filtered  into  a  watch  glass,  and  a  saturated  alcoholic  solution  of 
fuchsin  or  gentian  violet  is  added  drop  by  drop  to  the  filtrate  until  a 
metallic  sheen  appears  upon  the  surface  of  the  mixture,  indicating  that 
the  anilin  water  is  saturated  with  the  stain. 

2.  A  solution  of  fuchsin  or  gentian  violet  in  carbolic  water  (Ziehl- 
Neelsen).  One  gram  of  fuchsin  or  gentian  violet  is  mixed  with  10  c.c. 
■of  absolute  alcohol  and  100  c.c.  of  a  5  per  cent,  solution  of  carbolic 
water ;  or  a  saturated  alcoholic  solution  of  fuchsin  or  gentian  violet  may 
be  dropped  into  a  5  per  cent,  solution  of  carbolic  water  until  saturation 
takes  place  (formation  of  metallic  sheen  on  the  surface).  These  carbolic 
solutions  have  the  advantage  of  keeping  for  a  considerable  length  of 
time. 

3.  Czaplewsky  ^  recommends  the  use  of  the  following  solution  :  One 

^  Hyg.  Rundschau,  1896,  Xo.  21. 


MICROSCOPIC  EXAMINATION  OF  THE  SPUTUM.  595 

gram  of  fuchsin  ia  5  c.c.  acid,  carbol.  liquefact.  in  a  dish.  Fifty  cubic 
centimeters  of  glycerin  are  added,  stirring  constantly,  and  then  diluted 
with  100  c.c.  of  water.  This  solution  keeps  extremely  well  and  does 
not  need  to  be  filtered. 

Ordinary  aqueous  solutions  without  anilin  or  carbolic  acid  may  be 
used  (concentrated  alcoholic  stain  dropped  into  water  and  prepared  fresh 
each  time).  The  stain  is  somewhat  less  intense.  The  other  mixtures 
are  preferable  for  diagnostic  purposes. 

4.  The  best  decolorizing  method  is  that  of  Czaplewsky,  who  employs 
Ebner's  fluid,  consisting  of: 

Ijc    Acidi  hydroclilorici, 

Sodii  chloridi,  da      2.5 

AquiB  destillatse,  100.0 

Alcoholis,  500.0 

Before  the  employment  of  this  fluid  the  specimen  is  washed  with 
water ;  the  decolorizatiou  may  be  accelerated  by  treating  the  specimen 
alternately  with  Ebner's  fluid  and  water.  The  advantage  of  this  fluid 
is  that  the  acid-resisting  bacilli  are  decolorized  by  the  contained  alcohol 
and  cannot  be  confused  with  tubercle  bacilli,  as  was  the  case  with  the 
purely  aqueous  solutions  of  acids  previously  employed. 

Gabbet's  method  of  decolorizing  and  counterstaining  simultaneously, 
which  was  formerly  almost  universally  employed,  is  not  to  be  recom- 
mended, since  Gabbet's  solution  contains  no  alcohol,  and  consequently 
gives  rise  to  the  previously  mentioned  confusion. 

ISOLATING    TUBERCLE    BACILLI    FROM   OTHER  ACID-STAINING  BACILLI  IN 

THE  SPUTUM. 

(Occurrence  of  Smegma  Bacilli  in  the  Sputum.) 

Pappentteim/  in  Lichtheim's  Clinic,  recently  found  smegma  or  nearly  related 
bacilli  in  a  non-tubercular  afTection  of  the  lung.  They  closely  resemble  tubercle 
bacilli  in  their  affinity  for  acid  stains.  Laab  found  similar  bacilli  on  the  tonsils, 
on  the  tongue,  and  in  the  coating  about  the  teeth.  They  are  so  rare,  however, 
that  probably  no  serious  mistakes  have  occurred.  In  examining  urine  for  tubercle 
bacilli,  these  smegma  bacilli  are  of  considerable  importance.  To  avoid  any  mis- 
take, Pappenheim's  method  of  staining  should  be  employed.  This  colors  the 
tubercle  bacilli  red  and  the  smegma  bacilli  blue.  Pappenheim  recommends  the 
following  procedure  :  1.  Stain  in  carbol  fuchsin,  heat  to  boiling-point  for  a  few 
moments  ;  2,  pour  off  the  excess  of  carbol  fuchsin  ;  3,  decolorize  and  counter- 
stain,  without  washing,  with  the  following  solution,  pouring  it  slowly  three  to 
five  times  over  the  preparation  and  allowing  it  to  run  off:  One  part  of  corallin  is 
dissolved  in  100  parts  of  absolute  alcohol,  and  methylene-blue  added  till  satura- 
tion (a  considerable  amount  is  necessary  for  this  purpose)  ;  20  parts  of  glycerin 
are  then  added  ;  4,  wash  with  water,  dry,  and  mount.  Duration  of  entire  pro- 
cedure, three  minutes. 

Confusion  may  be  avoided  by  decolorizing  the  specimen  stained  in  carbol 
fuchsin  with  Ebner's  fluid,  as  described  above. 

SEDIMENTATION  OF  TUBERCLE  BACILLI. 

If  the  tubercle  bacilli  in  a  specimen  of  sputum  are  scarce,  the  examination 
may  be  facilitated  by  diluting  the  sputum  and  then  centriftigating  the  mixture. 

1  Berlin,  /din.  Woch.,  1898,  No.  37,  p.  809. 


596  EXAMINATION  OF  THE  SPUTUM. 

This  can  best  be  accomplished  as  recommended  by  Viedert.  One  to  2  c.c.  of 
sputum  are  placed  in  a  test  tube  with  six  to  eight  times  as  much  0. 2  per  cent, 
solution  of  sodium  hydrate,  and  then  boiled  once.  The  flocculent  residue  ob- 
tained (after  about  forty-eight  hours'  standing,  if  centrifuged)  is  used  for  making 
a  dry  preparation,  after  adding  some  of  the  original  sputum,  so  as  to  make  the 
layer  stick.  To  determine  the  other  micro-organisms  which  may  be  contained  in 
the  sputum,  an  antiseptic — for  instance,  one-fifth  volume  of  saturated  chloroform 
water — should  be  added,  so  as  to  prevent  the  growth  of  contaminating  bacteria. 
Tubercle  bacilli  and  other  bacteria  in  the  dilute  sodium  hydrate  above  mentioned 
survive,  and  the  tubercle  bacilli  will  often  be  found,  where  they  would  be  missed 
in  the  ordinary  dry  preparation. 

Spengler's  ^  method  of  making  the  sputum  homogeneous  by  pancreatic  diges- 
tion or,  so  as  to  prevent  decomposition,  by  peptic  digestion  in  acid  solution  has 
no  particular  advantage  over  Hiedert's  original  method,  according  to  the  data  the 
author  has  been  able  to  collect. 

Ilkewitsch  ^  recommends  another  method  which  is  very  useful  for  collecting 
tubercle  bacilli  in  the  sediment.  This  consists  in  stirring  the  sputum  for  quite  a 
while  with  twenty  times  as  much  water,  precipitating  with  acetic  acid  (mucin, 
nucleo-albumin),  and  then  centrifuging. 

EMPLOYMENT  OF  ANIMAL  EXPERIMENTS  FOR  DEMONSTRATING 
TUBERCLE  BACILLI  IN  SPUTUM.^ 

When  no  tubercle  bacilli  can  be  found  in  the  sputum  microscopically  even 
after  sedimenting,  animal  experiments  may  be  resorted  to  for  diagnostic  purposes. 
A  suspicious  portion  is  washed  repeatedly  and  rubbed  up  in  normal  saline  solu- 
tion, and  0.5  to  1.5  c.c.  of  the  fluid  injected  into  the  peritoneal  cavity  of  a 
guinea-pig. 

The  weight  of  the  animal  is  recorded,  and  it  is  killed  in  four  to  six  or  ten 
weeks,  according  to  the  diminution  in  its  weight.  An  examination  is  then  made 
to  ascertain  whether  tuberculosis  of  the  abdominal  organs  has  developed.  Some- 
times the  animals  die  in  twenty-four  to  seventy-two  hours,  from  an  infection  with 
pneumococci  or  streptococci.  The  experiment  should  then  be  repeated,  after 
heating  the  sputum  for  ten  minutes  at  60°  C,  a  temperature  which  will,  accord- 
ing to  the  investigations  of  Forster  and  his  pupils,  kill  all  inflammatory  organ- 
isms except  the  tubercle  bacilli. 

DEMONSTRATION  OF  OTHER  MICRO-ORGANISMS. 

These  may  be  demonstrated  in  dry  preparations  made  very  much  in 
the  same  way  as  those  for  tubercle  bacilli.  They  are  stained  witli  the 
same  solutions  and  according  to  the  same  methods,  but  the  acid  is 
omitted.  After  staining,  the  prej)arations  are  washed  in  water  only. 
If  the  stain  is  then  too  intense,  the  preparation  may  be  subjected  for  a 
very  few  moments  to  the  action  of  alcohol.  The  latter  will  remove  any 
color  which  has  been  precipitated  and  render  the  bacteria  more  distinctly 
visible.  Most  bacteria  possess  so  great  an  affinity  for  fuchsin  and 
gentian  violet  that  heating  is  unnecessary.  Cold  preparations  will  stain 
bacteria  sufficiently  inside  of  a  few  seconds  to  a  minute. 

Gram's  Method. — Some  bacteria  stain  very  intensely  with  Gram's 
method,  while  the  other  elements  of  the  sputum  are  decolorized.  A 
specimen  is  stained  with  anilin  gentian  violet  and  then  washed  with 

^  Zeits.f.  Hyg.,  1894,  vol.  xviii.,  part  2. 

^  Baumgarten' s  Jahresbericht,  1892,  vol.  viii.,  p.  664. 

*  See  Levy  and  H.  Bruno,  Deutsch.  med.  Wock,  1900,  No.  9,  p.  141. 


MICROSCOPIC  EXAMINATION  OF  THE  SPUTUM.  597 

water ;  Lugol  solution  ^  is  then  added  drop  by  drop.  The  iodin  solu- 
tion is  allowed  to  act  upon  the  preparation  from  one  to  three  minutes ; 
it  is  then  washed  with  absolute  alcohol  until  entirely  decolorized  micro- 
scopically. When  no  further  color  can  be  washed  away  the  specimen 
is  dried,  and  then  examined  in  cedar  oil.  The  nuclei  and  the  body  of 
the  preparation  will  appear  entirely  decolorized  or  very  slightly  yellow, 
but  the  micro-organisms  will  be  stained  intensely  blue  or  almost  black. 
By  subsequent  counterstaining  (Bismarck-brown  or  fuchsin  ten  times 
diluted,  Ziehl-Neelsen's  or  Czaplewsky's  solution)  a  capital  contrast 
stain  is  obtained. 

Beautiful  specimens  may  also  be  obtained,  according  to  Czaplewsky,  if 
Weigert's  modification  of  Gram's  method  be  combined  with  a  fuchsin  counter- 
stain.  Czaplewsky  describes  the  procedure  as  follows  :  Stain  for  one  minute  in 
carbolic  gentian  violet  (11  c.c.  of  a  concentrated  alcoholic  solution  of  gentian 
violet,  10  c.c.  of  alcohol,  50  c.c.  of  a  5  per  cent,  solution  of  carbolic  acid,  50  c.c. 
of  distilled  water)  ;  wash  thirty  to  sixty  seconds.     Lugol' s  solution  (1  iodin,  3 


FiQ.  214.— Frankel's  pneumococci  (from  a  photograph  by  Frankel)  (X  about  800). 

potassium  iodid,  200  aqua)  ;  wash,  dry,  differentiate  with  anilin-xylol  2  :  1,  to 
which  has  been  added  1.5  per  cent,  of  acetone  ;  wash  with  xylol,  dry,  counter- 
stain  with  diluted  carbol  fuchsin,  1  :  10  (see  p.  594),  for  about  one  minute,  during 
which  time  the  specimen  is  warmed  slightly.  The  specimen  is  then  washed, 
dried,  embedded  in  Canada  balsam,  and  examined  with  the  oil-immersion  lens. 

Staphylococci,  streptococci,  diphtheria  bacilli,  tubercle  bacilli  (stain- 
ing with  heat),  anthrax  bacillli,  bacilli  of  tetanus,  and  Frankel's  pneu- 
mococci stain  with  Gram's  stain  ;  whereas  typhoid,  influenza  and  cholera 
bacilli  and  Friedlander's  bacilli  of  pneumonia  decolorize  with  Gram's 
stain. 

This  property  of  decolorizing  is  only  a  relative  one,  for  individuals  of  certain 
species  which,  as  a  rule,  are  not  stained  by  Gram's  stain  may  retain  their  stain, 
and  vice  versa.     A  great  deal  depends  upon  the  intensity  of  action  of  the  decolor- 

^  This  solution  consists  of  1  part  of  iodin,  2  parts  of  potassic  iodid,  and  300  parts 
of  water.  These  are  the  original  directions ;  but  according  to  the  author's  experience, 
a  solution  of  gentian  violet  in  5  per  cent,  carbolic  water,  as  recommended  by  Ziehl- 
Neelsen  for  staining  tubercle  bacilli,  is  quite  as  good. 


598  EXAMINATION  OF  THE  SPUTUM. 

izing  method.  Where  mixtures  of  bacteria  and  not  pure  cultures  are  being 
treated,  as  in  the  examination  of  sputa,  the  question  whether  certain  bacteria 
decolorize  after  Gram's  stain  can  best  be  decided  by  subsequently  counterstaining 
with  a  fuchsin  solution  diluted  ten  times.  Bacteria  which  decolorize  after  Gram's 
stain  will  then  be  stained  red. 

The  demonstration  of  Frdnkel's  pneumococei  in  the  sputum  is  of  con- 
siderable diagnostic  importance.  They  are  usually  elongated,  lance- 
shaped  cocci,  generally  arranged  in  pairs  with  their  bases  approximated. 
They  are  surrounded  by  a  faintly  staining  capsule,  which  in  dry  prepara- 
tions usually  does  not  stain  at  all.  Frankel's  pneumococci  are  supposed 
to  be  the  cause  of  croupous  pneumonia.  They  must  not  be  confounded 
with  other  diplococci  found  in  the  sputum,  more  especially  with  Friedland- 
er's^  so-called  diplococci.  The  latter  also  possess  a  capsule,  but  they 
have  nothing  to  do  with  the  etiology  of  croupous  pneumonia,  although 
they  may  sometimes  be  present  with  pneumonia.  Friedlander's  cocci, 
when  strongly  magnified,  are  seen  to  be  short  bacilli.  Cultural  diflPer- 
ences  also  exist,  and  Gram's  stain  decolorizes  them,  but  stains  Frankel's 
diplococci.  W.  Wolf  has  furnished  us  with  a  very  useful  double  stain 
for  Frankel's  diplococci.  The  dry  preparation  is  first  of  all  stained 
in  anilin  water  saturated  with  fuchsin,  and  then  placed  one  to  two  min- 
utes in  a  diluted  aqueous  solution  of  methylene-blue.  The  cocci  stain 
blue,  the  capsule  rose  color,  and  the  body  of  the  preparation  a  bluish 
red. 

The  diagnostic  significance  of  pneumococci  is  limited,  because  the 
same  organism  may  be  found  in  the  normal  secretions  of  the  mouth  and 
in  non-pneumonic  sputum.  It  is  identical  with  the  organism  of  an 
experimental  sputum  septicemia  of  rabbits.  The  cocci,  however,  are 
found  in  very  small  numbers  in  normal  secretions  from  the  mouth. 
According  to  modern  views,  any  bacteria  found  in  the  body  normally 
may,  under  certain  conditions,  acquire  pathologic  significance,  so  that 
we  need  not  modify  the  etiologic  importance  of  Frankel's  cocci  in 
pneumonia. 

The  influenza  bacillus^  was  described  by  R.  Pfeiifer  as  the  cause 
of  the  great  epidemic  of  influenza  in  the  early  part  of  the  nineties.  It  is 
of  some  diagnostic  importance  (Fig.  215). 

It  is  a  very  small  bacillus  ;  is  hard  to  stain  ;  is  sometimes  arranged 
in  pairs ;  is  always  found  in  fresh  attacks  of  true  influenza,  and  usually 
in  very  great  numbers,  free  or  included  in  the  leukocytes.  In  parts  of 
the  sputum  it  may  be  obtained  practically  in  pure  cultures.  Pfeiffer 
obtained  the  best-stained  specimens  by  allowing  dry  preparations  to  float 
five  or  ten  minutes  on  a  very  thin,  pale-red  solution  of  carbol  fuchsin. 
Influenza  bacilli  are  only  two  to  three  times  as  long  as  they  are  broad. 
They  rarely  form  threads.  The  ends  are  rounded  off,  and  if  the  stain  is 
slight  will  be  somewhat  more  deeply  stained  than  the  center,  so  that  they 
may  resemble  a  diplococcus. 

This  appearance  may  also  be  produced  if  two  short  rods  lie  side  by 

^  [Friedlander's  micro-organism  is  a  species  of  bacillus  belonging  to  the  same  group 
as  the  various  species  designated  Bacillus  mucosus  capsulatus. — C.  N.] 
2  Zeits.  /.  Hyg.,  xiii.,  p.  357  et  seq.,  1893. 


MICROSCOPIC  EXAMINATION  OF  THE  SPUTUM. 


599 


side.  Influenza  bacilli  have  no  capsule  and  are  not  mobile.  They  do 
not  stain  by  Gram's  method.  The  bacillus  of  influenza  has  not  been 
found  in  late  years  in  so-called  attacks  of  influenza,  but  great  numbers 


Fig.  215.— Influenza  bacilli  (X  1000)  (after  Pfeififer). 

of  FrankePs  pneumococci,  even  when  there  were  no  signs  of  pneu- 
monia, but  only  bronchitis.  They  seem  to  be  of  etiologic  importance. 
If  the  influenza  observed  in  the  nineties  be  regarded  as  a  specific  disease 


|y 


Fig.  216.— Saprophytic  bacteria  of  the  mouth,  from  the  gums.    The  large  rods  are  Leptothrix 
buccalis  (X  about  800)  (after  Friinkel). 

produced  by  the  influenza  bacillus,  which  does  not  seem  to  the  author 
to  have  been  absolutely  established,  it  might  be  well  to  discontinue  using 
the  term  influenza  for  these  pneumococcic  infections  and  common  catarrhal 
conditions. 


600 


EXAMiyATIOX   OF  THE  SPUTUM. 


Influenza  bacilli  can  be  cultivated  only  on  media  containing  hemoglobin,  a 
fact  which  may  serve  to  diflerentiate  them,  for  instance,  from  the  colon  bacillus. 
An  appropriate  medium  can  be  easily  prepared  by  spreading  a  little  blood  with 
the  infected  material  upon  the  surface  of  ordinary  agar.  In  regard  to  the  char- 
acter of  the  colonies  and  the  restilts  of  animal  inoculations,  we  must  refer  to 
PfeiiFer's  original  work. 

Leptothrix  huccalis  and  other  sapropliytic  bacteria  are  often  observed 
in  fi'esh  sputum,  for  they  grow  in  the  normal  mouth  and  there  become 
mixed  with  the  expectoration  (Fig.  216).  They  may  multiply  in  the 
lung  and  appear  very  abundantly  in  the  sputum,  especially  in  putrid 
diseases  of  the  lung.  They  do  not  seem  to  have  any  special  pathologic 
significance,  except  that  they  may  play  a  very  considerable  part  in  the 
decomposition  of  secretions.  The  bacillus  known  as  Leptothrix  buccalis 
or  pulmonalis  may  be  easily  recognized  by  its  size  and  shape,  and  its 
peculiarity  of  frequently  (not  always)  staining  blue  with  Lugol's  solu- 


/      iv.v^ 


Fig.  217.— Micrococcus  tetragenus  (X  about  800) 
(after  FraDkel;. 


Fig.  218.— Streptococcus  pyogenes  (X  about  800) 
(after  Frankelj. 


tion.      This    latter    peculiarity    seems    to    depend    upon    the    kind    of 
medium. 

The  Micrococcus  tetragenus  may  be  found  in  the  sputum  in  various  conditions  : 
in  bronchitis,  in  cavities  of  the  lung  especially,  and  sometimes  in  the  sputum  of 
healthy  people.  It  is  pathogenic  in  animals,  and  may  also  produce  suppuration 
in  man.  Very  possibly  it  aids  the  tubercle  bacillus  in  destroying  the  lung  tissue 
in  phthisis. 

The  same  possibility  applies  to  the  strejAococci  and  staphylococci,  which  are 
(Fig.  218)  found  not  infrequently  in  very  great  numbers  in  tubercular  sputum. 

The  Micrococcus  catarrhalis  is  almost  always  found  in  the  nasal  secretion  in 
rhinitis,  and  is  quite  frequently  observed  in  the  sputum  from  the  lungs.  It  differs 
from  the  ordinarv-  staphylococci  by  its  much  larger  size,  by  its  decolorization  by 
Gram's  method,  and  by  its  position  in  the  cells.  With  the  exception  of  its  large 
size,  it  closely  resembles  the  gonococcus,  and,  like  the  ordinary  staphylococcus,  is 
frequently  grouped  in  pairs  as  a  diplococcus,  the  contiguous  sides  of  the  paired 
cocci  being  distinctly  concave. 

In  recent  years  bubonic  plague  has  occasionally  occurred  in  regions  in  which 
the  disease  is  not  endemic,  and  the  pest  bacillus  must  consequently  be  described. 
Although  bacteriologic  laboratories  v/ill  usually  make  the  bacteriologic  diagnosis 


MICROSCOPIC  EXAMINATION  OF  THE  SPUTUM. 


601 


of  bubonic  plague,  it  will  occasionally  happen  that  the  physician  will  be  forced 
to  make  his  own  diagnosis,  and  in  such  cases  he  should  "be  familiar  with  the 
method  of  bacteriologic  examination.  This  is  particularly  necessarj-  in  the  cases 
m  which  the  lungs  are  affected,  since  the  clinical  course  of  the  disease  may  then 
almost  exactly  correspond  to  that  of  an  ordinary  catarrhal  or  croupous  pneu- 


X 


'r-\. 


&- 


f 


^ 


♦  ** 


Fig.  219.— Staphylococcus    pyogenes    aureus         Fig.  220.— Aspergillus  fumigatus  (X  about  a50) 
(culture)  (X  1000)  (after  Weichselbaum).  (after  Frankel). 

monia.  Enormous  quantities  of  pest  bacilli  may  be  found  between  the  red 
blood-corpuscles  in  the  hemorrhagic  sputum  of  such  cases.  The  pest  bacilli  may 
also  be  present  in  the  expectoration  in  the  ordinary  bubonic  plague.  Czaplewsky 
describes  them  as  follows :  They  are  usually  short  rods  with  rounded  ends,  their 
length  being  two  to  three  times  greater  than  their  breadth.  They  are  occasionally 
so  short,  however,  that  they  resemble  cocci.     They  are  readily  stained,  the  poles 


Fig.  221.— Pest  bacilli  in  a  smear  made  from  a  bubo  ;  stained  with  methylene-blue  (Kolle). 

appearing  darker  than  the  central  portion,  which  may  be  pale  or  even  colorless 
(see  Fig.  221).  This  polar  stain  may  be  most  beautifully  obtained  by  staining 
the  bacilli  for  a  half-minute  in  dilute  borax-methylene-blue  (.stock  solution  with 
2  per  cent,  methylene-blue  and  5  per  cent,  borax).  The  pest  bacilli  are  de- 
colorized by  Gram's  method.     They  are  non-motile.      For  methods  of  cultivation, 


602  EXAMINATION  OF  THE  SPUTUM. 

the  reader  is  referred  to  the  official  communications  of  the  German  government 
for  the  bacteriologic  diagnosis  of  bubonic  plague  (published  by  J.  Springer, 
1902),  and  to  the  works  of  Kossel  and  Overbeck  (from  the  Imperial  Health 
Office,  1901,  I.  Heft). 

In  pulmonary  glanders  the  Bacilli  mallei  may  be  found  in  the  sputum. 
They  cannot  be  sufficiently  identified  by  microscoj^ic  examination,  but  require  to 
be  grown  in  cultures,  and  particularly  to  be  inoculated  into  the  lower  animals. 
They  are  of  about  the  same  length  as  tubercle  bacilli,  but  are  thicker  and  have 
rounded  ends.  They  are  motile,  and  are  decolorized  by  Gram's  method.  Par- 
ticularly characteristic  is  an  alkaline  potato  culture  which,  after  two  days  at  a 
temperature  of  37°  C,  presents  slimy  drop-like  colonies,  varying  in  color  from 
honey  yellow  to  copper  red,  about  which  the  potato  is  darkly  stained.  Experi- 
ments upon  animals  are  performed  as  follows :  A  guinea-pig  is  inoculated  subcu- 
taneously  with  the  suspicious  material.  From  the  resulting  swollen  glands  a 
piece  is  excised  and  introduced  into  the  peritoneal  cavity  of  a  second  male  guinea- 
pig.  Upon  the  second  or  third  day  this  second  animal  develops  a  characteristic 
orchitis  produced  by  glanders.  Since  other  bacteria  may  also  produce  an  orchitis, 
the  morphologic  and  cultural  characteristics  of  the  Bacillus  mallei  must  also  be 
taken  into  consideration. 

In  the  so-called  wool-sorters'  disease,  which  is  nothing  else  than  pulmonary 
anthrax,  the  Bacillus  anthracis  may  be  found  in  the  sputum  (see  Fig.  235). 
These  bacilli  are  easily  stained,  and  may  be  readily  recognized  by  their  size 
(length  5  to  10  //,  breadth  1  to  1.5  //).  The  ends  are  frequently  slightly  concave, 
giving  rise  to  the  so-called  bamboo  form.  They  liquefy  gelatin  and  grow  out 
into  long,  waving  chains,  which  develop  endogenous,  highly  refracting  spores. 
Mice  quickly  die  after  the  subcutaneous  inoculation  of  anthrax  bacilli ;  the 
edematous  fluid  at  the  site  of  the  inoculation,  and  the  blood  contain  large 
numbers  of  the  bacilli. 

The  occurrence  of  tyj^hoid  bacilli  in  the  sputum  is  of  slight  diagnostic  impor- 
tance. It  has  been  particularly  observed  in  the  pneumonia  of  typhoid  fever. 
The  author  himself  has  seen  a  case  of  tyj^hoid  in  which  a  serous  jaleuritis  exudate 
containing  large  numbers  of  typhoid  bacilli  perforated  into  the  respiratory 
passages  and  was  expectorated. 

The  presence  of  sarcince  in  the  sputum  possesses  a  certain  amount  of  interest. 
They  resemble  and  are  often  confounded  with  the  Micrococcus  tetragenus,  but  are 
considerably  larger.  They  are  very  rarely  found  in  the  sputum.  True  sarcinse 
are  best  seen  in  unstained  preparations.  Fig.  141,  c  and  d,  gives  some  idea  of 
their  appearance.  It  has  not  as  yet  been  definitely  settled  whether  or  not  the 
sarcinse  of  the  stomach  (described  above)  are  identical  with  those  of  the  lung. 
Sarcinse  have  been  found  in  the  sputum,  chiefly  in  gangrene  of  the  lung,  but  also 
in  tuberculosis,  bronchitis,  and  pneumonia  (pneumonomycosis  sarcinica).  Sarcinse 
should  probably  be  considered  saprophytic,  especially  when  we  consider  their 
occurrence  in  all  of  these  conditions.  The  same  type  of  sarcina  may  develop  in 
the  mucous  membranes  of  the  mouth  and  pharynx  of  debilitated  patients,  produc- 
ing the  grayish  spots  of  pharyngo-  or  stomatomycosis,  and  from  this  source  may  be 
found  in  the  expectoration. 

It  has  recently  been  found  that  various  kinds  of  molds  belonging  to  the  genus 
Aspergillus  (Figs.  220  and  222),  or  perhaps  to  the  genus  Mucor,  may  develop  in 
the  lung ;  but  practically  only  when  there  is  some  coexisting  cavity  formation. 
The  ca\'ities  where  these  molds  have  been  found  are  almost  exclusively  devoid  of 
odor.  The  relation  of  the  molds  to  putrefactive  bacteria  observed  outside  of  the 
body  would  seem  to  make  it  probable  that  the  constant  antagonism  between  these 
two  kinds  of  organism  continues  in  the  interior  of  the  body,  so  that  the  aspergilli 
protect  a  pulmonary  cavity  from  putrefactive  bacteria  ;  and,  conversely,  the  sap- 
rophytic bacilli  found  in  the  majority  of  cases  protect  the  lung  from  becoming 
overgrown  with  some  mold.  Molds  probably  do  not  invade  an  otherwise  healthy 
lung  ;  but  if  they  once  settle  there,  they  aid  in  the  general  destruction,  as  is  defi- 
nitely proved  by  the  examination  of  the  pathologic  jirocesses.  Verj'  likely  they 
may  even  displace  the  primary  pathogenic  bacilli.     Cases  where  pneumo7iomycosis 


MICROSCOPIC  EXAMINATION  OF  THE  SPUTUM. 


603 


aspergillina  or  mucorina  seems  to  be  primary  can  be  explained  in  this  way  ;  they 
probably  never  occur  primarily,  for  the  spores  of  aspergillus  are  everywhere,  and 
yet  aspergillus  mycosis  is  extremely  rare.  The  only  diagnostic  criterion  differen- 
tiating pneumonomycosis  asiiergillina  or  mucorina  from  ordinary  bronchitis, 
phthisis,  etc.,  is  the  demonstration  of  the  molds  in  a  fresh  specimen  of  sputum 
(Figs.  220  and  222)  (mycelium,  spores,  conidia).  The  varieties,  as  a  rule,  can 
be  separated  only  by  culture  (see  special  text-books). 


Fig.  222.— Aspergillus  fumigatus  of  the  lung  (partly  schematic) :  a.  Mycelium  of  aspergillus  in 
roset-like  rays;  &,  sporangium  (X  285)  (after  Weichselbaum). 

In  rare  cases  the  Oidium  albicans,  another  mold,  may  develop  in  the  lung.  It 
is  best  detected  in  fresh  unstained  preparations  of  sputum  (Fig.  223).  It  develops 
much  more  frequently  upon  the  mucous  membranes  of  the  mouth,  pharynx,  and 
esophagus  than  in  the  lung.  From  any  one  of  these  sources  it  may  be  found  in 
the  sputum  (Fig.  223). 

The  rare  cases  of  actinomycosis,  or  disease  caused  by  ray  fungi,  which  occur  in 
the  lung  should  be  mentioned.  Their  course  clinically  is  similar  to  that  of  tuber- 
culosis of  the  lung,  except  that  instead  of  the  tubercle  bacilli  this  fungus  is  found. 


Fig.  223.— Oidium  albicans  (X  400)  (after  Bizzozero). 


The  characteristic  yellowish  or  grayish-green  granules  of  actinomycosis  can 
generally,  but  not  always,  be  recognized  with  the  naked  eye  (Fig.  224).  The 
microscopic  examination  is  not  always  decisive,  either.  In  some  cases  the  micro- 
scopic rosets  of  the  fungus  are  to  be  found  ;  in  others  only  the  branching  threads 
staining  by  Gram's  method  (Fig.  225),  with  or  without  club-like  ends.  Occa- 
sionally even  coccus-like  structures  are  found,  the  actinomyces  belonging  to  the 
pleomorphic  class  of  streptotriches.  Generally  speaking,  microscopic  elements 
of  this  sort  make  the  diagnosis  of  actinomycosis  very  probable;  still,  it  is  wise  to 


604 


EXAMINATION  OF  THE  SPUTUM. 


follow  Silberschinidt's^  advice,  and  prepare  aerobic  and  anaerobic  bouillon  and 
agar  cultures  for  tbe  purpose  of  differentiation. 

The  direct  examination  of  fresh  sputum  expectorated  in  the  presence 
of  the  observer  is  of  much  more  value  for  differentiating  micro-organisms 


Fig.  224. — Young  actinomyces  granule  (prepared  section).  In  the  middle,  the  mycelium ;  on 
the  edge,  the  clubs,  which  become  much  thicker  with  maturity.  From  a  preparation  stained  by 
Gram's  method  (X  530j  (after  Weichselbaum). 

than  the  much  overrated  culture  methods  (see  Examination  for  Diph- 
theria Bacilli),  because  most  of  the  pathogenic  micro-organisms  which 
are  found  in  the  sputa  are  also  present  and  harmless  in  the  mouths  of 


Fig.  225.— Actinomvces  from  a  tumor  of  the  lower  jaw  of  a  cow :  1,  An  entire  granule  (X  500) ; 
2,  3,  4,  5,  6,  7,  different  forms  of  clubs ;  8,  9,  10,  round  elements  (X  1000)  (after  Mac^). 

healthy  people,  and  cultures  may  lead  to  an  erroneous  impression  con- 
cerning their  preponderance  over  the  other  bacteria.  Moreover,  certain 
pathogenic  micro-organisms  are  not  readily  cultivated  from  the  sputum. 

^  Zelts.  f.  Hyg.  u  Infectionskrankh.,  1901,  vol.  xxxvii.,  p.  345. 


CHIEF  CHARACTERISTICS  OF  IMPORTANT  TYPES  OF  SPUTA.   605 


CHEMICAL   EXAMINATION   OF   THE   SPUTUM. 

ALBUMIN   IN   THE   SPUTUM. 

Wagner  ^  calls  attention  to  the  diagnostic  importance  of  the  presence 
of  albumin  in  the  sputum.  The  greater  the  quantity  of  albumin  in  the 
expectoration,  the  more  marked  will  be  the  inflammatory  process  to 
which  the  sputum  owes  its  origin.  From  a  practical  standpoint,  Wag- 
ner directs  attention  to  the  fact  that  the  sputum  of  a  simple  chronic 
bronchitis  is  always  practically  free  from  albumin,  while  that  of  pulmo- 
nary tuberculosis  is  usually  characterized  by  a  distinct  quantity  of 
albumin. 

To  demonstrate  this  albumin,  a  measured  quantity  of  the  expectora- 
tion is  placed  in  a  glass  flask  with  a  3  per  cent,  solution  of  acetic  acid, 
and  violently  agitated  until  the  mucus  is  decomposed.  The  mixture  is 
Altered,  and  the  filtrate  is  washed  with  3  per  cent,  acetic  acid.  The  fil- 
trate, which  contains  the  albumoses  and  the  albumin  of  the  sputum 
without  the  mucin,  is  now  treated  with  sodium  hydroxid  until  it  is  only 
slightly  acid  in  reaction.  If  necessary  concentrated  saline  solution  may 
be  added,  after  which  the  albumin  may  be  coagulated  by  boiling.  The 
albumin  may  also  be  precipitated  from  the  strong  acetic  acid  solution  by 
potassium  ferrocyanid.  In  either  case  the  resulting  precipitate  gives  a 
qualitative  and  a  quantitative  test  for  the  amount  of  albumin  in  the 
sputum.  Esbach's  method,  as  applied  to  the  urine  (see  p.  505  et  seq.), 
may  also  be  employed  for  an  approximate  quantitative  estimation  of  the 
amount  of  albumin. 

CHIEF  CHARACTERISTICS  OF  THE   MOST   IMPORTANT 
TYPES  OF  SPUTA. 

SPUTUM  IN  CATARRH  OR  BRONCHITIS. 

Ordinarily,  catarrhal  sputum  is  essentially  mucopurulent  without  any  other 
admixtures.  In  the  beginning  of  an  acute  bronchial  catarrh  the  mucus  predomi- 
nates and  the  sputum  is  scant.  After  a  few  days  the  expectoration  becomes 
more  abundant,  less  tenacious,  and  considerably  more  purulent,  the  general  dis- 
comfort at  the  same  time  lessening.  As  recovery  progresses,  the  amount  of 
pus  diminishes  as  the  quantity  of  expectoration  becomes  less,  until  the  sputum 
disappears  entirely.  In  chronic  bronchitis  the  nature  of  the  expectoration  may 
vary  considerably,  being  at  times  more,  at  times  less  purulent.  Patients  usually 
feel  more  comfortable  when  the  sputum  is  fairly  abundant  ;  whereas  the  discom- 
fort is  increased  when  the  secretion  ceases  entirely  or  becomes  excessive. 

SPUTUM  IN  FIBRINOUS  OR  CROUPOUS  BRONCHITIS. 

The  sputum  of  croupous  differs  from  that  of  ordinary  bronchitis.  Fibrinous 
coagula  in  the  shape  of  casts  of  the  bronchi  appear  in  the  sputum  from  time  to 
time,  usually  associated  with  more  or  less  blood.  Charcot's  crystals  are  very 
frequently  found  in  these  formations.  The  larger  coagula  are  apt  to  be  expec- 
torated with  very  severe  paroxysms  of  coughing,  which  have  usually  been  pre- 
ceded by  more  or  less  dyspnea. 

^  Deutsch.  Arch.f.  klin.  Med.,  vol.  Ixxv.,  parts  3  and  4,  1902. 


606  EXAMINATION  OF  THE  SPUTUM. 

SPUTUM  IN  ORDINARY  PULMONARY  TUBERCULOSIS. 

Macroscopically,  this  cannot  be  absolutely  distinguished  from  simple  catarrhal 
sputum.  Any  type  may  be  present,  from  a  purely  mucous  to  an  almost  purely 
purulent  sputum.  In  well-advanced  ulcerative  types  of  phthisis  the  amount  of 
pus  is  usually  considerable.  Friable  opaque  white  particles  always  make  one 
suspect  tuberculosis.  The  sputum  of  tubercular  patients  frequently  has  a  very 
bad  odor,  especially  if  there  are  cavities  with  stagnating  contents.  A  positive 
diagnosis  can  be  made  only  when  the  tubercle  bacillus  is  found.  If  all  other 
destructive  processes  of  the  lung  can  be  eliminated,  elastic  fibers  are  very  sugges- 
tive. The  abundance  of  these  morphologic  elements  by  no  means  indicates  the 
severity  of  the  case.  There  are  very  severe  cases  of  tuberculosis  of  the  lungs 
where  no  bacilli  and  no  elastic  fibers  can  be  found.  These  are  frequently  very 
malignant  and  acute  cases,  where  the  constitution  is  undermined  before  dis- 
integration of  the  pulmonary  infiltration  begins,  or  cases  where  miliary  tubercu- 
losis is  alone  responsible  for  the  grave  symptoms.  Again,  if  the  catarrhal  secre- 
tion is  profuse,  which  is  common  especially  in  unfavorable  cases,  the  number  of 
tubercle  bacilli  in  the  sputum  will  seem  few  on  account  of  the  dilution.  On  the 
other  hand,  we  not  uncommonly  find  tubercle  bacilli  and  elastic  fibers  in  the 
sputum  of  early  tuberculosis  of  the  lung  where  physical  examination  reveals  no 
or  only  slight  signs.  The  significance  of  tubercle  bacilli  in  cases  of  this  sort  is 
of  very  decided  importance.  Naturally,  then,  any  variation  in  the  number  of 
elastic  fibers  or  of  tubercle  bacilli  which  are  present  in  the  same  individual 
cannot  be  interpreted,  in  and  of  itself,  as  indicating  any  marked  change  in 
the  course  of  the  disease.  In  judging  the  value  of  therapeutic  measures,  such 
false  interpretations  have  frequently  been  applied. 

SPUTUM  IN  ACUTE  MILIARY  TUBERCULOSIS. 

This  presents  the  characteristics  of  an  ordinary  catarrhal  sputum,  and  if  not 
complicated  by  ulcerative  phthisis  is  without  bacilli.  There  may  be  no  sputum 
at  all. 

SPUTUM  IN  CROUPOUS  PNEUMONIA. 

The  characteristic  feature  of  the  sputum  of  croupous  pneumonia  is  the  blood- 
content.  The  blood  is  usually  uniformly  mixed  in  a  glairy  menstruum,  the  sputum 
appearing  almost  transparent  and  homogeneous.  Not  infrequently,  however,  par- 
ticles of  sputum  free  from  blood  alternate  with  hemorrhagic  streaks  and  spots  or 
with  considerable  quantities  of  almost  pure  blood.  In  some  cases  the  original 
color  of  the  blood  is  almost  completely  preserved  ;  in  others,  especially  when  the 
blood  is  uniformly  mixed  with  the  glairy  mass,  the  blood-pigment  is  modified  to 
a  yellowish  or  brownish  red,  as  previously  described  {rusty  sputum,  sputa  crocea). 
Blood-corpuscles  can  be  recognized  microscopically  in  any  pneumonic  sputum, 
although  they  are  almost  completely  laked  out.  The  peculiar  change  of  blood- 
pigment  producing  green  and  yellow  sputa  has  been  already  considered  (p.  579). 
Pneumonia  not  infrequently  gives  rise  to  jaundice  (p.  43),  in  which  case  the 
sputum  is  apt  to  be  yellow  or  greenish  and  show  Gmelin's  reaction  (p.  472). 
Fibrin  coagula  are  not  uncommonly  found  in  the  sputum  of  pneumonia  ;  we 
have  already  considered  (p.  585)  their  peculiarities  and  the  method  of  demon- 
strating them.  If  a  catarrhal  bronchitis  of  the  larger  bronchi  is  associated  with 
the  croupous  pneumonia  and  a  fibrinous  bronchitis  of  the  smaller  bronchi  with 
which  it  is  almost  always  accompanied,  then  the  purely  pneumonic  sputum  will 
be  mixed  with  catarrhal  elements.  Pneumonic  sputum  is  usually  very  viscid,  on 
account  of  the  nuclein  it  contains,  so  much  so  that  the  spit  cup  may  be  com- 
pletely inverted  without  spilling  the  contents.  Thin  liquid  sputum,  especially  if 
it  is  abundant  and  dark  reddish  brown  in  color,  is  often  an  unfavorable  sign  in  pneu- 
monia, as  it  frequently  indicates  the  beginning  of  pulmonary  edema.  Such  a 
dark  sputum  has  been  called  "prune-juice"  sputum,  on  account  of  its  appear- 
ance. However,  we  should  not  make  a  prognosis  from  the  nature  of  the  sputum 
alone.     A  thin  liquid  sputum  is  an  unfavorable  sign  only  when  the  other  symp- 


CHIEF  CHARACTERISTICS  OF  IMPORTANT  TYPES   OF  SPUTA.   607 

toms  are  very  urgent,  for  not  infrequently  a  liquid  sputum  indicates  the  begin- 
ning of  resolution.  Frankel's  pneumococcus  can  always  be  demonstrated  in  the 
sputum  of  croupous  pneumonia  (Fig.  214). 

SPUTUM  IN  BRONCHOPNEUMONIA. 

We  include  here  deglutition  and  hypostatic  pneumonias.  In  these  disorders 
the  sputum  sometimes  resembles  bronchitic  sputum  or,  like  that  of  croupous 
pneumonia,  it  contains  blood.  This  is  easily  understood,  for  it  is  frequently  very 
difficult,  aside  from  the  macroscopic  distribution,  to  distinguish  broncho-  from 
croupous  pneumonia  histologically,  and,  like  the  latter,  bronchopneumonia  may 
also  be  hemorrhagic,  with  a  more  or  less  fibrinous  exudate.  The  bacteriology 
of  bronchopneumonia  sputum  may  vary  considerably.  Frankel's  pneumococci 
are  not  infrequently  found,  as  well  as  many  other  pathogenic  micro-organisms. 

SPUTUM    IN    PULMONARY    GANGRENE. 

This  is  characterized  mainly  by  its  intensely  disagreeable  odor.  It  is  usually 
very  abundant  and  liquid,  and  of  a  dark  dirty-greenish  or  brown  color.  Small 
pieces  of  necrotic  lung  tissue  can  be  found  macroscopically  in  it,  and  besides  them 
constituents  characteristic  of  hemorrhagic,  pneumonic,  catarrhal,  or  purulent 
sputum.  Odorless  gangrene  is  very  uncommon.  The  author  once  demonstrated 
an  abundance  of  sarcina^  in  the  necrotic  portions  from  a  case  of  this  sort.  If 
allowed  to  stand,  the  sputum  of  pulmonary  gangrene  usually  separates  to  form 
layers.  The  uppermost  layer  contains  mucus  and  necrotic  portions  which,  on 
account  of  the  air  contained,  float.  The  second  layer  is  liquid,  and  the  sediment 
consists  of  pus  corpuscles  and  necrotic  detritus.  Besides  the  ordinary  elements  of 
sputum,  abundant  bacteria  of  decomposition,  fatty  crystals,  cholesterin,  leucin 
and  tyrosin  crystals  (Fig.  211,  c),  pigment,  and  bits  of  destroyed  lung  tissue  are 
seen  microscopically.      Elastic  fibers  may  be  present. 

SPUTUM   IN    PULMONARY  ABSCESS. 

This  is  essentially  a  purulent  sputum,  and  often  has  a  very  foul  odor.  Char- 
acteristic for  the  pus  when  mixed  with  water  is  its  fine,  shredded,  flocculent  appear- 
ance (see  p.  584).  If  catarrh  exists  at  the  same  time,  the  pus  is  mixed  with  more 
or  less  abundant  catarrhal  sputum,  provided  the  abscess  has  perforated  slowly. 
If  perforation  takes  place  suddenly,  large  quantities  of  pure  pus  are  expectorated, 
which  contains  microscopically  elastic  fibers,  and  hematoidin,  cholesterin,  and 
fatty  crystals,  beside  lung  pigment  and  bacteria  (Fig.  211). 

SPUTUM   IN   PERFORATING   EMPYEMA. 

This  usually  resembles  very  closely  the  sputum  of  a  pulmonary  abscess. 
Elastic  fibers,  if  present,  occur  in  very  small  numbers.  Hematoidin  and  other 
crystals  may  be  present.  An  odorless  empyema  may  smell  very  badly  after  per- 
foration, because  the  empyema  cavity  becomes  infected  with  saprophytic  bacteria 
from  the  lung. 

SPUTUM   IN    PUTRID   BRONCHITIS. 

This  is  more  or  less  purulent,  with  a  foul  odor,  and  abundant  bacteria,  but 
without  any  elastic  fibers. 

SPUTUM    IN    BRONCHIECTASIS. 

The  sputum  of  bronchiectasis  with  circumscribed  cavities  is  mucopurulent, 
but  it  is  often  more  profuse  than  is  a  simple  catarrhal  sputum,  and  it  is  expecto- 
rated periodically.  Expectoration  is  easier  in  certain  positions  of  the  body, 
according  to  the  location  of  the  bronchiectasis.     The  odor  is  frequently  foul.     Its 


608  EXAMINATION  OF  THE  SPUTUM. 

microscopic  peculiarities  are  quite  like  those  of  the  sputum  of  putrid  bronchitis. 
In  diffuse  bronchiectasis  the  sputum  resembles  sometimes  the  above  type,  at  other 
times  that  of  simple  catarrhal  bronchitis.     The  odor  may  or  may  not  be  foul. 

SEROUS    SPUTUM    IN    PULMONARY   EDEMA    AND   IN 
PERFORATING    SEROUS    PLEURISY. 

The  sputum  in  edema  of  the  lung  is  usually  colorless  or  faintly  tinged  with 
blood,  foamy  and  somewhat  opaque,  and  usually  profuse.  It  separates,  upon 
standing,  into  a  lower  liquid  and  an  upper  foamy  layer.  The  latter  is  quite 
abundant.  At  the  bottom  there  may  settle  a  very  thin  layer  of  morphologic  con- 
stituents, which  consist  partly  of  white  blood-corpuscles  and  partly  of  other  ele- 
ments from  some  other  affection  of  the  lung  present  at  the  same  time  (bronchitis, 
pneumonia).  Otherwise  the  sputum  of  pulmonary  edema  consists  chiefly  of  pure 
or  slightly  bloody  serum  which  contains  a  moderate  amount  of  albumin  (demon- 
strated by  boiling  and  addition  of  acid).  The  sputum  raised  after  a  paracentesis 
for  pleurisy  may  present  all  the  characteristics  of  that  from  a  case  of  pulmonary 
edema.  The  French  call  this  expectoration  "  albumineuse. "  It  is  nothing  more 
than  the  product  of  an  acute  edema  of  the  lung  following  the  sudden  removal  of 
pressure  from  the  pulmonary  vessels.  Fortunately,  however,  paracentesis  is  not 
generally  followed  by  any  severe  symptoms.  If  a  serous  pleural  exudation  per- 
forates the  lung  and  is  then  expectorated,  the  sputum  viill  resemble  that  in  edema.  ^ 
This  is,  of  course,  very  rare,  but  it  does  occur.  The  sputum  from  a  pleurisy 
can  in  such  cases  be  differentiated  by  means  of  its  greater  albumin  content  fi-om 
the  sputum  in  edema,  the  fluid,  as  a  rule,  becoming  solid  after  addition  of  acid 
and  boiling. 

SPUTUM   IN    VARIOUS   KINDS   OF   PULMONARY   HEMORRHAGE 
AND    IN    HEMORRHAGIC   INFARCTION    OF  THE   LUNG. 

In  marked  hemorrhages  of  the  lung  proper,  such  as  occur  after  injury,  or 
erosion  of  vessels  by  tuberculosis,  or  new  growths,  the  sputum  may  consist  chiefly 
of  blood.  It  is  usually  bright  red,  whether  it  comes  from  the  pulmonary  artery 
or  from  one  of  the  veins,  because  the  dark  venous  blood  of  the  pulmonary-  artery 
in  its  course  along  the  bronchi  has  usually  been  sufficiently  aerated  to  be  rendered 
more  or  less  arterial.  The  admixture  of  the  blood  with  air  in  the  lung  causes  the 
frothy  nature  of  the  expectoration.  This  frothy  appearance  and  bright  red  color, 
and  the  fact  that  the  blood  is  coughed  up,  are  usually  characteristic  enough  to 
establish  the  diagnosis  that  the  seat  of  the  hemorrhage  is  in  the  lung. 

It  is,  however,  sometimes  difficult  to  determine  whether  the  blood  comes 
from  the  lung  or  from  the  digestive  tract,  especially  from  the  stomach.  Differ- 
entiation is  usually  easy,  provided  the  physician  himself  sees  the  hemorrhage 
occur,  but  it  is  often  very  hard  to  judge  from  the  patient's  statements.  In  the 
first  place,  the  patient  takes  no  special  note  of  his  condition,  on  account  of 
excitement,  and  is  not  sure  whether  he  coughed  or  vomited  the  blood  ;  and,  in 
the  second  place,  vomiting  may  be  produced  by  the  violent  paroxysms  of  cough- 
ing accompanying  a  pulmonary  hemorrhage  ;  or,  on  the  other  hand,  vomiting 
blood  from  the  stomach  may  start  a  fit  of  coughing,  on  account  of  the  aspiration 
of  blood  into  the  larynx. 

When  in  doubt,  reliance  must  be  placed  upon  the  objective  examination  of 
the  blood.  Frothy  bright-red  blood  favors  the  diagnosis  of  a  hemorrhage  from 
the  lung.  Blood  from  the  stomach  is  more  apt  to  be  dark  (methemoglobin  and 
hematin),  partly  coagulated  and  not  foamy,  because  it  has  been  more  or  less 
digested.  Bright-red  blood  may  come  from  a  hemorrhage  from  the  stomach 
where  an  ulcer  has  eroded  an  artery  of  the  stomach  and  the  blood  is  vomited  in 
such  large  quantities  that  it  is  still  bright  red  without  having  undergone  any 

^  Sahli,  "  Ueber  die  perforation  seroser  Exsudate,"  etc.,  Mitlheilungen  axis  Min.  u.  med. 
Instituten  der  Schweiz,  1894,  vol.  i.,  part  9. 


EXAMINATION  OF  THE  BLOOD.  609 

change.  On  the  other  hand,  in  exceptional  cases  dark  blood  is  observed  in  a 
hemorrhage  from  the  lung  when  the  eroded  vessel  is  a  large  branch  of  the  pul- 
monary artery,  from  v?hich  the  dark  venous  blood  has  been  expectorated  so 
quickly  that  it  has  undergone  no  change. 

The  reaction  is  frequently  mentioned  as  a  differential  point  between  blood 
from  the  lungs  and  that  from  the  stomach.  The  former  is  said  to  be  alkaline  ; 
the  latter  acid,  on  account  of  the  admixture  of  gastric  juice.  But  this  is  true 
only  when  the  stomach  contains  a  considerable  quantity  of  acid  secretion  at  the 
time  that  the  blood  is  vomited. 

No  one  point  can  be  considered  absolute  in  differentiating  between  a  hemor- 
rhage from  the  lung  and  one  from  the  stomach.  Nevertheless,  it  is  usually  not 
very  difficult  to  decide  in  any  given  case.  Examination  of  the  patient  is  more 
important  than  is  the  consistence  of  the  blood,  and  especially  a  careful  attention 
to  the  symptoms  preceding  or  following  the  hemorrhage.  A  patient  with  hemor- 
rhage from  the  stomach  usually  gives  a  history  of  previous  gastric  difficulty,  or 
such  a  disturbance  can  be  determined  after  the  hemorrhage  has  taken  place. 
Patients  who  have  had  a  hemorrhage  from  the  stomach  usually  pass  blood  in 
their  movements.  On  the  other  hand,  a  patient  with  hemorrhage  from  the  lung 
has  usually  been  subject  to  a  cough  before  or  after  the  bleeding.  The  expectora- 
tion is  usually  blood-tinged  for  days  after  the  hemorrhage,  either  blood  red 
or  brownish.  If  all  of  these  points  are  taken  into  consideration,  the  diagnosis 
will  not,  as  a  rule,  be  difficult. 

Slight  hemorrhages  from  the  lung,  as  contrasted  with  a  true  hemoptysis,  will 
cause  more  or  less  tinging  of  a  catarrhal  sputum.  The  blood  is  not  as  intimately 
mixed  with  the  expectoration  as  it  is  in  the  sputum  of  pneumonia,  but  occurs  in 
streaks.  A  sputum  of  this  sort  does  not  always  come  from  the  lung,  and  so  often 
causes  patients  quite  unnecessary  worry.  It  is  very  uncommon  to  have  hemoptysis 
proper  from  the  larynx  or  trachea  (for  the  simple  reason  that  there  are  no  large 
vessels  there).  But  slight  streak-like  hemorrhages  may  arise  from  the  small 
vessels  in  the  mucous  membrane  of  the  larger  bronchi,  the  trachea,  the  larynx, 
or  of  the  pharynx  itself.  Bronchitis  may  sometimes  be  hemorrhagic.  During  the 
last  influenza  epidemic  some  patients  expectorated  for  weeks  a  blood-tinged 
catarrhal  sputum  without  any  especial  disturbance  of  the  general  condition.  It 
is  not  always  possible  to  distinguish  between  these  various  conditions.  Besides 
this,  it  must  be  mentioned  that  the  clots  coming  from  a  nose-bleed  which  has 
occurred  during  sleep  may  become  mixed  with  the  sputum  in  the  pharynx  as  the 
blood  is  swallowed.  Such  sputum  may  be  erroneously  attributed  to  a  pulmonary 
hemorrhage.  A  careful  examination  of  the  anterior  and  posterior  nasal  passages 
will  generally  settle  the  diagnosis. 

Most  cases  of  hemorrhagic  infarction  of  the  lung  present  a  typical  sputum, 
dark  and  bloody  and  resembling  pure  blood.  In  its  tenacious  consistence,  how- 
ever, it  resembles  the  sputum  of  pneumonia.  In  fact,  the  sputum  in  these  cases 
is  an  intimate  mixture  of  blood  with  a  tenacious  exudation.  Besides  this  typical 
form,  the  sputum  of  infarction  shows  many  varieties,  in  some  cases  resembling 
the  sputum  of  tubercular  hemoptysis,  in  other  cases  that  of  pneumonia. 


EXAMINATION   OF  THE    BLOOD. 

The  examination  of  the  blood  furnishes  a  number  of  important 
diagnostic  data.  Several  of  the  methods  are  so  simple  that  they  can  be 
employed  at  the  bedside  in  daily  practice,  whereas  others  are  too  com- 
plicated for  such  a  purpose. 

39 


610 


EXAMINATION  OF  THE  BLOOD. 


METHOD   OF  OBTAINING  BLOOD  FOR   EXAMINATION. 

A  few  drops  are  sufficient  for  microscopic  examination  for  the  deter- 
mination of  the  coagulability  and  the  estimation  of  the  alkalinity  of 
the  blood.  This  may  be  obtained  by  puncturing  the  tip  of  a  patient's 
finger  or  the  lobe  of  his  ear  with  a  needle  or  sharp  lancet. 

Fraucke's  instrument  ^  (Fig.  226)  pierces  the  skin 
very  rapidly  with  a  narrow  needle-like  lancet  to  a 
depth  which  can  be  readily  regulated.  It  does  not 
cause  serious  pain.  Pressing  on  the  lever  suddenly 
releases  a  spiral  spring  in  the  interior  of  the  instru- 
ment, which  drives  the  point  of  the  lancet  into  the 
skin  to  a  depth  regulated  by  the  guard  (d).  The 
blade  may  be  easily  removed  and  cleansed.  The 
instrument  may  be  adjusted  so  as  to  obtain  sufficient 
blood  where  a  larger  quantity  is  needed  (alkalinity). 
The  skin  should  first  carefully  be  cleansed  (with 
alcohol)  and  then  thoroughly  dried. 

The  writer  has  constructed  a  simpler,  cheaper, 
and  more  compact  instrument,  in  which  the  punct- 
ure is  also  made  by  a  lancet.  It  is,  however, 
made  by  manual  instead  of  spring  pressure ;  its 
depth  is  regulated  by  an  adjustable  cover.  Since 
the  depth  of  the  puncture  cannot  exceed  the  length 
of  the  lancet  exposed,  the  stab  may  be  very  quickly 
made,  and  is  no  more  disagreeable  to  the  patient  than  when  Francke's 
needle  is  employed. 

If  several  cubic  centimeters  of  blood  are  required,  wet-cupping  may 
be  employed ;  but  since  the  blood  coagulates  so  rapidly  that  certain 
methods  of  investigation  are  difficult  of  execution,  it  is  better  to  use  a 
cannula  inserted  into  a  vein.     An  ordinary  hypodermic  syringe  with  a 


Fig.  226.— Francke's 
needle  for  removing 
blood  for  clinical  pur- 
poses (about  one-half 
its  natural  size). 


Fig.  227.— Blood-needle. 

large  needle  may  be  all  that  is  required ;  but  when  quite  large  amounts 
are  necessary  they  are  best  obtained  by  a  larger  cannula,  through  which 
the  blood  flows  directly  from  the  vein.  A  piece  of  tubing  is  attached 
to  the  end  of  the  cannula.     The  cannula  should  have  a  lumen  of  at  least 

1  See  Deutsch.  med.  Woch.,  1889,  No.  2,  p.  27.     [A  similar  one  is  made  by  Baker  & 
Cb.,  of  London.     It  is  smaller  and  very  satisfactory  (see  Fig.  227). — Ed.]. 


QUANTITY  OF  THE  BLOOD.  611 

1  mm.  Its  length  should  not  exceed  5  cm.,  otherwise  the  flow  of  blood 
will  soon  be  interrupted  by  coagulation ;  moreover,  a  longer  cannula  is 
difficult  of  manipulation.  Whether  a  needle  or  a  larger  cannula  is 
used,  it  should  be  very  sharp,  as  the  vein  may  easily  elude  the  puncture. 
In  introducing  the  cannula  the  median  vein  is  selected,  a  fillet  is  placed 
about  the  arm,  and  the  instrument  is  thrust  toward  the  periphery,  and 
as  nearly  parallel  as  possible  to  the  cutaneous  surface.  The  writer  has 
convinced  himself  that  this  method  is  not  adapted  to  the  quantitative 
examination  of  the  blood,  since  the  stasis  produced  by  the  fillet  quickly 
changes  the  composition  of  the  blood  withdrawn,  particularly  in  respect 
to  the  proportion  between  the  solid  constituents  and  the  water.  This 
condition  of  affairs  may  be  avoided,  however,  by  loosening  the  fillet 
before  the  blood  is  withdrawn. 

QUANTITY  OF  THE  BLOOD;  DIAGNOSIS  OF  HYDREMIC 

PLETHORA. 

As  yet  we  know  no  reliable  method  of  determining  tlie  exact  quantity  of 
blood  even  in  animals.  In  man  it  is  estimated  to  be  about  one-thirteenth  of  the 
body  weight,  but  it  is  very  probable  that  this  ratio  may  be  changed  under  patho- 
logic conditions.  There  are  as  yet  no  positive  data,  although  it  would  be  of  the 
greatest  clinical  interest  to  have  accurate  information  upon  this  point.  After 
acute  losses  of  blood  the  quantity  doubtless  remains  diminished ;  perhaps,  how- 
ever, only  for  a  short  time.  Furthermore,  when  the  body  is  deprived  of  water, 
the  liquid  portion  of  the  blood  is  utilized,  the  blood  becomes  somewhat  thicker, 
and  is  diminished  in  quantity.  This  probably  occurs  in  cholera  and  in  the  acute 
infantile  diarrheas,  judging  from  the  great  amount  of  water  lost,  the  slight  dis- 
tention of  the  vessels,  and  the  increased  hemoglobin.  Quantitative  spectroscopic 
examinations  and  hemoglobin  estimations  have  recently  shown  that  the  concen- 
tration of  the  blood  increases  after  marked  perspiration  and  after  the  use  of  saline 
cathartics  and  diuretics,  due  to  the  loss  of  water. 

The  demonstration  of  hydremic  plethora— i'.  e. ,  an  increased  quantity  of  blood 
due  to  the  retention  of  water — is  of  particular  clinical  interest.  This  demonstra- 
tion is  sometimes  possible  from  a  determination  of  the  hemoglobin  percentage 
(see  p.  616,  et  seq.),  which  falls  when  the  water  is  retained.  It  is  clear,  however, 
that  it  will  be  possible  to  base  a  diagnosis  of  hydremic  plethora  upon  the  oligo- 
chromemic  character  of  the  blood  only  when  the  latter  develops  acutely  under  the 
observation  of  the  physician,  and  when  hemorrhage  or  other  common  causes  of 
anemia  can  be  excluded.  With  these  limitations,  the  fall  of  the  hemoglobin 
percentage  is  a  useful  indication  of  hydremic  plethora,  since  hemoglobin  cannot 
quickly  enter  or  leave  the  vessels,  as  can  the  soluble  constituents  of  the  blood.  It 
consequently  follows  that  hydremic  plethora  is  frequently  to  be  recognized  only 
by  the  lowering  of  the  hemoglobin  percentage,  while  the  specific  gravity,  the  dry 
residue,  and  the  osmotic  pressure  remain  normal,  since  the  dissolved  constituents, 
particularly  the  salts,  may  remain  in  the  blood.  In  cases  of  nephritis,  for  exam- 
ple, the  hydremo-plethoric  blood  very  usually  exhibits  even  an  increased  osmotic 
pressure  (see  p.   669  et  seq). 

The  conditions  of  so-called  "  bloodlessness  " — the  various  types  of  a«e?nia — 
are  by  no  means  due  to  a  deficient  quantity  of  blood,  as  has  been  previously  sup- 
])0sed,  and  as  is  indicated  by  the  name.  But  the  constant  sign  of  anemia  (oligo- 
chromemia)— pallor  of  the  blood — is  due  to  a  diminution  in  the  percentage  of 
blood-pigment.  Traumatic  anemia,  due  to  loss  of  blood,  is,  of  course,  at  the 
first  associated  with  a  diminution  in  the  quantity  ;  but  even  this  condition  is 
rapidly  changed  to  a  simple  oligochromemia,  the  blood  lost  being  rapidly  replaced 
by  absorption  of  lymph  from  the  tissues. 


612  EXAMINATION  OF  THE  BLOOD. 

SPECIFIC  GRAVITY  OF  THE  BLOOD. 

The  specific  weight  of  the  blood  may  be  determined  in  two  ways — one  the 
* '  areometric ' '  method,  the  other  the  ' '  pyenometric. ' '  In  the  areometric  method 
(Roy,  V.  Jaksch,  Devoto,  et  al.),^  a  drop  of  blood  is  placed  in  fluids  of  different 
but  known  specific  gravity — i.  e.,  in  different  mixtures  of  water  and  glycerin. 
The  fluid  is  then  so  mixed  that  the  drop  remains  suspended,  when  the  specific 
gravity  will  be  the  same  as  that  of  the  fluid.  The  influence  of  coagulation  and 
diffusion  militates  against  this  method,  and,  besides,  it  is  difiicult  to  obtain  a  great 
many  drops  of  blood  successively  from  one  and  the  same  patient ;  it  has,  however, 
the  advantage  that  it  may  be  perfonned  at  the  bedside,  without  any  analytic 
balance. 

Hammerschlag's  Method. — Hammerschlag '^  modified  this  method  by  plac- 
ing a  mixture  of  benzol  chloroform,  of  an  average  specific  gravity  of  1050  to  1060, 
in  a  test  tube  or  in  a  urinometer.  A  drop  of  blood  is  then  allowed  to  fall  gently 
into  this  mixture,  and,  according  to  whether  the  drop  floats  or  sinks,  benzol  or 
chloroform  is  added  until  the  drop  is  exactly  suspended.  The  drop  of  blood  can 
then  be  easily  removed  by  filtering  through  a  piece  of  linen,  and  the  specific 
gravity  of  the  mixture  determined  with  the  az'eometer.  The  fluid  may  be  saved 
for  further  use. 

In  the  pyenometric  method,  Schmalz^  employs  a  capillary  tube  (capillary 
pycnometer)  IJ  mm.  in  internal  diameter  and  12  cm.  long,  slightly  constricted  at 
the  ends  so  as  to  easily  retain  its  contents.  This  tube  is  dried,  filled  with  dis- 
tilled water,  and  then  weighed.  It  is  then  carefully  dried  with  alcohol  and  ether, 
filled  with  the  blood  to  be  examined,  and  weighed  again.  If  c  equals  the  weight 
of  the  empty  capillary  tube,  c^  the  weight  of  the  capillary  tube  plus  the  water, 
and  (/'  the  weight  of  the  capillary  tube  plus  the  blood,  then  c' — c  will  be  equal 
to  the  weight  of  the  water,  and  (/^ — c  will  be  the  weight  of  an  equal  volume  of 

blood.     Therefore  the  specific  weight  of  the  blood  will  be  —^ 

Experiments  at  the  Berne  Clinic  have  proved  that  this  method  is  easy  and 
accurate  if  scales  weighing  to  ^^  mg.  are  used. 

The  results  of  determuiing  the  specific  gravity  of  the  blood  thus  far  have 
shown  that  it  is  diminished  in  all  anemic  conditions  (oligochromemia),  and  in 
some  other  cachectic  conditions  (nephritis,  digestive  disturbances),  although  the  per- 
centage of  hemoglobin  need  not  be  diminished.  The  normal  figures  vary  between 
10,455  and  10,665.  In  men  it  averages  about  10,550  ;  in  women,  10,535  ;  and 
in  children,  10,512  (Peiper). 

Hammerschlag  *  advocates  a  method  of  estimating  the  specific  gravity  of  the 
blood-plasma,  based  upon  the  above-described  areometric  principle.  The  blood 
is  drawn  into  a  capillary  tube  f  cm.  (probably  3  to  4  cm.  is  meant,  instead  of  f ) 
long,  and  1  to  2  mm.  in  diameter.  The  tube  should  be  pre^^ously  washed  out 
with  a  3  per  cent,  solution  of  oxalate  of  sodium,  to  prevent  coagulation,  and  then 
blown  out.  Both  ends  of  the  tube  are  closed  with  wax,  the  tube  is  set  in  a  ver- 
tical position,  and  the  blood  is  allowed  to  settle.  After  the  blood-corpuscles 
have  separated  from  the  plasma,  the  capillary  tube  is  filed  in  two  at  the  point 
where  the  two  layers  meet,  and  the  plasma  is  examined  according  to  Hammer- 
schlag's areometric  method.  The  admixture  of  the  sodium  oxalate  solution 
causes  a  slight  error  in  the  result,  but  so  slight,  according  to  Hammerschlag,  that 
it  need  not  be  considered  (?).  The  specific  gravity  of  blood-serum  maybe  deter- 
mined in  a  similar  way.  The  blood  is  allowed  to  coagulate  in  the  capillary  tube 
without  adding  the  oxalate,  and  to  stand  until  the  clot  has  pressed  out  a  sufficient 
quantity  of  serum.  According  to  Hammerschlag,  the  specific  gravity  of  blood- 
serum  varies  but  very  little  from  that  of  the  plasma.     The  specific  gravity  of  plasma 

'Roy,  Proc.  Physiol.  Soc,  1884;  Devoto,  Zeits.f.  Heilk.,  No.  11,  p.  175,  1889;  v. 
Jaksch,  Klin.  Diagnostic  1892.  ^  Zeits.  f.  klin.  Med.,  vol.  xx.,  p.  444,  1892. 

^Deutsch.  Arch./,  klin.  Med.  vol.  xlvii.,  p.  Mo,  1890,  and  Deutsch.  med.  Wocli.,  1891, 
No.  17,  p.  555.  *  Zeits./.  klin.  Med.,  vol.  xxi.,  p.  47q,  1892. 


REACTION  OF  THE  BLOOD.  613 

in  a  healthy  individual  ranges  from  1029  to  1032.  It  is  diminished  in  condi- 
tions associated  with  hydrops,  especially  in  nephritis.  In  these  conditions,  how- 
ever, the  specific  gravity  of  the  plasma  may  be  increased,  since  in  addition  to 
water  proportionately  larger  quantities  of  the  solid  constituents  may  be  retained 
in  the  blood. 

REACTION    OF   THE   BLOOD. 

The  normal  reaction  of  the  blood  is  alkaline,  the  degree  of  alkalinity  varj'ing 
under  pathologic  conditions.  According  to  Cantani,  blood  may  become  acid  in 
cholera.  ^ 

The  peculiar  color  of  blood  renders  titration  very  difiicult,  so  that  an  attempt 
has  recently  been  made  to  estimate  the  degree  of  alkalinity  by  determining  the 
amount  of  carbonic  acid  contained  in  the  blood,  on  the  ground  that  this  amount 
depends  essentially  upon  the  alkialinity.  Theoretically  this  deduction  is  question- 
able, and,  moreover,  the  method  of  estimating  carbonic  acid  is  too  complicated 
for  clinical  purposes  and  requires  altogether  too  much  blood. 

TITRATION  OF  OPAQUE  BLOOD   (after  Landois-v.  Jaksch.ji 

This  method  consists  in  a  modified  titration  of  minute  quantities  of  blood. 
A  series  of  tartaric  acid  solutions  of  known  acidity  is  kept  in  stock.  A  measured 
small  quantity'  of  blood — for  instance,  0.1  c.c. — is  added  consecutively  to  1  c.c. 
of  each  of  these  acid  solutions.  They  are  stirred  quickly,  and  the  reaction  is 
tested  with  some  very  sensitive  litmus  pajaer.  The  degree  of  acidity  of  the  tartaric 
acid  solution  which  is  exactly  neutralized  by  the  blood  indicates  the  alkalinity  of 
the  blood. 

V.  Jaksch  employs  the  following  eighteen  test  solutions  to  carrj^  out  this 
method : 

Solution    1  contains  in  1  c.c.  0.9  c.c.    j-g-g  ]  ."2       f  0.1  concent,  solution  of  Glaubei-'s  salt. 


1 

contains 

inl 

c.c.  0.9  c.c 

2 

11 

"  1 

"    0.8    " 

3 

a 

"  1 

"    0.7    " 

etc. 

etc. 

9 

It 

"  1 

"    0.1    " 

10 

is 

"  1 

"    0.9    " 

11 

a 

"  1 

"    0.8    " 

etc. 

etc. 

18 

(I 

"  1 

"    0.1    " 

A  o  ti  a  a 

etc.      etc.        etc.  etc. 


}-  =  S  ^   0.9 
■'  ■■      0.1         "  "  " 

etc.      etc.        etc.  etc. 

j^       L  0.9        " 

The  Glauber's  salt  solution  is  added  instead  of  distilled  water  to  presen-e  the 
red  blood-corpuscles  and  make  the  solution  permanent. 

V.  Jaksch  obtains  the  .specimen  of  blood  by  a  wet-cup.  Miss  Freundberg 
undertook  to  determine  the  alkalinit}^  of  the  blood  in  cases  at  the  Bern  Clinic. 
She  employed  Francke's  needle  (p.  610),  but  used  only  0.05  c.c.  of  blood,  because 
it  was  difficult  to  get  0.1  c.c.  from  so  small  a  jjuncture.  The  blood  is  sucked  into 
a  capillary  pipet.  Immediately  after  removal,  it  is  blown  into  a  watch  glass 
containing  0.5  c.c.  of  tartaric  acid  solution  of  an  average  degree  of  acidity. 
The  mixture  in  the  watch  glass  is  stirred  rapidly  with  a  little  glass  rod,  and  the 
reaction  tested  with  litmus  paper.  If  acid,  the  experiment  is  repeated  with  a 
weaker  solution  until  the  point  is  reached  when  the  amount  of  blood  employed 
neutralizes  the  acid  solution  exactly.  It  is  best  not  to  proceed  from  one  solution 
to  the  next,  but  to  skip  several,  so  that  the  outside  limits  between  which  the 
degree  of  acidity  lies  may  be  quickly  obtained.  Care  must  be  taken  to  remove 
the  blood  as  rapidly  as  possible,  as  a  considerable  amount  of  alkalinity  is  lost  by 
chemical  changes  outside  of  the  vascular  sy.stem.  Especial  care  must  also  be 
devoted  to  preparing  a  very  sen.sitive  litmus  paper.  (See  text-books  on  Chem- 
istry).'^    The  method  of  using  litmus  paper  is  as  follows  :  A  drop  of  the  mixture 

^  Landois,  Eulenburffs  Re(dencyklnpddie,\o\.  iii.,  p.  161,  2d  ed.,  1895;  v.  Jaksch, 
ZeUs.f.  klin.  Med,  vol.  x'iii.,  p.  350,'l887. 

*  Cf.  Fresenius,  Qualitative  Analyse,  1895,  16th  ed.,  p.  100,  note. 


614  EXAMINATION  OF  THE  BLOOD. 

of  blood  and  acid  is  dropped  upon  the  paper  with  a  glass  rod,  and  the  fluid 
immediately  removed  with  a  piece  of  white  filter  paper  which  is  known  to  be 
neutral.  The  blood-pigment,  which  is  the  disturbing  factor,  is  taken  up  by  the 
filter  paper,  leaving  an  unmistakable  spot  on  the  litmus  paper,  provided  neutral- 
ization is  not  complete.  Only  natural  litmus  paper  can  be  used  for  testing, 
because  the  blood-pigment,  even  after  it  has  been  taken  up  with  filter  paper, 
renders  it  impossible  or  very  difficult  to  recognize  the  reaction  upon  red  acid 
litmus  paper.  For  this  reason  blue  litmus  paper  should  be  used.  Successively 
weaker  solutions  of  tartaric  acid  should  be  tried  until  no  red  spot  remains. 

It  has  not  yet  been  definitely  determined  whether  this  method  of  blood-titra- 
tion  with  litmus  paper  gives  reliable  results.  The  uncertainty  depends  upon  the 
well-known  peculiarity  of  litmus  pigment  to  react  amphoterically  to  mixtures  of 
both  alkaline  phosphates  contained  in  the  blood  (primary  and  secondary). 

The  principal  fact  obtained  by  v.  Jaksch  with  this  method,  and  corroborated 
by  Miss  Freudberg,  is  that  the  alkalinity  of  the  blood  diminishes  in  all  anemias. 
V.  Jaksch  found  the  same  to  be  true  for  diabetes  mellitus,  for  uremia,  and  for  fever. 

The  normal  alkalinity  of  the  blood  determined  in  this  way  corresponds, 
according  to  v.  Jaksch,  to  0.26  to  0.30  sodium   hydroxid,  for  100  c.c.  of  blood. 

TITRATION    OF  LAKED    BLOOD    (after  Lowy  and  Engel)» 

In  the  method  of  titration  described  above  it  is  doubtful  how  much  the  red 

blood-corpuscles,  which  are  preserved  by  the  addition  of  Glauber's  salt,  influence 

the  reaction.     For  this  reason  Lowy  employed  lake  blood.     A  test  tube  provided 

with  a  long,  narrow,  partially  graduated  neck,  capable  of  containing  50  c.c,  is 

filled  with  45  c.c.  of  \  per  cent,  solution  of  oxalate  of  ammonia  and  5  c.c.  of 

blood.     This  solution  of  oxalate  of  ammonia  lakes  the  blood,  and  at  the  same 

N 
time  prevents  coagulation.     Titration  is  performed  with  a  —  tartaric  acid  solution 

(see  above)  and  lackmoid  ^  paper,  which  has  been  saturated  with  a  concentrated 

solution  of  magnesium  sulphate.     The  5  c.c.  of  blood  may  be  taken  from  a  vein 

(see  1^.  610).     With  fi-esh  human  blood  Lo^vy's  values  varied  between  400  and  600 

mg.  NaOH  pro  100   c.c.  of   blood.     These  are  higher  values  than  v.   Jaksch 

obtained  with  unlaked  blood.     H.  Strauss'^    values  were  medium,  300  to  350  mg. 

pro  100  c.c.  of  blood. 

S.  Engel  ^  modified  this  method  by  using  a  melangeur,  diluting  0. 05  of  blood 

100  times  with  neutral  distilled  water.     With  this  mixture  in  a  small  beaker 

glass  he  then  titrates  from  a  buret,  graded  into  -^^  c.c,  dropping  with  great  care 

N 
a  —tartaric  acid  solution  (1  gr.   of  tartaric  acid  to  1  liter  of  water).     The  end 

reaction  is  tested  after  the  addition  of  each  drop  from  the  buret  by  wetting  a  piece 
of  lackmoid  paper  with  one  drop  of  the  solution  from  a  glass  rod,  and  then  deter- 
mining the  moment  when  the  yellowish  drop  (hemoglobin)  shows  a  sharp  red 
line  around  its  margin.  Engel' s  and  Lowy's  results  correspond.  The  relation 
of  lackmoid  pigment  to  mixtures  of  primary  and  secondary  alkaline  phosphates 
should  be  more  carefully  examined  before  any  judgment  is  formed  as  to  the 
reliability  of  Lowy's  or  Engel's  method.  The  close  correspondence  of  their 
values  with  those  of  Salkowski  is  in  favor  of  their  accuracy. 

From  a  practical  standpoint,  it  is  interesting  to  note  that  Magnus-Levy,*  by 
the  use  of  Lowy's  method,  in  diabetic  coma,  has  observed  extraordinarily  marked 
diminutions  of  the  alkalinity  of  the  blood — diminutions  corresponding  to  220  to 
260  mg.  NaOH  to  100  c.c.  of  blood.  He  attributes  this  diminished  alkalinity 
partly  to  neutralized  carbonates  and  partly  to  the  combination  of  the  proteids 
with  acids,  which  consequently  lessens  the  quantity  of  acid  to  be  neutralized  by 
titration. 

^  Cf.  Bockmann,  Chem.-techn.   Uniersuchungsmethoden,  Berlin,  1893. 

2   Zeits.f.  klin.  Med.,  1896,  vol.  xxx.  ^  Berlin  klin.  Woch.,  1898,  vol.  xiv.,  p.  308. 

*  Arch./,  exp.  Pathol.,  vol.  xlii,  1899,  p.  197. 


COAGULATION  TIME  OF  THE  BLOOD.  615 

SALKOWSKI'S  METHOD  OF  DETERMINING  THE  ALKALINITY  OF  THE  BLOOD. 

Salkowski  ^  lias  recently  announced  a  method  of  determining  the  alkalinity 
of  the  blood  which  has  the  advantage  of  avoiding  direct  titration  with  all  its 
associated  difficulties  (color  of  the  blood,  uncertainty  of  the  indications  in  titra- 
tion in  phosphate  mixtures).  Schlosing's  apparatus  for  determining  the  amount 
of  ammonia  in  urine  is  employed.  A  known  quantity  of  sulj^hate  of  ammonia 
is  added  to  the  blood  the  alkalinity  of  which  is  to  be  determined,  and  the  amount 
of  ammonia  liberated  from  the  alkalies  of  the  blood  is  then  estimated  by  Schlosing's 
method.  The  technic  is  as  follows  :  Twenty  grams  of  finely  pulverized  sulphate 
of  ammonia  are  placed  in  the  large  lower  dish  of  Schlosing's  apparatus,  and 
then  dissolved  by  adding  20  c.c.  of  water.  Ten  cubic  centimeters  of  a  normal 
solution  of  sulphuric  acid  are  placed  in  the  upper  dish  containing  the  ammonia 
sulphate.  It  is  well  to  wash  the  graduate  in  which  the  blood  is  measured  with 
a  1  per  cent,  solution  of  sodium  oxalate,  so  as  to  prevent  coagulation.  The 
blood  is  mixed  with  the  solution  of  ammonia  sulphate,  and  the  globe  placed  over 
it  as  soon  as  possible. 

After  five  or  six  days  all  the  ammonia  that  has  been  freed  has  been  taken  up 
by  the  sulphuric  acid,  and  can  then  be  estimated  by  titration.  The  entire  quan- 
tity of  sulphuric  acid  must  be  taken  into  account  in  the  titration  because,  as  has 
been  pointed  out  by  Waldvogel,  the  volume  of  the  acid  may  change  on  account 
of  water  being  given  off  and  combined  with  the  sulphate  of  ammonia  solution. 

Waldvogel  gives  as  normal  values  for  men  350  to  400  mgr.  NaHO  pro  100  c.c. 
of  blood  ;  for  women,  300  to  350.  In  febrile  and  also  in  anemic  conditions 
the  values  were  lower.  The  blood-corpuscles  doubtless  enter  into  the  reaction  in 
this  method.  The  correspondence  of  the  values  found  by  Waldvogel  with  those 
obtained  by  Lowy  would  seem  to  support  the  value  of  the  method. 

Dare's  Spectroscopic  Method  for  the  Determination  of  the  Alkalinity  of  the  BIood» 

Dare  ^  has  recently  suggested  a  method  of  determining  the  alkalinity  of  the 

N 

blood  by  titrating  laked  blood  with  a  tartaric  acid  solution.     The  end  re- 

^  *  1000 

action  in  this  method  is  the  disappearance  of  the  characteristic  siJectrum  of  hemo- 
globin and  its  replacement  by  that  of  methemoglobin,  the  author  assuming  that  the 
disappearance  of  the  hemoglobin  spectrum  is  coincident  with  neutralization. 
Further  investigations  are  necessary,  however,  to  determine  the  utility  of  this 
method,  since  it  has  not  yet  been  conclusively  shown  that  the  hemoglobin  is  not 
destroyed  before  complete  neutralization,  and,  furthermore,  the  spectroscopic 
changes  dependent  upon  variations  in  the  reaction  are  quite  slow  in  their 
appearance. 

COAGULATION  TIME  OF  THE  BLOOD. 

The  time  elapsing  before  coagulation  of  blood  occurs  varies  decidedly  under 
pathologic  conditions.  It  is  difficult  to  give  any  constant  normal  figures,  because 
coagulation  depends  so  much  upon  external  conditions,  such  as  temperature,  the 
shape  of  the  vessel  in  which  coagulation  takes  place,  the  amount  of  blood  used, 
and  the  nature  of  the  wound  from  which  the  blood  is  taken.  This  is  the  reason 
why  so  little  is  as  yet  known  regarding  pathologic  variations. 

H.  Vierordt  ^  recommends  a  method  for  determining  the  coagulation  time  of 
human  blood  which  can  be  performed  with  very  small  amounts  of  blood.  The 
technic  is  as  follows  :  A  capillary  glass  tube,  about  5  cm.  long  and  1  mm.  in  internal 
diameter,  is  filled  with  blood  for  about  one-half  cm.  From  the  other  end  there  is 
introduced  through  the  blood  a  white  horsehair  (about  10  cm.  long),  which  has  pre- 

^  Genlralhl.  f.  die  med.  Wissemchaften,  1898.  Kef.  in  Maly's  Jahresbericht,  1898,  aiuc] 
Waldvogel,  Deutsch.  med.  Woch.,  1900,  No,  43. 

^  Proc.  Pathol.  Soc.  of  Philadelphia,  April,  1903. 
=*  Arch,  der  HeilL,  1878,  vol.  xix.,  p.  193. 


616  EXAMINATION  OF  THE  BLOOD. 

viously  been  carefully  boiled  witb  alcohol  and  ether,  care  being  taken  not  to  touch 
.  the  end  which  comes  in  contact  with  the  blood.  At  first  no  blood  sticks  to  it, 
but  the  moment  coagulation  begins  the  horsehair  will  show  a  reddish  discoloration. 
As  soon  as  coagulation  is  complete,  the  horsehair  will  appear  white  when  pushed 
further  into  the  tube,  or  the  entire  quantity  of  blood  will  adhere  to  it  as  a  com- 
pact clot.  In  order  to  determine  more  accurately  the  length  of  time  necessary 
.  for  complete  coagulation,  it  has  been  the  writer' s  custom  to  knot  the  posterior 
portion  of  the  horsehair.  At  the  moment  of  complete  coagulation  the  entire 
coagulated  blood-column  may  be  drawn  out  of  the  tube  as  a  compact  mass  when 
this  knot  is  brought  in  contact  with  its  posterior  portion.  Vierordt  found  the 
average  time  of  coagulation  with  this  method  was  nine  minutes.  The  writer  has 
found,  however,  that  this  is  subject  to  extreme  variations  dependent  upon  the 
external  temperature  and  the  diameter  of  the  capillary  tube,  so  that  the  time  of 
coagulation  can  be  assumed  to  be  pathologic  only  when  it  is  compared  with  a  con- 
trol test  in  which  normal  blood  is  employed  under  exactly  similar  conditions. 
The  time  of  coagulation  is  shortened  by  stasis,  after  transfusion,  after  hemorrhage, 
by  hunger,  and  by  the  majority  of  diseases.  The  statement  that  the  coagulation, 
time  of  the  blood  is  shortened  when  it  is  taken  from  an  area  of  passive  congestion 
is  in  marked  contradiction  to  the  fact  that  the  blood  in  the  corpse  after  suffocation 
is  usually  liquid.  In  the  intervals  between  the  hemorrhages  of  hemophilia  the 
writer  has  found  the  coagulation  time  to  be  markedly  prolonged.  During  the 
hemorrhage,  however,  this  coagulation  time  may  be  even  shorter  than  that  ob- 
served in  normal  blood.  For  further  details  in  this  connection  the  reader  is- 
referred  to  the  writer's  article  in  the  Zeitschrift  fur  klinische  Medicin,  190'4-05 — 
."Ueber  das  Wesen  der  Hamophilie." 

DETERMINATION  OF  THE  HEMOGLOBIN  IN  THE  BLOOD. 

A  large  number  of  methods  have  been  recommended  for  use  in  this  important 
part  of  blood-diagnosis.  The  methods  available  for  clinical  purposes  indicate 
only  the  relative  amount  of  hemoglobin  contained  in  the  blood  examined  com- 
pared with  the  normal.  Clinically  these  relative  values,  expressed  in  percentages 
of  the  normal,  are  of  primary  interest.  It  is  very  easy  to  obtain  from  them  abso- 
lute figures  if  the  normal  amount  of  hemoglobin  contained  in  the  blood  is  known. 
This  is  in  a  normal  adult  13  to  14  gm.  in  100  c.c.  of  blood.  As  hemoglobin  con- 
tains about  0.4  per  cent,  of  iron,  this  would  correspond  to  about  0.05  per  cent, 
of  iron  content.  Leichtenstern  found  the  following  values  for  the  hemoglobin 
content  at  the  various  ages,  expressed  in  grams  per  100  c.c.  of  blood  : 


36  hours. 

19.329 

3  vears 

. 

10.971 

2  days. 

21.160 

4*  c, 

11.341 

3       '^' 

20.451 

5     " 

11.151 

4      " 

19.488 

6-10  years. 

11.796 

8      " 

17.869 

11-15 

11.701 

10      " 

17.129 

16-20 

13.034 

14      " 

16.124 

21-25 

13.870 

3  weeks. 

15.023 

26-30 

14.727 

4      " 

15.362 

31-35 

15.013 

10      " 

14.293 

36-40 

14.685- 

12      " 

13.828 

41-65 

14.420 

14      " 

14.388 

46-50 

12.484 

20       " 

12.928 

51-55 

12.696 

^-1  year. 

11.373 

56-60 

13.150 

2          " 

11.151 

Over  60 

years. 

14.790 

In  this  table  a  large  number  of  observations  were  made  on  middle-aged  and 
old  people,  and  average  figures  were  taken ;  but  for  the  earlier  periods  of  life  only 
single  observations  were  made.  Nevertheless  the  amount  of  hemoglobin  contained 
in  the  blood  in  the  first  week  of  life  is  without  doubt  one-third  larger  than  the 


DETERMII^ATION  OF  THE  HEMOGLOBIN  IN  THE  BLOOD.  617 

average  during  the  third  and  fourth  decades.  During  the  following  weeks  the 
quantity  gradually  diminishes,  and  remains  one-fourth  to  one-iifth  below  the 
average  from  the  second  half  of  the  first  year  to  about  pubert}\  From  puberty 
to  the  forty-fifth  year  of  life,  it  remains  about  at  the  average,  and  then  gradually 
diminishes.  These  figures  correspond  very  closely  to  the  variations  in  the  number 
of  blood-corpuscles,  except  that  they  are  somewhat  more  striking. 

The  percentages  upon  clinical  hemoglobinometers  corresponding  to  these  abso- 
lute values  can  be  readily  calculated  from  the  above  table  if  13  to  14  gm.  of 
hemoglobin  in  100  c.c.  of  blood  is  taken  as  100  per  cent.  Stierlin^  calculated 
these  percentages,  and  found  them  to  be  as  follows  : 

Newborn  (1st  to  3d  day)  138.88 

^-5  years  76.58   )    „p.  .. 

5-15   "  80.50   J     '*•**• 

15-25  "  88.88 

25-45  "  100.00 

45-60  "  87.50 

Hemoglobin  determinations  are  of  great  value  (any  practitioner  can  employ 
the  Gowers'  instrument  or  Tallquist's  book  at  the  bedside).  Only  since  we  have 
been  able  to  determine  the  amount  of  hemoglobin  have  we  recognized  that  an 
individual  who  is  very  pale  need  not  necessarily  be  anemic,  and  that  the  pallor  of 
the  skin  of  the  face  may  be  due  to  lack  of  cutaneous  transparency,  or  to  the  fact 
that  the  skin  contains  only  a  very  slight  amount  of  blood.  And  only  since  we 
have  been  able  to  limit  iron  therapy  to  diseases  where  there  is  really  a  deficient 
amount  of  hemoglobin  has  it  become  rational  therapy. 

Clinically  the  anemias  include  those  conditions  in  which  there  is  deficient 
percentage  of  hemoglobin  (oligochromemia).  Increased  percentages  of  hemo- 
globin up  to  from  110  to  120  per  cent,  are  by  no  means  uncommon  in  so-called 
full-blooded  healthy  individuals. 

Numerous  observations  have  established  the  fact  that  the  hemoglobin  per- 
centage increases  with  increased  altitude,  just  as  does  the  number  of  blood-cor- 
puscles (compare  p.  628). 

GOWERS'  HEMOGLOBINOMETER. 

This  instrument  (Fig.  228)  consists  of  two  glass  tubes  (a  and  b) 
about  11  cm.  long  and  0,8  cm.  in  diameter.  One  of  them  (a)  contains 
2  c.c.  of  standard  picrocarmin  solution,  the  shade  of  which  corresponds 
as  closely  as  possible  to  a  1  per  cent,  solution  of  normal  blood.  The 
other  tube  is  closed  at  one  end,  and  graduated  so  that  the  level  to  which 
2  c.c.  of  fluid  will  reach  corresponds  to  100.  If  the  calibers  of  the 
two  are  exactly  alike,  this  will  be  exactly  the  level  of  the  standard 
fluid  in  the  other  tube.  Below  the  100  mark  the  tube  is  subdivided 
into  100  equal  parts,  every  ten  of  which  are  numbered.  Each  of  these 
parts  contain  20  c.mm.  Both  tubes  can  be  held  in  a  vertical  position 
by  setting  them  into  a  perforated  rubber  block  (e).  A  capillary  pipet 
(e)  containing  20  mm.,  with  a  small  rubber  tube  attached,  is  used  for 
convenience  in  sucking  up  the  blood.  A  non-graduated  pipet  (d)  is 
used  for  making  the  approyjriate  dilution.  It  contains  about  3  c.c, 
with  an  opening  so  small  that  water  which  has  been  sucked  into  it  can 
only  escape  drop  by  drop. 

The  technic  of  estimating  the  amount  of  hemoglobin  is  as  follows  : 

'  Blutkorperchenziihlungen  und  Haemoglobinbestimmungen  bei  Kindem,  Arch.f. 
klin  Med.,  vol.  xlv.,  1889. 


618 


EXAMINATION  OF  THE  BLOOD. 


Twenty  c.mm.  of  blood  are  sucked  up  in  the  capillary  pipet  as  quickly 
as  possible,  so  as  to  avoid  coagulation.  The  point  of  the  pipet  is  wiped 
oflp,  care  being  taken  not  to  allow  blood  to  escape  from  the  lumen. 
Its  contents  are  then  quickly  blown  out  into  the  graduated  tube  (6) 
partly  filled  with  water.  The  blood  and  water  are  intimately  mixed 
by  stirring,  and  the  pipet  washed  by  repeated  sucking  up  and  blowing 
out  of  the  fluid.  Tube  b  with  the  blood-mixture  and  tube  a  with  the 
colored  solution  are  now  set  up  side  by  side  in  the  rubber  block.  A 
thin  piece  of  white  tissue  paper  is  held  behind  the  tubes,  and  their 
colors  are  compared  by  transmitted  light.  Water  is  added  from  the 
larger  pipet,  drop  by  drop,  with  repeated  stirring,  until  the  color  in 


FiQ.  228.— Gowers'  hemoglobinometer  (about  two-thirds  the  natural  size). 

both  tubes  is  as  nearly  alike  as  possible  by  transmitted  light.  The  line 
to  which  the  mixture  reaches  at  this  moment  indicates  the  percentage  of 
hemoglobin  in  the  specimen  of  blood  examined.  This  instrument  is 
accurate  within  5  or  10  per  cent.,  provided  that  the  shade  of  the  standard 
solution  exactly  corresponds  to  the  color  of  blood.  The  disadvantages  of 
the  instrument  are,  first,  that  it  is  quite  difficult  to  make  the  standard 
solution  so  that  it  will  exactly  match  the  color  of  normal  blood,  and,  sec- 
ondly, that  its  color  will  change  after  a  certain  length  of  time.  A  special 
standard  solution  must  be  used  if  the  examination  is  made  by  artificial 
light.  In  view  of  these  disadvantages,  the  writer  has  constructed  a 
new  hemometer,  in  which  some  of  the  "principles  of  Gower's  instrument 
are  retained,  and  which  will  meet  with  the  requirements  of  daily  prac- 


DETERMINATION  OF  THE  HEMOGLOBIN  IN  THE  BLOOD.   619 

tice.     The  standard  solution,  however,  is  made  up  with  blood-pigment 
instead  of  picrocarmin  (see  p.  621  et  seq.). 

FLEISCHL'S  HEMOMETER  WITH  MIESCHER'S  IMPROVEMENTS. 

Fig.  229  represents  Fleischl's  instrument  for  the  clinical  determination  of 
hemoglobin  with  Miescher'  s  improvements.  The  principle  of  the  instrument  is 
as  follows  :  The  stand  is  like  that  of  a  microscope.  In  the  central  opening  of 
the  objective  stage  is  placed  a  cylindric  chamber,  divided  into  two  parts  by  a 
vertical  partition.  This  chamber  {m)  has  a  glass  floor.  One-half  (a)  is  filled 
with  a  diluted  solution  of  the  blood  to  be  examined.  The  other  half  is  filled 
with  water.  A  glass  wedge  stained  purple  slides  beneath  the  chamber  by  means 
of  the  screw  T  R.  The  glass  wedge  and  the  chamber  are  illuminated  from  below 
by  a  plaster-of-Paris  reflector  P  S.     The  colors  in  the  two  halves  of  the  chamber 


Fig.  229.— The  new  Fleischl-Miescher  hemometer. 

are  compared  from  above  by  transmitted  light.  The  glass  wedge  is  then  adjusted 
until  both  sides  of  the  chamber  show  the  same  shade — i.  e.,  until  the  portion 
of  the  glass  wedge  underneath  the  chamber  filled  with  water  has  the  color  of  the 
blood-solution  to  be  examined.  The  position  of  the  wedge  is  read  off  through 
the  window  (m)  in  percentage  of  hemoglobin.  Artificial  light  must  be  employed, 
best  a  candle  light. 

The  modifications  of  Fleischl's  old  apparatus  introduced  by  Miescher  are 
as  follows:  1.  The  amount  of  blood  employed  can  be  much  more  accurately 
measured  with  the  specially  constructed  pipet  (melangeur)  than  with  Fleischl's 
former  capillary  tubes.  2.  Blood  of  varying  degrees  of  concentration  can  be  com- 
pared with  the  aid  of  this  melangeur  so  that  a  control  is  kept  of  the  individual 
examinations  and  of  the  evenness  of  the  coloring  of  the  glass  wedge.  ^  3.  The  scale 
of  the  new  hemometer  is  supplied  with  a  caliber  table  for  each  instrument  of 
absolute  hemoglobin  values  (in  milligrams),  whereas  the  scale  of  the  old  instrument 
showed  the  percentage  of  hemoglobin  in  relation  to  a  more  or  less  arbitrarily 
selected  average.  In  this  way  many  of  the  errors  which  with  the  old  appa- 
ratus were  due  to  the  irregular  coloring  of  the  glass  slide  are  avoided.     4.  The 


620  '  EXAMINATION  OF  THE  BLOOD. 

chamber  is  covered  with  a  glass  (D)  before  attempting  to  read  the  percentage,  and 
also  with  a  diaphragm  (Bl),  so  that  the  fields  examined  are  sharply  defined  on 
all  sides  without  any  meniscus.  5.  The  coloring  of  the  glass  wedge  has  been 
improved  upon  technically,  and  is  much  more  even  than  in  Fleischl's  original 
instrument. 

The  mixing  pipet  above  mentioned  (melangeur)  (Mel.  Fig.  229)  is  made 
like  a  blood-counter.  It  consists  of  a  capillary  portion  and  a  chamber  200  times 
the  capacity  of  the  former.  This  contains  a  glass  pearl  in  the  interior.  A  rubber 
tube  is  attached  to  the  melangeur.  The  drop  of  blood  is  obtained  in  the  same 
way  and  under  the  same  precautions  as  for  counting  the  blood-corpuscles.  To 
dilute  200  times,  blood  is  sucked  up  into  the  capillary  portion  to  the  mark  1,  and 
then  the  diluting  fluid  (1  per  cent,  soda  solution),  until  the  chamber  is  filled.  It 
is  then  well  shaken.  There  are  two  other  marks  on  the  mixing  pipet  (|  and  J), 
one  of  which  corresponds  to  a  dilution  of  the  blood  of  1  :  300,  and  the  other  of 
1 :  400.  If  the  blood  does  not  suck  up  readily  enough  to  the  desired  mark,  and 
there  is  danger  of  coagulation,  the  deficiency  or  excess  in  the  quantity  of  blood 
may  be  determined  by  the  small  cross-lines  above  and  below  the  main  marks. 
Each  of  these  accessory  marks  corresponds  to  the  Yho  ^f  the  entire  blood-column 
(up  to  1),  so  that  the  excess  or  deficiency  of  aspirated  blood  may  easily  be 
deducted  or  added  later. 

For  accurate  comparison  of  the  color  shades,  the  solution  of  blood  must  be 
perfectly  clear ;  otherwise  the  blood  always  seems  somewhat  darker  than  the  color 
of  the  glass  wedge.  This  is  the  reason  that  we  employ  a  solution  of  soda,  which 
dissolves  the  stroma  of  the  blood-corpuscles.  This  soda  solution  must  be  reason- 
ably fresh,  as  othei^wise  the  blood  will  not  appear  perfectly  clear,  on  account  of 
the  formation  of  bicarbonate  of  soda. 

The  details  of  technic  in  using  the  Fleischl-Miescher  instrument  for  deter- 
mining hemoglobin  are  clearly  described  in  the  directions  accompanying  the 
apparatus.  They  are  copied  from  an  article  by  Vaillon.^  Jaquet^  claims  from 
numerous  experiments  that  the  margin  of  error  in  the  absolute  quantity  of  hemo- 
globin determined  by  this  instrument  does  not  exceed  0.15  to  0.22  per  cent,  by 
weight  of  the  blood,  provided  all  precautions  are  taken.  This  instrument  is 
therefore  almost  as  accurate  as  the  spectrophotometer,  and  is  much  simpler. 

SAHLI'S  NEW  HEMOMETER. 

In  the  previously  described  clinical  methods  for  the  estimation  of 
hemoglobin,  Avhieh  are  those  most  commonly  employed,  the  solution  of 
blood  is  compared  with  an  artificially-  colored  substance — /.  e.,  either 
with  a  colored  wedge  of  glass  or  with  a  solution  of  picrocarrain. 

To  meet  the  demands  of  accurate  colorimetry,  however,  the  colored 
fluid  to  be  examined  should  not  be  compared  with  a  different  substance 
similar  in  color,  but  with  a  solution  of  known  strength  of  the  same 
coloring  matter.  This  is  the  only  method  by  which  the  ability  of  the 
human  eye  to  differentiate  shades  can  be  completely  utilized.  In  addi- 
tion to  the  great  difficulty  in  obtaining  a  standard  color  exactly  like 
the  color  of  the  blood,  whether  it  be  by  means  of  a  glass  wedge  or  a 
picrocarmin  solution,  the  shades  of  the  two  colors  will  not  coincide  for 
all  dilutions  unless  the  standard  color  be  made  with  the  same  substance 
as  that  contained  in  the  fluid  to  be  examined.  This  difficulty  is  quite 
apparent  in  any  colorimetric  appliance,  such  as  the  Fleischl-Miescher 
hemometer,  in  which  different  shades  of  the  standard  color  must  be 

^  ArcXf.  exp.  Pathol,  n.  Pharmakol.,  vol.  xxxix.,  1897,  p.  385. 
^  Correspondenzbl.  f.  Schweizer  Aerzte,  1897,  pp.  129  and  164. 


DETERMINATION  OF  THE  HEMOGLOBIN  IN  THE  BLOOD.   621 

compared  with  different  concentrations  of  the  blood  to  be  examined. 
For  analogous  reasons,  an  artificial  standard  color  can  never  be  pro- 
duced the  shade  of  which  will  coincide  with  that  of  the  blood  both  with 
natural  and  with  artificial  light. 

The  difficulty  in  applying  this  colorimetric  principle  lies  in  the  fact 
that  solutions  of  hemoglobin  are  not  permanent.  It  consequently  fol- 
lows that  if,  in  the  interest  of  accuracy,  we  avoid  employing  artificial 
colors,  we  must  utilize  some  permanent  hemoglobin  derivative  in  making 
the  standard  solution.  The  blood -solution  to  be  examined  is  then  con- 
verted into  a  solution  of  the  same  derivative,  when  a  comparison  may 
be  accurately  made.  The  application  of  this  principle  is  limited  prac- 
tically by  the  necessity  of  employing  only  those  derivatives  of  hemo- 
globin which  may  be  produced  in  solutions  of  blood  by  simple  chemical 
reactions. 

After  numerous  attempts  the  author  has  succeeded  in  devising  a 
method  by  which  the  hemoglobin  of  a  solution  of  blood  may  be  trans- 
formed into  a  derivative  by  quite  a  simple  chemical  reaction.  With 
this  derivative  permanent  standard  solutions  and  colorimetric  estima- 
tions may  be  made  in  accordance  with  accurate  colorimetric  principles. 

The  procedure  consists  simply  in  diluting  the  blood  with  10  times 

N  .        . 

its  volume  of  —    hydrochloric  acid.     After  a  few   seconds  the  fluid 

becomes  dark  brown  from  the  formation  of  minute  particles  of  hematin 
hydrochlorate.^  Although  this  substance  is  not  held  in  true  solution, 
it  has  the  a])pearance  of  being,  and  when  diluted  with  water  forms  a 
clear  brownish-yellow  fluid,  the  pigment  percentage  oF  which  may  be 
colorimetrically  determined  by  comparison  with  a  permanent  standard 
solution  of  the  same  substance. 

The  color  comparison  may  be  made  by  means  of  any  of  the  color- 
imetric appliances,  such  as  the  colorimetric  double  pipet  (see  below). 
In  the  author's  hemometer  he  has  employed  the  same  principle  of  com- 
parison that  is  found  in  Gowers'  instrument  (see  p.  618),  and  which  has 
proved  to  be  so  well  adapted  to  the  requirements  of  the  practitioner. 
The  standard  hydrochloric  acid  solution,  in  a  concentration  corre- 
sponding to  a  1  per  cent,  solution  of  normal  blood,  is  sealed  in  a  gradu- 
ated glass  tube.     A  similar  accurately  graduated  tube,  each  division  of 

which  corresponds  to  20  c.mm.,  is  filled  to  the  mark  10  with  —  hydro- 
chloric acid  which  has  been  saturated  with  chloroform.  With  a  capil- 
lary pipet  like  that  employed  in  Gowers'  instrument,  20  c.mm.  of  blood 
are  introduced  into  the  tube  and  well  shaken.  As  soon  as  the  mixture 
approaches  a  clear  dark -brown  color,  ordinary  water  is  added  until  the 
shade  of  the  mixture  exactly  corresponds  to  that  of  the  standard  solu- 

^  The  substance  produced  is  not  niethenioglobin,  since  the  shade  diffei-s  from  that  of 
metheraoglobin  formed  in  hemoglobin  sohitions  by  the  addition  of  other  acids.  Its 
spectrum  also  differs  from  that  of  niethenioglobin.  The  author  has  recently  succeeded 
in  producing  Teichmann's  hemin  crystals  from  this  fluid  by  extraction  with  acetic 
alcohol  and  subsequent  evaporation. 


622  EXAMINATION  OF  THE  BLOOD. 

tion,  when  the  hemoglobin  percentage  may  be  directly  read  oif,  as  in 
Gowers'  instrument.  The  author  has  kept  this  standard  solution  for  three 
years  without  beiug  able  to  detect  the  slightest  change  in  color,  and 
consequently  is  sure  that  it  is  permanent.  He  must,  however,  call 
attention  to  the  fact  that  after  long  disuse  the  suspended  particles 
(which  are  not  in  solution,  see  above)  may  be  deposited  upon  the  walls 
of  the  tube,  by  reason  of  which  the  fluid  appears  lighter  in  color.  After 
such  a  period  of  disuse  the  mixture  may  be  easily  made  homogeneous 
again  by  gently  shakiug  and  repeatedly  inverting  the  tube.  AY  hen  this 
is  done  a  cloud  of  pigment  may  be  seen  to  diffuse  itself  gradually 
throughout  the  fluid.  The  pigment  never  adheres  firmly  to  the  glass. 
Violent  agitation  must  be  avoided,  since  it  fills  the  fluid  with  air 
bubbles,  which  do  not  disappear  for  several  hours,  and  make  an  accu- 
rate comparison  impossible. 

Physicians  have  repeatedly  sent  the  author  standard  tubes  which 
appeared  to  be  too  light  in  color,  and  which  consequently  gave  rise  to 
the  suspicion  that  the  fluid  became  lighter  with  age.  The  author  does 
not  believe  that  this  is  the  case,  but  has  been  able  to  show  that  the 
error  was  due  to  the  fact  that  the  glass  blower,  when  filling  the  tubes, 
neglected  to  agitate  the  stock  mixture  sufficiently,  and,  since  this  con- 
tained minute  particles  in  suspension  instead  of  in  solution,  the  individual 
tubes  did  not  receive  the  proper  quantity  of  the  pigment.  In  such 
cases  the  faulty  tubes  were  replaced  free  of  cost  by  the  manufacturing 
firm. 

The  standard  solution  was  purposely  made  somewhat  dark — i.  e., 
corresponding  to  the  highest  hemoglobin  percentage  of  normal  blood  as 
found  in  the  author's  strongest  assistants.  The  author  emphasizes  this 
point,  since  an  absolute  standard  does  not  exist,  and  variations  amount- 
ing to  20  per  cent,  (by  his  hemometer)  occur  in  healthy  individuals.  The 
occurrence  of  such  marked  variations  was  first  brought  to  his  attention 
by  the  use  of  this  instrument,  which  is  based  upon  reliable  coloriraetric 
principles.  He  was  led  to  employ  the  bloods  richest  in  hemoglobin  for 
the  purpose  of  making  a  standard  color  by  observing  that  a  com- 
parison can  be  more  accurately  made  with  the  darker  than  with  the 
lighter  sliades.  The  standard  fluid  now  furnished  in  his  hemometer 
corresponds  to  a  blood  which,  in  a  dilution  of  1  :  200  in  the  Fleischl- 
Miescher  instrument,  furnishes  a  reading  of  109,  or  an  absolute  quantity 
of  hemoglobin  of  17.2  per  cent. 

The  author  has  further  improved  this  instrument,  as  compared  with 
Gowers'  (see  Fig.  230),  by  placing  the  two  tubes  in  a  perforated  black 
stand  of  hard  rubber,  which  serves  as  a  colorimetric  shield.  When 
the  tubes  are  compared  by  transmitted  light,  the  rays  passing  through 
the  sides  of  the  glass  blend  with  the  side  light,  and  the  colored  surfaces 
are  seen  upon  a" black  background.  The  stand  is  also  provided  with 
a  ground-glass  plate  which  diffuses  the  light  before  it  reaches  the 
tubes,  and  obviates  all  disturbing  reflections.  By  means  of  these 
appliances  the  optical  impression  obtained  is  that  the  fluid  is  con- 
tained in  a  small  compartment  with  plane  parallel  sides.     Such  com- 


DETERMINATION  OF  THE  HEMOGLOBIN  IN  THE  BLOOD.  623 


partments  are  really  necessary  for  accurate  colorimetric  estimations,  in 
order  to  compare  completely  homogeneous  colored  surfaces.  They  are 
very  dear,  however,  and  cannot  be  obtained  in  the  small  size  necessary 
for  the  minute  quantity  of  blood  which  is  procured  for  examination. 
The  appliance  above  described  renders  the  employment  of  plane  parallel 
glass  vessels  entirely  superfluous,  as  may  be  demonstrated  by  the  effect 
upon  the  eye.  In  addition  to  these  improvements,  the  scale  of  the 
graduated  tube  may  be  turned  completely  behind  the  margin  of  the 
stand,  so  that  it  is  not  seen  until  the  moment  when  the  percentage  is  to 
be  read.  This  has  a  twofold  advantage  in  that 
the  homogeneity  of  the  colored  surface  is  not 
disturbed  by  the  scale,  and  that  the  investi- 
gator, in  adding  the  diluting  fluid,  is  not  influ- 
enced by  a  preconceived  opinion  in  reference  to 
the  expected  percentage.  The  method  may  be 
made  still  more  objective  by  covering  all  but 
the  lowermost  portion  of  the  tube  with  black 
paper,  so  that  the  height  of  the  fluid  may  not 
be  seen  at  all. 

The  author  has  reached  the  conclusion  that 
by  means  of  these  various  contrivances,  but 
chiefly  on  account  of  the  absolute  chemical 
cougruity  of  the  compared  fluids,  the  simple 
hemometer  devised  by  him,  and  made  by  the 
optician  Biichi  in  Bern,  gives  as  accurate  re- 
sults as  the  most  exact  methods  of  colorime- 
tric examination  of  the  blood,  not  excepting 
the  more  complicated  ones.  Furthermore,  it  is 
clear  that  the  instrument  must  give  the  same 
result  with  both  artificial  and  natural  light, 
which  is  of  the  greatest  advantage  to  the  prac- 
titioner, who  must  work  under  the  most  varied 
conditions.  The  most  accurate  result  will  pos- 
sibly be  obtained  in  a  dark  room  with  artificial 
light,  since  under  these  conditions  the  eye  is 
the  most  sensitive  to  light  and  color ;  but  even  with  daylight  the 
results  are  quite  exact.     The  procedure  is  almost  as  simple  as  Gowers'. 

The  author  would  finally  call  attention  to  the  fact  which  he  has 
directly  proved  experimentally,  and  upon  which  the  entire  procedure  is 
based,  that  the  brownish-yellow  color  produced  by  the  addition  of  hydro- 
chloric acid  and  subsequent  dilution  with  water  is  directly  proportional 
to  the  hemoglobin  percentage  of  the  blood  examined.  In  other  words, 
the  accuracy  of  the  colorimetric  dilution  method  is  not  impaired  by  a 
dissociation  of  the  hematin  hydrochlorid  combination  which  is  formed. 


Fig.  230.— Salili's  new  clinical 
hemometer. 


HEMATOSPECTROPHOTOMETER. 

The  most  accurate  method  of  determining  the  amount  of  hemoglobin  is  by 
means  of  the  spectrophotometer,  first  used  by  Vierordt  and  perfected  by  Hiifher. 


624  EXAMINATION  OF  THE  BLOOD. 

This  instrument,  however,  is  much  too  complicated  and  too  expensive  for  practical 
purposes,  so  that  the  author  will  refer  for  a  description  to  Hiifher's  essay  in  the 
third  volume  of  the  Zeitschrift  fiir  Physiologische  Chemie,  p.  560. 

THE  HOPPE-SEYLER  COLORIMETRIC  DOUBLE  PIPET. 
This  very  excellent  apparatus  is  also  too  complicated  for  clinical  purposes,  i 

THE  COUNTING  OF  BLOOD-CORPUSCLES. 

THE  COUNTING   OF   RED   BLOOD-CORPUSCLES    (Erythrocytes.) 

It  is  almost  impossible  to  form  any  idea  of  the  number  of  red  blood- 
corpuscles  contained  in  the  blood  by  simply  inspecting  a  microscopic 
preparation,  unless  the  number  is  so  greatly  diminished  that  the  prep- 
aration shows  few  or  no  rouleaux.  Actual  counting  is  the  only  proper 
procedure.  Numerous  methods  of  counting  have  been  advocated.  In 
all  of  them  a  known  quantity  of  blood  is  diluted  to  a  definite  propor- 
tion with  a  solution  which  preserves  the  red  blood-corpuscles,  and  then 
those  contained  in  a  definitely  measured  space  are  counted.  The  num- 
ber of  red  blood-corpuscles  in  1  c.c,  of  undiluted  blood  can  then  easily 
be  calculated  by  simple  multiplication. 

The  simplest  and  most  practical  blood-counting  apparatus  is  that  constructed 
by  Thoma  and  Zeiss  (Fig.  231).  It  is  based  upon  the  older  principles  of  Malassez, 
Hayem,  and  Gowers.  It  consists  of  two  parts,  a  counting-chamber  upon  a  slide, 
and  a  melangeur  pipet.  The  latter  consists  of  a  capillary  pipet  with  a  bulb  con- 
taining a  freely  movable  glass  pearl.  As  is  shown  in  the  figure,  the  melangeur  is 
so  constructed  that  the  bulb  contains  100  times  the  cubic  contents  of  the  capillary 
tube.  A  rubber  tube  is  attached  to  the  upper  end  for  convenience  in  sucking  up 
the  blood. 

The  counting-chamber  itself  is  represented  in  Fig.  231,  B  from  above  and 
C  in  cross-section.  Two  plane  glass  plates  are  cemented  to  a  slide.  The  smaller  (/) 
is  circular;  the  larger  (e,  e,  e,  e)  is  square,  somewhat  thicker  than  /,  and  with  a 
circular  opening  in  the  center,  in  which  (/)  is  centered,  leaving  between  the  two  a 
circular  moat  (g).  The  floor  of  the  moat  is  formed  by  the  slide  itself.  The  upper 
surface  of  /  is  exactly  0. 1  mm.  below  that  of  e.  In  the  center  of  /,  which  forms 
the  floor  of  the  counting-chamber,  1  sq.  mm.  of  the  glass  is  ruled  with  a 
microscopic  scale  into  400  (20  X  20)  squares  (Fig.  231,  D).  Each  square  has  a 
surface  of  ^^^  sq.  mm.,  each  side  being  ^^^  mm.  This  chamber  is  covered  with  a 
carefully  ground  cover-glass,  made  thick  enough  not  to  bend.  The  chamber  is 
therefore  divided  into  little  square  prisms,  each  one  of  which  has  a  cubic  content 
of  ^QQQ  c.mm.  This  fraction  forms  the  basis  of  subsequent  calculations.  The 
chaqaber  is  very  carefully  ground,  and  to  avoid  error  the  cover-slip  should  rest 
very  accurately  upon  the  slide.  It  is  carefully  pressed  down  upon  the  square 
glass  e,  €,  e,  e  until  the  ' '  Newton' s  rings ' '  which  are  produced  remain  per- 
manently— ^.  e.,  after  the  pressure  has  been  removed — merely  fi'om  the  adhesion 
between  the  cover-slip  and  the  margin  of  the  chamber.  The  moat  {g,  g)  around 
the  glass  (/)  prevents  the  blood-mixture  upon  /  from  running  in  between 
the  cover-slip  and  the  square  glass  (e,  e,  e,  e),  and  so  altering  the  depth  of  the 
chamber. 

The  method  of  procedure  is  as  follows  :  In  extracting  the  blood  we  must 
avoid  any  pressure  in  the  vicinity  of  the  puncture,  otherwise  congestion  or  lymph 
exudation  may  make  the  results  inaccurate.     The  blood  is  sucked  up  into  the 

^  Zeits.  f.  Physiol.  Chem.,  vol.  xvi.,  1892,  p.  505,  and  Lehrb.  der  physioL-chem.  Analyse, 
1893,  p.  414. 


THE  COUNTING   OF  BLOOD-CORPUSCLES. 


625 


capillary  tube  to  the  mark  1 ;  the  bulb  is  then  filled  up  to  the  mark  101  with  a 
3  per  cent,  solution  of  sodium  chlorid  or  a  5  per  cent,  solution  of  Glauber's  salts, 
or  better  still,  Hayem's  fluid.  ^  While  sucking  up  the  diluting  fluid,  the  melan- 
geur  should  be  held  vertically  and  slightly  rotated  to  whirl  the  glass  pearl  a  little, 
and  so  free  it  from  any  adherent  air  bubbles  which  would  make  the  degree  of  dilu- 
tion inaccurate.  A  1  :  100  dilution  of  the  blood  is  thus  prepared  tor  counting. 
After  thorough  shaking,  2  or  3  drops  of  the  fluid  are  first  blown  out,  the  point  of 


r 

ii  In 


Wf 


m 


^    ^  J'  ff  e 


A  E  .  D 

Fig.  231.— Thoma-Zeiss  blood-conntlng  apparatus :  A,  Melanf?eur;  B,  counting-cliamber,  seen 
irom  above ;  t  profile  of  counting-chamber ;  D,  microscopic  picture  of  a  portion  of  ruled  field 
with  blood-cells ;  E,  white  counter. 

the  pipet  is  wiped  off,  and  a  small  drop  of  the  solution  is  carefully  placed  upon 
the  center  of  the  counting-chamber — i.  e.,  over  the  ruled  scale.  The  cover- 
glass  is  now  adjusted,  and  pressed  down  at  the  margin  until  Newton's  rings  appear. 

'Hayem's  fluid:  Sublimate,  0.5;  sodium  sulphate,   5;  .sodium    chlorid,    2;    aquje 
destillatse,  200.     This  also  preserves  the  red  color  of  the  cells,  and  facilitates  a  distinction 
between  the  red  and  the  white  blood-corpuscles. 
40 


626  EXAMINATION  OF  THE  BLOOD. 

If  these  do  not  remain  after  removal  of  the  pressure,  the  preparation  must  be 
made  over  again.  The  chamber  and  cover-glass  must  then  be  still  more  carefully 
cleansed,  for  the  trouble  is  usually  due  to  dust  getting  between  the  margin  of  the 
chamber  and  the  cover-glass.  The  slide  is  allowed  to  remain  horizontal  for  about 
a  minute,  until  the  blood-corpuscles  have  settled  to  the  bottom  of  the  chamber, 
and  then  the  corpuscles  are  counted.  For  greater  accuracy  two  counting-chambers 
may  be  prepared,  and  compared  to  be  sure  that  the  blood-coi-puscles  are  about 
evenly  distributed  in  each.  If  this  is  not  the  case,  fresh  preparations  should  be 
made  after  repeatedly  shaking  the  melangeur.  A  medium  power  is  the  best  for 
counting  ;  for  instance,  a  Leitz  No.  5  or  a  Zeiss  C  or  D  objective. 

In  the  modern  apparatus  each  fourth  and  fifth  division  line  of  the  chamber  is 
more  heavily  ruled,  and  an  extra  line  is  ruled  halfway  between  them  (Fig.  231,  D). 
This  device  is  helpful  in  pointing  out  the  squares  more  plainly,  and  series  of  16 
(4  X  4)  or  36  (6  X  6)  squares  can  be  counted  more  rapidly. 

To  determine  the  number  of  cells  contained  in  1  c.mm.  of  blood,  we  divide 
the  number  of  cells  counted  by  the  number  of  squares  ;  the  resulting  quotient  is 
the  number  of  cells  in  one  square  ;  this  we  multiply  by  the  dilution,  and  divide 
by  the  size  of  the  tiny  prism.  Suppose,  for  example,  that  in  counting  100  squares 
we  find  980  cells. 

Number  of  cells,       980^.  ^„„.^,      ,.,     . 

Number  of  squares,  100  ^  ''' ^^^^  ^^^'^t^^^)  ><  ^^^^  ^  ^'^^O^OOO 

The  size  of  each  tiny  square  prism  is  marked  upon  the  counting-slide,  and  so 
need  not  be  memorized. 

Unless  there  is  a  decided  diminution  of  red  cells  (anemia),  it  is  easier  to  count 
a  preparation  diluted  200  times.  For  such  a  dilution  we  suck  up  blood  to  the 
first  mark  0.5,  and  then  suck  the  diluting  fluid  to  the  101  mark  (just  above  the 
bulb).  Some  examiners  find  that  a  sliding  stage  makes  counting  easier  and  more 
accurate.     The  more  cells  we  count,  the  more  accurate  our  result. 

THE    COUNTING   OF  THE  WHITE    BLOOD   CORPUSCLES   (Leukocytes). 

It  is  very  difficult  to  judge  the  number  of  leukocytes  in  a  specimen 
of  undiluted  blood,  because  they  are  usually  distributed  very  irregularly, 
and  often  seem  to  be  hidden  or  jammed  in  between  the  rouleaux  of  the 
red  blood-corpuscles.  For  this  reason  we  dilute  the  blood,  and  count 
them  as  explained  in  the  following  : 

Two  conditions  must  be  ftiltilled:  first,  the  leukocytes  must  be  made  easily 
recognizable  with  the  rather  low  power  used  in  counting;  and  second,  consider- 
ably larger  amounts  of  blood  must  be  used  than  in  counting  red  blood-corpuscles, 
because  the  number  of  leukocytes  is  so  small  (unless,  of  course,  they  are  very 
considerably  increased,  leukemia).  The  blood  is  diluted  with  a  ^  per  cent, 
aqueous  solution  of  acetic  acid.  This  solution  dissolves  the  red  blood-corpuscles, 
leaving  the  remaining  cells  leukocytes.  A  special  melangeur  (Fig.  231,  E)  is  used  ; 
its  bulb  contains  only  10  times  as  much  fluid  as  the  capillary  tube.  After  preparing 
the  mixture,  the  technic  is  very  similar  to  that  for  counting  red  cells.  It  is  advan- 
tageous, however,  to  employ  a  larger  counting-chamber,  such  as  those  devised  by 
Elzholz,  Tiirk,  and  B.  Breuer.  On  account  of  its  clearness,  Breuer's  chamber 
seems  best.  Fig.  232  shows  how  it  is  divided.  The  depth  of  this  chamber  is  0. 1 
mm. ,  as  in  that  of  Thoma,  but  the  sides  are  3  mm.  in  length,  so  that  the  square 
has  a  surface  of  9  sq.  mm.  The  units  for  calculation  are  the  elongated  rectangles 
seen  in  the  illustration.  The  triple  line  is  merely  for  the  puqjose  of  orientation. 
Upon  request,  the  Zeiss  firm  will  furnish  this  counting-chamber  with  the  central 
square  millimeter  subdivided  into  smaller  squares  of  -^^  sq.  mm.,  as  in  the 
counting-chamber  of  Thoma,  so  that  this  portion  of  the  field  may  be  utilized  for 
counting  red  blood-corpuscles,  making  a  second  counting-chamber  unnecessary. 


THE  COUNTING   OF  BLOOD-CORPUSCLES. 


627 


The  division  of  Turk's  counting-chamber  is  also  very  practical.^  With  this  large 
chamber  a  great  number  of  leukocytes  may  be  rapidly  counted,  and  this  is  some- 
thing which  is  necessaiy  in  the  interest  of  accuracy  (see  below).  After  the  drop 
of  diluted  blood  has  been  placed  upon  the  floor  of  the  counting-chamber,  it  should 
be  examined  wdth  a  low  power,  so  that  the  examiner  may  convince  himself  that 
the  leukocytes  have  been  homogeneously  dis- 
tributed. Just  as  in  counting  erythrocytes,  it  is 
best  to  employ  two  counting-chambers  simultane- 
ously, and  to  be  sure  that  the  leukocytes  are 
present  in  about  the  same  proportions  in  both 
chambers. 

Instead  of  the  ^  per  cent,  acetic  acid  solution, 
we  may  employ  the  same  3  per  cent,  sodium  chlorid 
solution  which  was  mentioned  for  counting  the 
red  cells,  adding  gentian  violet  in  the  proportion 
of  1 :  10,000.  This  will  stain  the  leukocytes,  but 
does  not  dissolve  the  red  cells,  so  that  it  is  not  as 
convenient  nor  as  accurate  as  the  acetic  acid  solu- 
tion. 

Turk  recommends  counting  300  to  1000  leuko- 
cytes.    This  is  very  easy  if  Elzholz's  chamber  is 
used.     Eeinert  found  that  the  probable  error  was  3. 6  per  cent,  one  way  or  the 
other  even  when  4000  cells  were  counted. 

In  pathologic  cases  the  count  should,  if  possible,  be  taken  just  before  a  meal — 
i.  e.,  at  a  time  to  avoid  the  leukocytosis  of  digestion.  The  leukocytosis  of  diges- 
tion is  almost  always  absent  if  very  small  and  frequent  meals  of  fatty  and  starchy 
food  are  taken  (Rieder). 


Fig.  232.— The  divisions  of  Breuer's 
counting-chamber  for  leukocytes. 


NUMBER  OF  RED  AND  WHITE  BLOOD-CORPUSCLES  UNDER 
PHYSIOLOGIC  CONDITIONS. 

The  number  of  red  blood-cells  (Vierordt)  in  1  c.mm.  of  blood  is 
5,000,000  in  man  and  4,500,000  in  women.  In  Switzerland  the 
counts  show  that  healthy  women  have  5,100,000  or  over,  and  men 
about  6,000,000.  These  correspond  very  well  with  the  following 
figures  which  S5rensen  published  to  show  the  variation  in  the  number 
of  blood-corpuscles  at  different  ages  : 

Table. 


Males. 

Females. 

Age. 

Number  of  red 

cells  in  1  c.mm. 

of  blood. 

Age. 

Number  of  red 

cells  in  1  c.mm. 

of  blood. 

Odd 

111 
P  S  X 

Newborn    .... 

Children 

Adults \ 

(Students)      J 

Adults ) 

(Young  physi-  > 
cians;          j 

Adults 

Adults 

5-8  days  | 

5  years! 

19K-22"    1 

25-30"   1 

50-52"    1 
82    " 

5,769,500 
(5,284,500-6,105,000) 

4,950,000 
(4,750,000-5,145,000) 

5,606,000 
(5,422,000-5,784,000) 

5,340,000 
(4,900,000-5,800,000) 

5,137,000 

(4,910,000-5,359,000) 

4,174,700 

}      ^ 

1 

1-14  days  j 

2-10  yrs.  1 

15-28   "     1 

41-61    "      f 
(Nurses)  \ 

5,560,800 
(5,262,500-5,960,000) 

5,120,000 
(4,980,000-5,260,000) 

4,820,000 
(4,417,000-5,350,000) 

5,010,000 
(4,800,000-5,470,000) 

}' 

^  Tiirk,  Vorlesungen  uher  klinische  Hdmalologie,  W.  Bi-aumiiller,  Wien  and  Leipzig, 
1904,  p.  95. 


628  EXAMl^\lTION  OF  THE  BLOOD. 

A  number  of  physiologic  conditions  have  some  influence  upon  the  number  of 
red  blood-cells.  As  to  the  influence  of  food,  the  authorities  differ.  According  to 
the  obsei"V'ations  of  Yierordt  and  Limbeck,  there  is  usually  a  slight  diminution  in 
the  number  of  red  cells  after  eating  or  drinking,  probably  to  be  explained  by  the 
dilution  of  the  blood  due  to  absorption  of  fluid.  On  the  other  hand,  fasting  pro- 
duces a  relative  increase.  Obese  people  average  a  somewhat  lower  red  blood-cell 
count  than  thin  j^eople  (Leichtenstern).  Menstruation  and  pregnancy  seem  to 
have  no  especial  influence  uison  the  number  of  blood-cells.  Cathartics  and  diu- 
retics increase  the  number  of  red  cells  if  their  action  is  ven,"  marked,  possibly  on 
account  of  the  removal  of  water.  A  cold  bath  temporarily  increases  the  number 
of  red  cells.  The  cause  of  this  phenomenon  is  not  known.  The  influence  of 
climates  and  high  altitudes  upon  the  number  of  red  blood-corpuscles  is  interesting. 
According  to  Yiault,  Miescher,  Egger,  Jaquet,  and  others,  the  number  of  red 
blood-cells  is  considerably  increased  in.  altitudes  of  1000  to  2000  meters  above  the 
level  of  the  sea.  This  increase  occui's  within  a  very  short  space  of  time.  In 
Arosa,  Egger  found  that  inside  of  two  weeks  the  number  of  red  blood-corpuscles 
increased  in  newcomers  from  5,000,000  to  6,000,000.  Egger  has  proved  that  this 
increase  is  due  neither  to  diminution  of  the  plasma,  owing  to  the  dry  air  of  the 
high  altitude,  nor  to  a  mere  difference  in  the  distribution.  (See  Miescher's  His- 
tochemic  and  Histologic  "Works,  Leipzig,  1897.)  Gottstein  claimed  that  this 
state  of  affairs  was  an  illusion,  due  to  the  fact  that  the  depth  of  the  counting- 
chamber  was  greater  with  a  low  than  with  a  high  air  pressure;  but  physics 
contradicts  such  an  hypothesis.  Besides,  the  hemoglobin  percentage  increases 
correspondingly. 

The  ratio  of  the  ^vliite  to  the  red  blood-corpuscles  varies  between 
1  :  300  and  1  :  700.  This  wide  range  is  probably  due  to  the  difference 
of  the  ratio  in  individual  cases,  to  the  leukocytosis  of  digestion,  and  to 
the  var\-ing  number  of  red  blood-corpuscles.  Rieder  examined  fasting 
people,  and  found  that  the  ratio  of  the  white  to  the  red  l)lood-cells  in 
healthy  adults  with  a  normal  red  blood-count  is  1  :  651,  and  in  children 
(nine  to  fifteen  years)  1  :  518.  Considering  the  varying  number  of  red 
cells,  these  comparative  figures  are  of  less  value  than  the  absolute  num- 
ber per  cubic  millimeter.  Rieder  found  in  fasting  adults  an  average 
number  of  7680,  and  in  children  9660.  (Compare  p.  646  with  refer- 
ence to  the  increased  number  of  leukocytes  in  the  newborn.) 

NUMBER  OF  RED  BLOOD-CELLS  AND  PERCENTAGE  OF  HEMOGLOBIN 
IN   BLOOD   UNDER   PATHOLOGIC    CONDITIONS, 

(Compare  p.  659  et  seq.) 

All  conditions  included  under  the  title  "  anemia  "  produce  a  more  or 
less  marked  diminution  in  the  number  of  red  blood-cells  and  in  the 
hemoglobin.  Any  acute  or  chronic  illness  may  diminish  both  the  hum- 
l)er  of  blood-cells  and  the  amount  of  hemoglobin,  and  so  produce  an 
anemia.  This  is,  however,  by  no  means  always  the  case.  In  acute 
febrile  infectious  diseases  the  red  blood-corpuscles  and  the  hemoglobin 
are  as  often  increased  as  diminished,  the  increase  being  due  to  the  dimi- 
nution in  the  amount  of  blood-plasma,  the  decrease,  to  the  retention  of 
the  water  and  the  destruction  of  the  red  blood-cells.  Xo  accurate  diag- 
nostic or  prognostic  conclusions  can  as  yet  be  drawn  from  these  condi- 
tions. 

Chronic  cachexia  generally  tends  to  diminish  both  the  amount  of 


THE  COUNTING   OF  BLOOD-CORPUSCLES.  629 

hemoglobin  and  the  number  of  red  cells.  In  the  cachexia  of  cancer  the 
anemia  may  be  very  marked  and  diagnostically  important.  Whenever 
a  marked  anemia  accompanies  cancer,  the  growth  has  almost  always 
caused  a  loss  of  blood.  This  loss  may  be  very  gradual  and  not  noticed 
at  the  time  (carcinoma  of  the  stomach  and  intestines).  The  blood  of 
tuberculous  patients  shows  at  times  a  diminished  quantity  of  hemoglobin 
and  a  smaller  number  of  red  blood-corpuscles.  This  is,  however,  by  no 
means  the  rule.  Many  tuberculous  patients  with  marked  pallor  and 
cachexia  frequently  show  a  normal  blood.  Neurasthenic  patients  rarely 
show  a  diminution  in  the  coloring  matter  of  the  blood.  Determining 
the  amount  of  hemoglobin  in  these  cases  is  of  great  value  with  refer- 
ence to  the  treatment,  as  we  have  repeatedly  Emphasized,  for  a  pale 
appearance  is  often  deceptive.  (See  section  on  the  Color  of  the  Skin, 
and  p.  662,  on  Secondary  Anemia.) 

In  venous  congestion  both  the  hemoglobin  and  the  number  of  blood- 
cells  are  increased.  This  is  a  purely  mechanical  result,  due  to  the  slowing 
of  the  blood-stream,  which  leaves  the  blood-cells  in  the  capillaries.  This 
condition  does  not  exclude  an  increase  in  the  amount  of  water  contained 
in  the  blood-plasma,  nor  hydremic  plethora.^ 

The  Hemoglobin  Quotient  or  Hemoglobin  Value  of  the  Red  Blood-corpuscles  {the 
So-called  Blood-corpuscle  Quotient  or  Value). — If  the  quantity  of  hemoglobin  and  the 
number  of  blood-cells  in  any  given  disease  are  expressed  in  percentages  of  the 
normal,  and  the  percentage  of  hemoglobin  is  divided  by  the  percentage  of  the 
number  of  red  cells,  a  fraction  is  obtained  which,  as  will  readily  be  seen,  indicates 
how  much  hemoglobin  any  one  blood-cell  contains,  as  compared  with  the  normal 
amount.  This  fraction  is  called  the  color  index,  the  blood-corpuscle  quotient  or 
value.  In  order  to  avoid  confusion  with  the  volume  quotient  described  on  p.  639, 
the  author  would  suggest  using  "hemoglobin  quotient"  or  "hemoglobin  value."  _ 
Normally  this  equals  1,  but  in  certain  anemias  it  sometimes  exceeds  1  (pernicious 
anemia),  or  is  less  than  1  (chlorosis) — e.  g., 

Hgb.         =  45  per  cent. 
Eed  cells  =  2,000,000  (40  per  cent.). 
C.I.         =|§  =  1.1+. 
or,  Hgb.         =  40  per  cent, 

Eed  cells  =  4,000,000  (80  per  cent.). 
C.  I.         =|-§  =  0.5. 

VOLUME  OF  BLOOD-CORPUSCLES  CONTAINED   IN  A  GIVEN 
QUANTITY   OF  BLOOD;    HEMATOCRIT. 

An  attempt  has  recently  been  made  to  supplant  the  counting  of  blood-cor- 
puscles by  estimating  the  volume  which  they  occupy  as  compared  with  that  of  the 
plasma.  The  method  recommended  by  Blix-Hedin,  and  modified  by  Gartner, 
consists  in  first  adding  a  definite  amount  of  a  solution  to  a  certain  amount  of  blood 
in  order  to  preserve  the  corpuscles  and  prevent  coagulation  (Miiller's  fluid),  and 
then  centrifuging  in  a  graduated  capillary  tube  closed  at  one  end.  This  is  known 
as  a  hematocrit.  The  specimen  is  centrifuged  about  five  minutes,  until  the 
blood-corpuscles  are  packed  into  the  end  of  the  capillary  tube,  so  that  their  volume 
can  no  longer  be  diminished  by  further  centrifuging.  The  red  blood-corpuscles 
form  a  red  layer  at  the  bottom  of  the  capillary  tube,  and  above  them  comes  a 
white  layer  of  leukocytes.     The  method  is  easy,  but  cannot  take  the  place  of 

^  See  K.  BaranofF,  Beitrage  zur  Theorie  der  Flussigkeitsentziehtmg  und  der  Behandlung 
der  Circulaiionssiorungen,  J.  A.  D.,  Bern,  1895. 


630  EXAMINATION  OF  THE  BLOOD. 

counting  the  blood-corpuscles,  as  was  first  thought,  because  there  are  several 
sources  of  error.  For  a  detailed  description  of  the  hematocrit,  we  refer  to  the 
original  communication  of  Blix-Hedin^  and  Gartner. '■' 

According  to  Capps,^  more  accurate  results  are  obtained  with  the  hematocrit 
if  pure  blood  is  used  without  any  diluting  fluid.  In  this  case,  however,  the  work 
must  be  done  very  rapidly  to  avoid  coagulation,  and  the  centrifuge  must  be  a 
powerful  one,  propelled  preferably  by  electricity.  The  investigations  in  reference 
to  the  volume  quotient  of  the  erythrocytes,  described  upon  p.  639,  were  carried 
out  by  this  method,  and  demonstrated  that,  in  view  of  the  variations  in  size  of  the 
erythrocytes,  the  hematocrit  can  never  replace  the  actual  count  of  the  latter,  but 
that  it  may  give  valuable  information  when  they  are  of  the  average  size. 

POWER  OF  RESISTANCE  OF  THE  ERYTHROCYTES  TO 
HYPOSMOTIC   INJURY. 

It  is  well  known  that  when  a  small  amount  of  blood  is  placed  in  an  excessive 
quantity  of  a  hypotonic  saline  solution,  the  blood-pigment  passes  out  of  the 
erythrocytes,  so  that  a  so-called  laked  blood  results.  In  such  experiments  the 
stromata  of  the  erythrocytes  are  not  dissolved.  In  saline  solutions  which  are 
isotonic  or  hypertonic  to  the  blood-plasma,  the  blood-pigment  does  not  pass  out,  at 
least  not  within  a  limited  period  of  time.  For  this  reason  it  was  formerly  believed 
that  the  osmotic  pressure  of  the  blood-plasma  could  be  determined  by  finding  the 
concentration  of  the  saline  solution  which  would  preserve  the  erythrocytes  intact. 
It  has  nevertheless  been  shown  that  the  escape  of  the  hemoglobin  from  the 
erythrocytes  under  these  conditions  is  by  no  means  a  pure  osmotic  phenomenon, 
but  that  it  is  also  dependent  upon  the  specific  sensibility  of  the  cortical  layer  of 
the  erythrocyte,  which  holds  the  hemoglobin  within  the  corpuscle.  This  has  been 
absolutely  proved  by  the  observation  that  all  of  the  erythrocytes  of  an  individual 
are  not  equally  sensitive  to  the  same  hypotonic  solution.  In  a  slightly  hypotonic 
saline  solution,  the  osmotic  concentration  of  which  closely  approximates  that  of 
the  blood,  a  number  of  erythrocytes  are  destroyed  by  the  escape  of  their  hemo- 
globin, while  others  do  not  lose  their  pigment  until  the  saline  solution  is  much 
more  markedly  diluted.  This  could  not  be  the  case  were  the  phenomenon  purely 
osmotic  in  character.  For  this  reason  we  are  no  longer  justified  in  assuming  that 
the  osmotic  concentration  of  the  blood-plasma  may  be  indirectly  obtained  by 
determining  the  resistance  of  the  erythrocytes  to  saline  solutions  of  varying  con- 
centration. This  false  idea  is  also  responsible  for  the  incorrect  supposition  that  a 
saline  solution  of  0. 6  or  even  0. 7  per  cent,  is  physiologic — i.  e. ,  isotonic  with  the 
blood-plasma — when  as  a  matter  of  fact  the  direct  determination  of  the  osmotic 
pressure  of  the  blood  by  means  of  cryoscopy  (see  p.  667)  has  shown  that  a  0.9  per 
cent,  saline  solution  is  isotonic  with  human  blood. 

The  above  facts  should  be  borne  in  mind  in  utilizing  Limbeck's*  modification 
of  Hamburger' s  '"  method  for  determining  the  resistance  of  the  erythrocytes  to 
hypotonic  saline  solutions.  Limbeck's  modification  is  as  follows:  One  cubic 
centimeter  of  a  sodium  chlorid  solution  of  varying  concentration  is  placed  in  each 
of  a  series  of  16  small  glasses.  The  weakest  is  0.4  per  cent.,  and  the  concentra- 
tion increases  from  one  glass  to  the  next  by  0. 03  per  cent. ,  so  that  the  series  varies 
from  0. 4  to  0.85  per  cent.  A  small  amount  of  blood  is  taken  from  a  punctured 
wound  of  the  finger  by  means  of  a  glass  rod,  and  placed  in  each  glass  of  the 
series.  The  blood  is  well  mixed  with  the  saline  solution  and  allowed  to  stand  for 
six  hours.  After  the  lapse  of  this  period  of  time  the  mixtures  are  inspected,  to 
determine  Avhich  solution  has  preserved  the  blood  without  extracting  its  pigment. 
The  lower  the  concentration  of  the  saline  solution  fulfilling  this  requirement,  the 
greater  will  be  the  resistance  of  the  erythrocytes. 

1  Skandin.  Arch.f.  Physiol,  1890,  p.  134.  ^  AUg.  Wien.  med.  Zeit.,  1892. 

3  Jour.  Med.  Research,  vol.  x..  No.  3,  1903. 
*  Grundriss  der  klin.  Pathologie  des  Blutes,  Jena,  Fischer,  1896. 

5  Arch,  der  Physiol.,  von  Du  Bois  Reymond,  1886,  p.  476 ;  1887,  p.  31,  Zeits.  f.  Biol., 
26,  neue  Folge,  viii.,  p.  414. 


OTHER  MORPHOLOGIC  RELATIONS  OF  THE  BLOOD.         631 

Tliis  method  is  open  to  a  number  of  objections,  however,  in  reference  to  which 
the  reader  is  referred  to  the  monograph  of  G.  Lang. '  The  chief  difficulty  depends 
upon  the  different  degrees  of  resistance  exhibited  by  the  individual  corpuscles  of 
the  same  patient.  Lang's  monograph  gives  a  number  of  methods  proposed  by 
Janowski  for  the  purpose  of  avoiding  these  difficulties. 

In  carcinoma  and  icterus  it  has  been  observed  that  the  erythrocytes  exhibit  a 
most  marked  degree  of  resistance  to  hyposmotic  saline  solutions. 

The  determination  of  the  power  of  resistance  of  the  erythrocytes  to  hyposmotic 
injury  is  not  sufficient  to  settle  all  of  the  questions  in  reference  to  their  resisting 
power,  since  Chvostek  ^  found  that  in  paroxysmal  hemoglobinuria  the  power  of 
resistance  of  the  erythrocytes  to  saline  solutions  was  normal,  while  they  showed 
but  slight  resistance  to  mechanical  injury  (shaking)  and  to  stasis  within  the  body. 

OTHER    MORPHOLOGIC    RELATIONS    OF    THE  BLOOD. 

TECHNIC  OF   THE   MICROSCOPIC  EXAMINATION  OF  THE  BLOOD. 

For  this  purpose  either  fresh  or  stained  dried  preparations  may  be 
employed. 

MICROSCOPICAL  EXAMINATION  OF  FRESH  BLOOD. 

The  most  important  alterations  in  the  blood  which  are  peculiar 
to  diseases  of  the  blood  proper  may  be  recognized  in  fresh  speci- 
mens. Certain  precautious  should  be  taken  in  preparing  the  latter. 
Too  much  pressure  applied  near  the  puncture  to  increase  the  flow  may 
deform  the  red  blood-corpuscles.  A  scrupulously  clean  cover-slip 
should  be  very  gently  touched  to  the  drop  of  blood,  so  that  only  a  very 
tiny  amount  of  blood  adheres.  Too  large  a  drop  makes  too  thick  a 
preparation  and  too  pronounced  a  rouleaux  formation,  so  that  the  finer 
details  cannot  be  detected.  The  cover-slip  is  immediately  dropped  very 
carefully  upon  a  clean  slide.  Pressure,  pulling,  or  sliding  the  cover- 
slip  should  be  avoided.  Unless  these  precautions  are  observed,  a  most 
beautiful  micro-  or  poikilocytosis  (compare  below)  may  be  artificially 
produced.  The  blood  should  be  distributed  under  the  cover-slip  in  a 
uniformly  thin  layer,  but  this  effect  must  be  produced  entirely  by  capil- 
lary action.  The  preparation  should  be  examined  immediately,  because 
the  blood-corpuscles  soon  begin  to  shrink  from  loss  of  water,  and  assume 
all  sorts  of  bizarre  shapes. 

PREPARATION  AND  STAINING  OF  DRIED  SPECIMENS. 

The  staining  of  the  histologic  elements  of  the  blood  is  almost  exclu- 
sively confined  to  dry  preparations.  These  stained  specimens  give  infor- 
mation in  regard  to  the  granulation  of  the  leukocyte  protoplasm  discov- 
ered by  Ehrlich,  as  well  as  to  the  coarser  morphologic  conditions  and 
staining  propensities  of  the  nuclei  and  of  the  protoplasm  of  all  the  blood- 
cells.  Ehrlich,  by  a  careful  study  of  the  staining  peculiarities  of  the 
granulations  with  various  anilin  colors,  has  found  that  with  given  mix- 
tures of  anilin  dyes  they  possess  elective  aflinities  and  stain  differently. 
He  classifies  the  available  anilin  dyes,  which  are  chemical  salts,  into  an 

^  Zeits.f.  klin.  Med.,  vol.  xlvii.,  parts  1  and  2,  1902. 

*  Ueber  das  Wesen  der  paroxysmalen  Hdmoglobinurie,  Wien,  F.  Deuticke,  1894. 


632  EXAMINATION   OF  THE  BLOOD, 

acid  group,  in  which  the  acid  radicle,  and  a  basic  group,  in  which  the 
basic  radicle,  determines  the  staining  property  of  the  dye,  and  further 
into  a  neutral  group,  in  which  both  radicles  possess  staining  properties. 
Eosin  and  add  fuchsin  are  types  of  acid  stains,  methylene-hlue  and 
-green  of  basic  stains,  and  rosanilin  and  picric  acid,  of  neutral  stains. 

He  found  that  certain  granulations  in  the  white  blood-corpuscles 
stained  only  with  acid,  others  only  with  basic  stains ;  a  third  group 
could  be  stained  with  both  dyes,  and  a  fourth  by  neutral  pigments  only. 
On  the  strength  of  this  he  distinguishes  (a)  oxyphilic,  (/J)  amphophilic, 
(r  and  o)  basophilic,  (e)  neutrophilic  granulations.  The  difference 
between  y  and  o  is  chiefly  in  the  size  of  the  granules.  The  (y)  granules 
are  the  so-called  mast-cell  granules  ;  they  are  basophilic  and  larger  than 
all  the  others.  According  to  Ehrlich,  each  leukocyte  contains  only  one 
kind  of  granule.     The  /3  and  o  varieties  are  not  found  in  human  blood. 

The  following  rules  should  be  followed  in  preparing  dry  specimens  : 
Very  thin  cover-slips  (less  than  0.1  mm.)  should  be  cleansed  with  the 
utmost  care.  Fat  can  be  removed  with  a  mixture  of  ether  and  alcohol 
and  a  soft  linen  cloth  without  shreds.^  In  subsequent  manipulations 
the  cover-slips  should  be  touched  only  with  dry  finger-tips  or  with 
forceps,  and  best  at  the  corner.  A  very  minute  drop  of  freshly  removed 
blood  from  the  tip  of  a  finger  or  the  lobe  of  the  ear  is  touched  to  a 
cover-slip,  and  a  second  slide  laid  on  top  of  this  without  pressure. 
Within  a  few  minutes,  by  capillary  action,  the  blood  will  spread  out 
between  the  cover-slips  in  a,  uniform  layer  ;  then,  without  exerting  any 
pressure,  the  slips  can  be  slid  rapidly  apart  and  dried  in  the  air. 

Fixing  or  hardening  of  the  dry  preparation  can  be  accomplished  by 
drying  in  the  air,  or,  according  to  Erhlich's  original  method,  by  heating 
in  an  incubator  at  110°  to  120°  C.  for  several  minutes  up  to  an  hour, 
according  to  the  stain  used.  A  simpler  method  later  recommended  by 
Ehrlich  is  to  place  a  copper  plate  horizontally  upon  a  stand,  and  to  heat 
one  end  with  a  flame.  After  a  short  time  each  individual  portion  of 
the  plate  will  remain  at  a  uniform  temperature,  the  part  nearest  the 
flame  hottest,  the  more  distant  portions  less  so.  The  spot  upon  the 
plate  is  determined  where  a  drop  of  oil  of  toluol  no  longer  boils,  but 
presents  Leidenfrosfs  phenomenon.^  The  cover-glass,  after  being  dried 
in  the  air,  is  placed  at  this  spot.  The  temperature  is  about  111°  C. 
(with  barometer  760  mm.).  It  should  remain  here  from  one-half  to 
one  minute  if  ordinary  stains  (hematoxylin,  eosin,  triacid)  are  to  be 
used.  With  many  other  stains  the  cover-slip  must  be  left  there  longer 
or  a  higher  temperature  employed. 

Rubinstein  ^  recommends  more  intense  heat  even  for  the  triple  stain. 
For  this  purpose  he  places  the  cover-slip  face  down  at  a  spot  on  the 
copper  plate  where  a  drop  of  water  still  shows  Leidenfrosfs  phenomenon, 

[1  Soap  and  hot  water  and  careful  rubbing  with  a  soft  linen  cloth  will  cleanse  them 
thoroughly.  Occasionally  it  may  be  necessary  to  wash  new  cover-slips  in  strong  acid  to 
remove  the  glaze. — Ed.] 

^  The  drop  runs  around  without  wetting  the  copper. 

^  Zeits.  f.  wissensch.  Mikroskopie,  vol.  xiv.,  1897,  p.  456. 


OTHER  MORPHOLOGIC  RELATIONS  OF  THE  BLOOD.         633 

and  in  such  a  way  that  a  corner  of  the  glass  reaches  over  toward  the 
cooler  end  of  the  plate. 

Preparations  may  also  be  fixed  by  immersing  them  for  five  minutes 
in  absolute  alcohol,  or  by  boiling  them  in  it  for  one  minute,  or  by 
immersing  them  in  a  1  per  cent,  solution  of  formalin  for  about  one 
minute.  After  fixation  the  specimen  may  be  stained  immediately  or 
later. 

A  simple  method  which  usually  suffices  for  recognizing  the  coarser 
relations  consists  in  immersing  the  specimen  in  a  saturated  solution  of 
eosin  in  5  per  cent,  carbolglycerin  for  several  hours  (Rieder).  The 
color  is  then  washed  off  with  water,  and  it  is  counterstained  for  a 
minute  with  50  per  cent.  Delafield's  hematoxylin.^  After  repeated 
washings,  the  preparation  is  dried  in  the  air  and  mounted  in  Canada  bal- 
sam. The  red  blood-corpuscles  and  eosinophilic  granules  are  stained 
red,  nuclei  and  cell  membranes  dark  blue,  and  the  protoplasm  of  the 
white  cells  violet  or  reddish  (see  Plate  8,  Figs.  4  and  5). 

To  recognize  tlie  finer  details  of  the  nuclear  structure,  and  especially  of  the 
mitoses,  Rieder  recommends  that  blood-films  be  first  fixed,  and  then  immersed  in 
a  saturated  aqueous  solution  of  picric  acid.  They  should  then  be  washed  for  one 
or  two  days  in  running  water,  and  stained  several  hours  with  a  very  dilute  Dela- 
field  hematoxylin  ;  then  washed  in  water_  again,  and  finally  in  water  containing 
hydrochloric  acid,  dried  in  the  air,  and  mounted  in  Canada  balsam. 

Ehrlich's  triple  stain  is  usually-  employed  when  examining  for  Ehrlich's 
granules.     This  is  prepared  in  the  following  way  : 

Saturated  aqueous  solution  of  orange-G.,  120  to  125  c.c;  saturated  aqueous 
solution  of  acid  fuchsin,  80  to  165  c.c;  saturated  aqueous  solution  of  methylene- 
green,  125  c.c;  water,  300  c.c;  absolute  alcohol,  200  c.c;  glycerin,  100  c.c 

Fixed  dry  preparations  are  immersed  in  this  solution  for  two  minutes,  washed 
in  water,  and  then  dried  and  mounted.  The  neutrophilic  granules  are  most  dis- 
tinctly stained.  The  hemoglobin  is  orange-colored,  the  nuclei  green,  the  neutro- 
philic granules  violet,  the  eosinophilic  granules  copper-colored,  and  the  basophilic 
granules  indistinctly  stained. 

Excellent  results  are  also  obtained  by  the  use  of  Jenner's  stain,^  which  con- 
tains eosin  and  methylene-blue,  probably  as  a  chemical  combination,  in  solution 
in  methyl  alcohol.  This  stain  is  prepared  with  difiiculty,  but  may  be  obtained 
from  Dr.  Griibler,  Bayrische  Strasse,  Leipzig,  or  of  still  better  quality  from  Baird 
and  Tatlock,^  Cross  St.,  Hatton  Gardens  14,  London.  The  great  advantage  of 
this  method  is  that  the  specimen  does  not  require  a  previous  fixation,  since  the 
methyl  alcohol  in  the  solution  fixes  the  blood  while  it  is  being  stained.  The 
specimens  are  almost  as  good  as  those  obtained  by  the  use  of  the  tri-acid  stain, 
and  successful  results  are  much  more  readily  attained.  The  illustrations  upon 
Plate  6,  are  from  specimens  stained  by  Jenner's  method.  According  to  May 
and  Griinwald,  it  is  important  to  wash  specimens  stained  in  this  manner  with  dis- 
tilled and  not  with  hydrant  water. 

Chenzinsky's  eosin-methylene-blue  solution  is  to  be  recommended  for  cer- 
tain purposes.     Forty  cubic  centimeters  of  concentrated  aqueous  methylene-blue 

^  Two  solutions :  (a)  1  gm.  of  a  crystalline  hematoxylin  dissolved  in  6  c.c.  of  abso- 
lute alcohol;  {h)  15  gm.  of  ammoniate  of  alum  dissolved  in  100  c.c.  of  distilled  water, 
and  filtered  after  cooling.  These  solutions  are  mixed  in  an  open  dish,  and  exposed  to 
light  three  days.  The  mixture  is  then  filtered,  and  mixed  with  25  c.c.  of  pure  glycerin 
and  25  c.c.  of  methyl  alcohol.  After  three  days  this  mixture  is  filtered  and  kept  in 
stock.  -^  Lancet,  1899,  p.  370. 

*  [A  very  good  preparation  can  be  obtained  from  Dougherty,  West  Fifty-ninth 
Street,  or  from  Eiraer  &  Amend,  Third  Avenue  and  Eighteenth  Street,  New  York 
City.— Ed.] 


634  EXAMINATION  OF  THE  BLOOD. 

solution,  20  c.c.  of  ^  per.  cent,  eosin  solution  in  70  per  cent,  alcohol,  and  40  c.c. 
of  distilled  water  are  mixed.  This  mixture  should  always  be  filtered  before 
using.  Six  to  twenty-four  hours  in  an  incubator  are  necessary  for  staining.  The 
nuclei,  the  mast-cell  granules,  and  the  basophilic  granules  of  red  blood-corpuscles 
appear  intensely  blue,  malaria  plasmodia  sky  blue,  the  red  blood-corpuscles  and 
eosinophilic  granules  red. 

Willebrandt's  Method.' — Willebrandt  claims  that  all  the  granules  of  human 
blood  may  be  very  well  seen  after  staining  with  a  solution  of  methylene-blue  and 
eosin.  A  solution  is  prepared  in  the  following  way:  One-half  per  cent,  of  eosin 
in  70  per  cent,  alcohol  is  mixed  with  an  equal  quantity  of  concentrated  aqueous 
solution  of  methylene-blue.  Willebrandt  describes  the  peculiarities  of  this  solu- 
tion as  follows  : 

The  fluid  usually  stains  the  preparation  diffusely  blue,  on  account  of  the  pre- 
ponderance of  methylene-blue.  If,  however,  dilute  acetic  acid  (1  per  cent.)  is 
added  drop  by  drop — usually  10  or  15  drops  to  50  c.c.  of  solution — the  eosin  will 
gradually  acquire  an  increased  staining  power  until  it  becomes  quite  efficient. 
After  experimenting  a  little,  it  is  always  possible  to  prepare  a  solution  that  stains 
well  and  gives  a  characteristic  picture.  The  solution  should  always  be  filtered 
before  using.  The  blood-preparation  should  always  be  carefully  fixed,  otherwise 
the  stain  will  not  be  successfiil.  The  staining  requires  five  to  ten  minutes  with 
repeated  heating  until  steam  is  given  off".  The  specimen  is  then  washed  in  water 
without  any  other  decoloration.  The  stain  from  this  method  is  very  instructive. 
The  red  blood-corpuscles  appear  red,  the  nuclei  dark  blue  and  sharply  outlined, 
the  neutrophilic  granules  of  the  mast  cells  intensely  violet.  This  method  has  the 
advantage  of  staining  all  the  granules  and  the  nuclei  at  the  same  time. 

In  staining  for  special  granules,  the  eosin  hematoxylin  stains  eosinophilic 
granules  very  well,  while  a  saturated  aqueous  solution  of  methylene-blue  is  best 
adapted  for  basic  granules  (stain  for  several  minutes),  and  the  neutrophilic  gran- 
ules are  best  stained  with  Ehrlich's  triple  stain. 

Ehrlich's  directions  are  the  best  for  demonstrating  microscopic  iodin  reac- 
tion of  the  blood.  The  dried  blood-film  (which  must,  however,  not  be  heated)  is 
immersed  in  a  solution  of  iodin  and  gum  arable  (iodin  1,  potassic  iodin  3,  water 
50,  and  enough  gum  arable  to  render  the  fluid  thick).  Ehrlich^  has  since 
announced  that  it  is  an  advantage  to  substitute  iodin  itself  for  the  solution  of 
iodin.  This  is  done  by  placing  the  preparations  dried  in  the  air  under  a  closed 
glass  containing  crystals  of  iodin,  for  several  minutes,  until  the  color  is  dark 
brown.  The  preparation  should  then  be  examined  in  a  saturated  syrupy  solution 
of  levulose  ;  and  to  preserve  it,  should  be  surrounded  with  varnish.  The  color  of 
the  leukocytes  varies  in  individual  cases.  The  red  blood-cells  are  stained  diffusely 
brown,  although  this,  at  present  at  least,  has  no  special  interest.  Zollikofer 
has  established  the  following  facts  with  regard  to  the  leukocytes.^  Under 
physiologic  conditions,  brown-stained  protoplasmic  granules  are  found  most  fre- 
quently in  lymphocytes,  oftentimes  in  mast  cells,  and  exceptionally  in  the  large 
mononuclear  cells  ;  the  polynuclear  neutrophilic  cells  are  faintly  stained  brown. 
If  the  last-mentioned  cells  show  distinct  deposits  of  brown-stained  granules  and 
flakes,  it  is  considered  pathologic.  This  condition  is  the  one  which  authors  have 
paid  most  attention  to  up  to  the  present  time.  It  is  ordinarily  spoken  of  as 
the  iodin  reaction  of  the  leukocytes  or  the  intracellular  iodin  reaction  of  the  blood. 
Zollikofer' s  brown  granules  are  very  rarely  found  in  eosinophiles,  and  then  under 
conditions  which  are  not  understood  or  defined.  They  are  never  found  in  the 
neutrophilic  mononuclear  cells  (myelocytes).  Ehrlich*  has  also  described  a 
so-called  extracellular  reaction,  in  which  stained  brown  granular  masses  are 
found  outside  of  the  leukocytes,  Gabritschewski  ^  and  Zollikofer  have  shown, 
however,  that   these   formations  are  blood-plates,   which   under   conditions   not 

1  DeuUch.  med.  Woch.,  1901,  No.  4,  p.  57. 

*  Ehrlich  and  Lazarus,  "  Die  Aniimie,"  Nothnagel's  Sp.  Path,  and  Therap.,  1898. 
^  Zur  lodreaction  der  Leukocyten,  J.  A.  D.,  Bern,  1899. 

*  Zeits.  f.  klin.  Med.,  1883,  vol.  vi.         ''  Arch.  f.  exp.  Path.  u.  Pharm.,  1891,  vol.  xxviii 


OTHER  MORPHOLOGIC  RELATIONS  OF  THE  BLOOD.         635 

definitely  known  give  the  iodin  reaction,  at  times  in  normal  blood,  at  times  under 
pathologic  conditions,  especially  in  diabetes  mellitus.  This  reaction  does  not 
necessarily  accompany  the  intracellular  reaction. 

This  brown-staining  substance  is  generally  supposed  (and  by  Ehrlich,  too)  to 
be  crlycogen.  But  Czerny,i  Kamminer,^  and  especially  Zollikofer,  discredit  this 
theory.  Very  likely  it  is  related  to  amyloid.  Under  certain  conditions  it  is 
stained  violet  and  not  brown  by  iodin,  which  favors  this  latter  view. 

The  pathologic  iodin  reaction,  at  present  at  least,  applies  only  to  the  appear- 
ance of  brown-stained  granules  in  the  polynuclear  neutrophiles.  Very  little  can 
be  said  as  yet  in  regard  to  the  clinical  importance  of  this  "iodin  reaction."  It 
is  almost  always  present  with  leukocytosis,  especially  in  purulent  conditions,  but 
not,  for  instance,  in  erysipelas. 

According  to  the  investigations  of  Zollikofer  in  the  Bern  Clinic,  the  presence 
of  this  reaction— e.  g.,  in  appendicitis— does  not  always  prove  the  presence  of 
pus  neither  does  its  absence  exclude  the  presence  of  pus.  About  the  same  results 
were  observed  in  cases  which  recovered  spontaneously  and  m  those  which  came 
to  operation.  No  definite  conclusions  can  be  drawn  from  the  absence  or  presence 
of  the  iodin  reaction  in  diabetes  mellitus,  although  several  observations  of  Zolli- 
kofer's  would  seem  to  indicate  that  a  diminution  of  diabetic  acidosis  is  associated 
with  diminution  of  the  reaction.  It  was  thought  that  the  reaction  might  possibly 
be  used  in  the  diagnosis  of  amyloid  degeneration,  an  opinion  based  upon  the 
chemical  nature  of  the  brown-staining  substance,  and  upon  the  observations  ot 
Czerny  relative  to  the  presence  of  the  iodin  reaction  in  artificially  produced  amy- 
loid degeneration  ;  but  observations  in  the  author's  clinic  have  disproved  this. 
Zollikofer  found  that  if  iodin  vapor  acted  upon  moist  preparations,  the  reaction 
was  considerably  increased,  so  that  even  in  normal  blood  fine  brown  granules 
appeared  in  the  neutrophilic  leukocytes,  instead  of  the  diffused  light-brown  stam. 
The  absence  of  these  normal  granules  in  the  dry  specimens  treated  with  lodin  is 
due,  according  to  Zollikofer,  to  the  disintegration  of  the  granules  m  the  interior 
of  the  cells  during  the  process  of  drying. 

Examination  of  the  Blood  in  Reference  to  the  Formation  of  Rouleaux. 
Under  normal  conditions,  in  fresh  microscopic  blood-specimens  which 
are  not  too  thin,  we  find  the  red  blood-corpuscles,  as  a  result  of  their 
peculiar  disk-like  shape  and  the  viscosity  of  the  blood,  standing  upon 
their  edges  and  arranged  in  cylindric  conglomerations  which  have  been 
compared  to  a  roll  of  coins.  This  formation  occurs  in  the  circulation 
only  when  the  blood  stagnates,  but  it  normally  occurs  quite  rapidly  (in 
a  few  seconds)  outside  of  the  body.  This  process  is  known  as  the 
formation  of  rouleaux.  It  will  easily  be  understood  that  the  formation 
of  rouleaux  must  be  influenced  by  the  number  of  the  red  blood-corpus- 
cles. We  consequently  find  a  diminished  formation  of  rouleaux  in  all 
conditions  which  are  associated  with  a  diminution  in  the  number  of  the 
red  blood-corpuscles,  and  wdth  a  properly  made  specimen  the  dimin- 
ished tendency  to  form  rouleaux  may  be  made  the  basis  of  a  probable 
diagnosis  of  a  decreased  number  of  red  blood-cells.  By  a  properly 
prepared  specimen  we  mean  one  having  a  sufficient  thickness  to  allow 
the  erythrocytes  to  stand  upon  their  edges.  If  the  preparation  be  too 
thin,  the  erythrocytes  are  flattened  out  by  the  cover-glass  and  cannot 
adhere  to  each  other  by  their  flat  surfaces.  When  a  specimen  of  proper 
thickness  is  immediately  examined,  individual  erythrocytes  should  be 

^  Arch.  f.  exp.  Path.  u.  Pharin.,  vol.  xxxi. 
2  Deutsch.  med.  Woch.,  1899,  vol.  xv. 


636  EXAMINATION  OF  THE  BLOOD. 

visible  standing  upon  their  edges.  In  order  to  obtain  a  layer  of  blood 
of  the  requisite  depth,  we  should  vary  the  size  of  the  drop  of  blood 
upon  the  slide  and  avoid  exerting  any  pressure  upon  the  cover-glass. 
The  specimen  should  not  be  too  thick,  since  this  interferes  not  only  with 
the  formation  of  rouleaux,  but  also  with  their  recognition.  Poikilocytosis, 
as  well  as  a  diminished  number  of  erythrocytes,  naturally  tends  to  pre- 
vent the  formation  of  rouleaux.  From  our  investigations  up  to  this 
time  we  cannot  say  whether  the  formation  of  rouleaux  is  disturbed  by 
a  diminished  viscosity  of  the  blood. 

Microscopic  Determination  of  the  Amount  of  Fibrin  in  the  Blood. 

In  addition  to  the  quantitative  estimation  of  the  separated  and  puri- 
fied fibrin  from  a  given  quantity  of  blood,^  the  microscopic  examination 
of  a  fresh  blood-specimen  may  sometimes  give  a  fair  idea  of  the  amount 
of  contained  fibrin.  If  a  fresh  blood-specimen  be  protected  against 
drying  by  smearing  the  edges  of  the  cover-glass  with  paraffin,  and 
allowed  to  stand  for  a  quarter  or  a  half-hour,  the  separated  fibrin  may 
be  recognized  by  strong  magnification  in  the  shape  of  a  fine  network 
more  or  less  distinctly  spread  out  between  the  red  blood-corpuscles. 
In  order  to  form  a  conception  of  the  quantity  of  fibrin  present,  the 
thickness  of  the  specimen  must  be  considered,  since,  other  things 
being  equal,  the  thicker  the  specimen,  the  more  marked  will  be 
the  fibrin  network.  If  the  specimen  be  very  thin,  the  fibrin  network 
may  entirely  escape  observation.  A  place  in  the  specimen  should 
consequently  be  selected  which  fulfils  the  requirements  laid  down  for 
the  examination  of  the  blood  for  rouleaux  (p.  635) — i.  e.,  immediate 
observation  should  reveal  isolated  red  blood-cells  standing  upon  their 
edges,  and,  subsequently,  distinct  spaces  should  be  seen  between  well- 
formed  rouleaux.  When  the  blood  is  rich  in  fibrin,  as  in  inflammatory 
affections  and  particulary  in  pneumonia,  the  spaces  between  the  rou- 
leaux are  entirely  filled  by  a  thick  fibrin  network ;  while  if  the  blood 
contain  but  little  fibrin,  it  is  concentrated  about  the  collections  of  blood- 
platelets,  in  the  shape  of  poorly  formed  stars.  In  general  the  quantity 
of  fibrin  in  the  blood  goes  hand  in  hand  with  the  degree  of  leukocy- 
tosis ;  and  in  leukopenic  diseases,  such  as  typhoid  fever,  a  pronounced 
diminution  of  the  amount  of  fibrin  is  consequently  not  without  diag- 
nostic importance. 

MICROSCOPIC  APPEARANCE  OF  ERYTHROCYTES. 

(Poikilocytosis ;  Staining  Capacity  of  the  Red  Blood-cells ;  Polychromatophilic  Changes ; 
Granular  Basophilic  Degeneration.) 

The  red  cells  or  erythrocytes  are  normally  biconcave  disks.  Under 
pathologic  conditions,  however,  they  may  present  very  abnormal  shapes, 
a  condition  which  has  been  called  by  Quincke  poikilocytosis.  Poikilo- 
cytes  may  assume  any  shape  (compare    Fig.    233).     Their  size,  too, 

^  After  washing  the  clot  with  chloroform  water,  alcohol,  and  ether,  the  quantitative 
estimation  may  be  made  either  by  weighing  or  by  Kjeldahl's  method. 


been  considered  to  be  the  result  of  drying.     The  blood- 


ance,   which,   according  to  Maragliano,    has  jncorrectly        n 
corpuscles  gradually  become  more   and  more  deformed        r\     f^   \> 


OTHER  MORPHOLOGIC  RELATIONS  OF  THE  BLOOD.         637 

may  vary  considerably.  Poikilocytosis  is  observed  in  all  cases  o^  grave 
anemia,  especially  in  pernicious  types,  in  leukemia,  in  the  cachexia  of 
carcinoma  of  the  stomach,  and  rarely  in  the  innocent  types  of  anemia, 
such  as  chlorosis. 

Maragliano  considers  these  degenerative  types  of  red  blood-cells.  Thus,  if 
normal  blood  is  examined  under  a  cover-glass  at  the  temperature  of  about  26°  to 
27°  C,  a  number  of  progressive  changes  occur  in  the  corpuscles,  and  these  same 
changes  are  found  in  the  fresh  blood  under  pathologic  conditions.  After  thirty  to 
seventy  minutes  the  so-called  endoglobular  changes  occur..  A  colorless  region 
irregularly  outlined  develops  from  the  center  and  shows 
an  ameboid  motion.      Considerably  later,   three  to   four  Q) 

hours,  so-called  total  alteration  of  the  blood-cells  begins,  (f%    ^   ^ 

and  the  external  shape  is  changed.     This  change  com-       /?  ^ 

mences  with  the  formation  of  a  mulberry-like  appear-  (1      rf)  fo\ 

) 

(ten  to  twelve  hours);  pseudopodia  develop  very  much        v     '^ 

with  an  ameboid-like  motility  like  that  of  the  decolorized     y\g.  233.— Poikilocytes  iu 

spots  above  described.     Poikilocytes  are  formed  in  this  pernicious  anemia. 

way.     Maragliano  has  called  attention  to  the  fact  that 

not  only  poikilocytes,  but  all  the  other  types  of  degeneration  described,  especially 

the  crenated  types  of  blood-cells,  may  be  found  in  the  fresh  preparation  of  severe 

blood-diseases.     Less  serious  pathologic  changes  of  the  blood  manifest  themselves 

by  the  fact  that  these  changes  take  place  outside  of  the  body  sooner  than  in  normal 

blood-specimens. 

These  changes  have  diagnostic  value  only  when  they  are  seen  in  absolutely 
fresh  specimens.  Pressure  on  the  tissues  when  removing  the  blood  and  on  the 
cover-glass  must  be  avoided,  because  this  may  produce  artificial  deformity  of  the 
blood-cells.  On  the  other  hand,  the  abnormally  rapid  appearance  of  deformity 
in  blood  apparently  normal  on  removal  indicates  a  certain  lack  of  resistance  of 
the  red  cells,  and  is  not  entirely  without  diagnostic  interest.  The  crenated  types 
are  of  especial  interest  in  this  respect,  although  they  have  not  yet  been  studied 
from  a  clinical  standpoint. 

So  far  as  the  staining  capacity  of  the  blood-corpuscles  is  concerned,  the  dry 
preparations  take  acid  stains  very  readily  (eosin,  orange-G).  The  intensity  of  this 
stain  depends  upon  the  amount  of  hemoglobin  contained  in  the  cells.  This  is  of 
practical  importance,  because  after  a  little  practice  the  degree  of  anemia  and  the 
oligochromatic  quality  of  the  blood  can  be  made  out  from  dry  specimens.  The 
diiference  between  normal  red  cells  and  those  deficient  in  hemoglobin  is  much 
more  striking  in  the  stained  dry  preparation  than  in  unstained  cells. 

Degeneration  of  the  red  cells  described  by  Maragliano  may  be  demonstrated  by 
staining.  .  Living  red  cells  are  achromatophilic — i.  e. ,  they  do  not  take  any  stain. 
After  they  have  been  fixed  by  drying  and  heating,  they  stain  with  eosin  and  the 
chemically  related  acid  pigments.  Endoglobular  degenerated  blood-cells  devoid 
of  color  in  the  center  do  not  act  in  this  way.  The  decolorized  portion  in  dry 
preparations  stains  with  hematoxylin,  whereas  the  peripheral  region  containing 
hemoglobin  stains  with  eosin.  To  demonstrate  this,  the  normal  staining  methods 
described  upon  p.  631  may  be  employed.  The  fact  that  the  endoglobular  region 
stains,  proves  that  it  is  not  a  vacuole,  as  was  formerly  believed,  a  view  which 
is  still  held  by  some  authorities. 

The  change  in  tinctorial  properties  of  the  red  cells,  termed  "anemic  degener- 
ation" by  Ehrlich,  and  " jwli/ehromatophilic  degeneration"  by  Gabritschewski, 
is  as  yet  little  understood.  In  this  condition  the  normal  red  blood-cells  and  the 
poikilocytes,  which  stain  with  the  acid  component  (eosin)  in  the  usual  staining 
mixtures,  are  tinged  various  shades,  from  eosin-red  with  a  bluish  tinge  to  pure 
violet,  when  they  are  treated  with  eosin  methylene-blue  (Chenzinski's  solution) 


638  EXAMINATION  OF  THE  BLOOD. 

or  eosin  hematoxylin.  This  change  has  been  noticed  in  nucleated  red  cells,  and, 
like  poikilocytosis,  is  found  in  all  severe  cases  of  anemia.  Occurring  under  such 
conditions,  it  is  suggestive  of  degeneration,  and  was,  therefore,  described  as  such 
by  Ehrlich  and  Gabritschewski.  This  view,  however,  has  become  untenable, 
since  we  know  that  polychromatophilic  staining  is  present  in  the  early  develop- 
mental stages  of  erythrocytes.  It  could  be  imagined  quite  as  easily  that  the 
polychromatophilic  changes  were  indicative  of  processes  of  regeneration;  at  any 
rate,  it  is  well  for  the  present  time  to  avoid  the  term  degeneration. 

Another  peculiar  change  is  the  so-called  granular  {granular  basophilic)  degen- 
eration of  the  erythrocytes.  This  has  been  closely  studied  by  Lazarus,  Askanazy, 
Plehn,  Grawitz,!  ^^^  others.  In  specimens  stained  with  Jeimer's  solution, 
Chenzinski's  solution,  or  by  brief  immersion  in  Loffler's  methyl ene-blue,^  some 
of  the  erythrocytes  are  seen  to  contain  a  number  of  bluish-black  (basophilic) 
granules  (see  Plate  6,  Fig.  4,  a).  This  change  has  been  found  chiefly  in  con- 
ditions associated  with  destruction  of  the  erythrocji:es,  such  as  pernicious  anemia, 
leukemia,  certain  forms  of  tropic  anemia,  carcinoma,  chronic  lead-poisoning, 
sepsis,  and  malaria.  Basophilic  granulation  is  of  the  greatest  diagnostic  import- 
ance in  the  recognition  of  chronic  lead-poisoning  (Nageli).  The  statement  of 
Grawitz,  that  granular  basophilic  degeneration  has  never  been  found  in  chlorosis, 
has  not  been  confirmed.  Eosin  and  Biber  state  that  they  have  observed  basophilic 
granules  in  the  erythrocytes  of  healthy  individuals.  Grawitz  succeeded  in  pro- 
ducing this  change  in  mice  by  overheating  the  animals.  Lazarus  and  Askanazy 
look  upon  the  basophilic  granules  as  the  remains  of  disintegrated  nuclei  ("kary- 
olytic  fragments"),  but  Grawitz  attributes  them  to  degenerative  changes  in  th& 
stromata  of  the  erji^hrocytes.  Others,  on  the  contrary,  regard  the  basophilic  gran- 
ulation as  a  phenomenon  holding  some  relation  to  the  regeneration  of  the  blood. 
Jawein,3  for  instance,  observed  this  change  in  a  patient  recovering  from  a  Both- 
riocephalus  anemia.  It  is  probable  that  basophilic  granulation  is  intimately 
related  to  erythrocytic  polychromatophilia,  with  which  it  is  frequently  associated. 
Ehrlich  and  Lazarus  designate  these  red  blood-corpuscles  by  the  non-committal 
term  "punctate  erythrocytes."  They  are  also  spoken  of  as  erythrocytes  with, 
basophilic  granulation. 

ERYTHROCYTIC   SHADOWS. 

These  forms  appear  in  the  blood  and  have  the  shape  of  red  blood- 
corpuscles,  but  are  absolutely  devoid  of  color,  so  that  the  central  depres- 
sion can  no  longer  be  distinctly  recognized.  They  are  the  stromata  of 
red  blood-corpuscles  which  have  lost  their  color.  They  are  produced 
artificially  when  sufficient  water  to  lake  the  red  blood-corpuscles  is 
added  to  normal  blood.  They  are  found  pathologically  where  red 
blood-corpuscles  are  being  rapidly  destroyed,  as  in  hemoglobinuria 
occurring  independently  or  as  the  result  of  poisoning  with  chlorate  of 
potash  or  other  blood-poisons.  They  may  also  be  found,  although  in 
smaller  numbers,  in  pernicious  anemia. 

VARIATION    IN   THE    SIZE    OF   RED    BLOOD-CORPUSCLES. 

Even  in  a  healthy  individual  all  the  red  blood-corpuscles  are  not  of 
the  same  size.  The  normal  size  varies,  according  to  diiferent  authors, 
between  6  and  9  [i  (averaging  about  7).  The  very  large  cells  are  called 
giant  corpuscles,  or  raacrocytes ;  the  small  ones,  microcytes.    According 

1  Deutseh.  med.  Woch.,  1899,  No.  36,  and  1900,  No.  9. 

2  Concenti-ated  alcoholic  solution  of  methylene-blue  30.0,  0.01  per  cent,  potassium 
hydroxid  100.  ^  Berlin,  klin.  Woch.,  1901,  p.  35. 


OTHER  MORPHOLOGIC  RELATIONS  OF  THE  BLOOD.         639 

to  Gram,  the  red  blood-corpuscles  are  larger  in  northern  than  in  southern 
countries.  There  may  be  very  great  differences  in  size  in  the  same 
blood  under  pathologic  conditions,  especially  in  so-called  pernicious 
anemia,  where  both  macrocytes  and  microeytes  are  numerous.  The 
latter  are  assumed  to  represent  broken-down  poikilocytes.  The  presence 
of  macrocytes  seems  to  bear  some  relation  to  the  megaloblasts  ;  they  are 
therefore  more  or  less  peculiar  to  pernicious  anemia. 

The  Volume  Quotient  or  the  Volume  Value  of  the  Erythrocytes.— We  are 

indebted  to  J.  A.  Capps  ^  for  an  interesting  study  of  the  size  of  the  erythrocytes. 
By  means  of  the  hematocrit  and  without  the  addition  of  fluid  (see  p.  629)  this 
author  has  determined  the  volume  of  the  erythrocytes  as  compared  to  the  volume 
of  the  whole  blood.  In  normal  cases  he  obtained  a  volume  of  50  per  cent.  If 
this  value  be  regarded  as  1,  the  volume  in  pathologic  cases  may  be  calculated  in 
per  cent,  of  the  normal  volume,  just  as  is  the  amount  of  hemoglobin.  Capps 
next  counts  the  erythrocytes  in  the  blood  under  observation,  and  expresses  this 
number  in  per  cent,  by  comparing  it  with  the  normal  number  of  erythrocytes. 
By  dividing  the  volume  of  the  erythrocytes  by  the  number  of  the  erythrocytes 
(both  expressed  in  percentages)  he  obtains  the  so-called  volume  index  of  the 
erythrocytes,  for  which  expression  the  author  would  suggest  substituting  "volume 
quotient"  or  "volume  value"  of  the  erythrocytes,  analogous  to  the  hemoglobin 
quotient  or  hemoglobin  value  of  the  erythrocytes.  This  quotient  is  the  measure 
of  the  average  volume  of  the  individual  erythrocyte.  Under  normal  conditions, 
it  is  evidently  equal  to  1.  Capps  found  that  an  increase  in  the  volume  quotient 
of  the  erythrocytes  is  one  of  the  most  constant  and  accurate  characteristics  of  per- 
nicious anemia,  which  agrees  with  the  well-known  fact  that  many  macrocytes  are 
present  in  this  disease,  and  that  the  hemoglobin  quotient  is  likewise  greater  than 
1.  In  contrast  to  this,  the  so-called  secondary  anemias  usually  show  a  diminished 
volume  quotient  of  the  erythrocytes.  The  same  is  true  of  chlorosis,  in  which 
affection  a  normal  or  slightly  diminished  volume  quotient  gives  a  good  prognosis, 
while  a  markedly  diminished  volume  quotient  is  less  favorable.  When  utilized 
in  this  manner,  the  volume  quotient  is  much  more  reliable  for  prognosis  in  chlo- 
rosis than  is  the  hemoglobin  percentage  or  the  hemoglobin  quotient. 

Capps  also  found  that  in  normal  erythrocytes  with  a  volume  quotient  of  1, 
the  discoplasm  is  saturated  with  hemoglobin,  so  that  if  the  hemoglobin  quotient 
becomes  greater  than  1,  it  indicates  an  enlargement  of  the  erythrocytes.  Upon 
the  other  hand,  the  hemoglobin  quotient  may  fall  irrespective  of  a  corresponding 
diminution  of  the  volume  quotient.  It  consequently  follows  that  if  the  hemo- 
globin quotient  of  the  erythrocytes  is  above  normal,  the  volume  quotient  must 
also  be  increased  ;  while  if  the  hemoglobin  quotient  is  below  normal,  the  volume 
quotient  is  not  necessarily  diminished.  The  osmotic  pressure  of  the  blood-plasma 
seems  to  haye  an  influence  upon  the  volume  quotient ;  this  is  difiicult  to  ujider- 
stand,  and  requires  further  investigation. 

NUCLEATED   RED    CELLS    (ERYTHROBLASTS)    AND    FREE    NUCLEL 

Nucleated  red  blood-corpuscles  do  not  occur  in  normal  blood.  They 
may  be  considered  as  evidence  of  some  abnormal  condition  of  develop- 
ment. They  are  found  especially  in  anemic  conditions.  Ehrlich  sub- 
divides the  nucleated  red  blood-cells  into  normoblasts  and  megaloblasts. 
The  normoblasts  are  red  blood-corpuscles  about  the  size  of  normal  cells, 
with  one  or  sometimes  several  nuclei.  These  nuclei  stain  intensely  with 
nuclear  stains,  such  as  hematoxylin,  usually  much  more  intensely  than 
the  nuclei  of  leukocytes  or  than  any  other  nuclei.  This  staining  quality 
^  Jour.  Med.  Research^  vol.  x.,  3,  Boston,  1903. 


640  EXAMINATION  OF  THE  BLOOD. 

is  very  characteristic,  and  enables  us  to  recognize  the  free  nuclei  of 
normoblasts  when  found  in  the  blood.  Unstained,  the  nuclei  of  normo- 
blasts appear  as  bright  centers  in  the  red  blood-corpuscles,  free  from 
hemoglobin.  They  differ  from  the  normal  depression  of  red  cells  by 
their  sharp  outline,  and  from  endoglobular  degeneration  in  being  some- 
what granular  (a  normoblast  is  represented  in  Plate  6,  Fig.  4),  Megal- 
oblasts,  which  are  also  nucleated  red  cells,  are  considerably  larger  than 
normoblasts — two  to  four  times  as  large.  The  nucleus  is  somewhat 
larger  than  that  of  a  normoblast,  but  occupies  a  comparatively  smaller 
portion  of  the  cell.  It  is  less  distinctly  outlined,  and  does  not  have  the 
same  affinity  for  nuclear  stains,  so  that  it  is  usually  but  very  faintly 
stained.  Megaloblasts  not  infrequently  show  polychromatophilia.  It 
is  usually  easy  to  differentiate  well-marked  normoblasts  from  megal- 
oblasts,' but  many  nucleated  red  blood  corpuscles  are  difficult  to  classify. 
Most  hematolooists  ao-ree  with  Ehrlich  that  there  is  a  distinct  diiference 
between  normoblasts  and  megaloblasts,  that  the  former  represent  the 
type  of  blood-formation  iu  the  adult,  and  the  latter  the  embryologic 
stage  of  blood  formation.  The  fate  of  the  nuclei  in  the  tAvo  types 
varies.  The  normoblasts  become  fully  developed  red  blood-cells  by 
extrusion  of  the  nuclei ;  the  megaloblasts,  by  disintegration  of  the 
nuclei  inside  of  the  corpuscle.  Of  clinical  significance  is  the  fact  that 
normoblasts  are  observed  in  those  anemic  conditions  in  which  the 
erythrocytes  develop  after  the  type  of  the  fully  grown  organism.  To 
this  group  belong  cases  of  acute  and  chronic  hemorrhages,  and  anemia 
following  inanition,  cachexia,  blood-poisoning,  hemoglobinemia,  etc. — 
i.  e.,  in  so-called  secondary  anemias  and  also  in  chlorosis.  Megaloblasts, 
on  the  contrary,  seem  to  l)e  the  clinical  indication  of  some  severe  degen- 
erative change  of  the  bone  marrow,  which  it  is  presumed  is  subjected  to 
abnormal  chemical  (toxic)  iuflnences.  They  are  frequently  found  in 
pernicious  anemia.  This  occurrence  makes  the  prognosis  grave  and 
unfavorable,  except  in  the  type  of  anemia  which  is  due  to  the  presence 
of  the  Bothriocephalus.  In  leukemia  both  normoblasts  and  megal- 
oblasts are  observed,  the  latter  predominating. 

In  secondary  anemia  large  numbers  of  normoblasts  may  at  times  be  found  in 
the  blood,  tbe  so-called  "blood-crises"  of  v.  Noorden.  Megaloblastic  blood-crises 
have  not  been  observed. 

In  poikiloc\i;osis,  deformed  blood-corpuscles  with  nuclei  are  sometimes  found. 
They  are  termed  poikiloblasts,  and  according  to  their  morphology  may  be  normo- 
blasts or  megaloblasts. 

VARIETIES   OF  LEUKOCYTES. 
The   following  varieties  of  white   blood-corpuscles   may  be   differ- 
entiated (Ehrlich  and  Lazarus)  :^ 

I.    LEUKOCYTES    IN    NORMAL   BLOOD. 

(o)  lyymphocytes. — These  are  derived  from  the  lymph  glands. 
They  are  small  cells  about  the  size  of  red  blood-corpuscles,  with  a  large 
centrally  placed  nucleus  and  a  small  margin  of  proto])lasm.     The  nucleus 

^  Die  Aniimie,  Nothnagers  Sp.  Path,  and  Therap.,  1898. 


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DESCEIPTION  OF  PLATE  6. 

Fig.  1. — Pernicious  Anemia :  a,  Normal  erj-throcytes ;  b,  erythrocytes  poor  in  hemoglobin ;  c, 
poikilocytes ;  c',  microcytes;  c?, macrocytes  :  e,  polychromatophil erythrocytes;/,  basophil  erythro- 
cytes ;  g,  polychromatophil  megaloblast ;  h.  polynuclear  neutrophil  leukocyte.  (Magnified  -570 : 
oil-immersion  Leitz  ^'j,  oc.  1 :  tube-length  170  mm.  Jenner's  stain). 

Fig.  2.— Myelemia :  a,  Erythrocytes ;  b.  polynuclear  neutrophil  leukocytes ;  c,  neutrophil 
myelocytes  with  large  nuclei ;  d,  neutrophil  myelocytes  with  small  nuclei ;  e,  polynuclear  eosin- 
ophil leukocyte ;  /,  eosinophil  myelocytes  ;  g,  mast-cell.    (Magnification  and  stain  as  in  Fig.  1.) 

Fig.  3.— Simple  Elements  of  the  Blood :  a,  Basophilic  erythrocyte  ;  b-g,  various  forms  of  ery- 
throcytes ;  6,  normoblast ;  c,  polychromatophil  megaloblast :  d,  poikilomegaloblast ;  e,  polychro- 
matophil erythroblast  the  size  of  which  corresponds  with  the  megaloblasts,  but  the  nucleus  of 
which  is  of  the  normoblast  type  :  /,  punctate  megaloblast;  g,  megaloblast  with  nucleus  split  into 
four  parts ;  h-l,  various  forms  of  small  normal  lymphocytes  from  the  same  preparation ;  k,  the 
most  common  form ;  m  and  n  (see  also  Fig.  4  x),  large  normal  lymphocytes  (in  the  common  form): 
these  all  stain  more  deeply  than  the  pathologic  lymphocytes  shown  in  Fig.  4;  o,  large  mononu- 
■clear  leukocyte  from  normal  blood ;  p,  form  intermediary  between  the  mononuclear  and  poly-  ■ 
nuclear  leukocyte  containing  sparse  granules.    (Magnification  and  staining  as  in  Fig.  1.) 

Fig,  4.— Acute  Lymphoid  Leukemia:  a,  Erythrocytes ;  6,  polynuclear  neutrophil  leukocytes; 
-c,  large  lymphocytes ;  d,  neutrophil  myelocyte ;  e.  polychromatophil  erythroblast ;  /,  free  nuclei 
of  normoblast.    (Magnification  and  staining  as  in  Fig.  1.) 


PLATE  6. 


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Fig.  4. 


OTHER  MORPHOLOGIC  RELATIONS  OF  THE  BLOOD.         641 

Stains  rather  intensely  with  nuclear  stains,  especially  hematoxylin,  and 
somewhat  less  intensely  with  methlyene-blue  and  the  triple  stain.  The 
protoplasm  is  free  from  granules.  In  children  and  in  lymphatic  leuke- 
mia so-called  "  large  lymphocytes  "  are  found  as  well  as  the  small  ones. 
These  may  be  double  the  size  of  red  blood-corpuscles,  but  are  otherwise 
very  much  like  the  smaller  ones  in  appearance.  The  nucleus  may  be 
irregular  or  may  be  composed  of  several  parts.  The  normal  number 
of  lymphocytes  is  22  to  25  per  cent,  of  the  total  number  of  leukocytes — 
i.  €.,  1500  to  1700  per  cubic  millimeter. 

According  to  Pappenheim,^  lymphocytes  are  also  found  in  the  bone  marrow; 
in  fact,  he  believes  that  these  lymphocytes  of  the  bone  marrow  are  the  progenitors 
of  all  the  myeloid  elements.  This  conception,  if  it  prove  correct,  has  a  far-reach- 
ing significance,  since  the  principal  difference  between  lymphatic  and  myelogenic 
leukemia,  in  reference  to  the  localization  of  the  changes,  would  then  disappear, 
and  this  is  what  Pappenheim  actually  alaims.  A  fact  in  favor  of  this  supposition 
is  that  a  myeloid  metamorphosis  of  the  lymphatic  glands  has  occasionally  been 
observed  in  myeloid  leukemia. 

(b)  I^arge  Mononuclear  I^eukocytes. — These  are  cells  two  or 
three  times  as  large  as  red  blood-corpuscles,  with  large  oval  nuclei, 
usually  situated  eccentrically  and  staining  faintly.  There  is  a  relatively 
large  amount  of  protoplasm,  which  is  also  free  from  granules.  They 
are  frequently  mistaken  for  large  lymphocytes,  but  have  more  protoplasm, 
and  a  nucleus  which  stains  very  faintly.  They  are  derived  in  all  prob- 
ability from  the  bone  marrow,  and  should  be  considered  the  parent  types 
of  the  following  cells  (c  and  rZ),  The  normal  percentage  of  this  group 
is  about  1  per  cent,  of  the  leukocytes — i.  e.,  70  for  each  cubic  millimeter. 

(c)  Transitional  Cells. — These  are  very  much  like  (6),  except 
that  the  nucleus  is  quite  irregular  in  shape  and  stains  more  readily,  and 
the  protoplasm  contains  scattered  neutrophilic  granules.  The  number 
of  transitional  cells  is  normally  from  2  to  4  per  cent,  of  the  leukocytes 
— i.  e.,  140  to  380  per  cubic  millimeter.  In  counting  they  are  usually 
included  in  one  group  with  the  related  type  (6).  The  normal  number 
for  the  combined  group  (6  and  c)  is  about  3  to  5  per  cent — i.  e.,  210  to 
350  per  cubic  millimeter. 

(d)  Polynuclear  or,  better,  polymorphonuclear  neutrophilic 
leukocytes,  are  characterized  by  a  polymorphous,  irregularly  shaped 
or  bent  nucleus,  which  may  be  readily  confounded  with  multiple  nuclei. 
Indeed,  acted  upon  by  acetic  acid,  it  may  be  separated  into  several 
nuclei,  a  change  which  also  occurs  probably  when  the  leucocytes  leave 
the  vascular  system  and  become  pus  corpuscles  (hence  the  incorrect  name 
"  polynuclear  cells,"  which  is  almost  impossible  to  eradicate).  The 
nuclei  stain  very  intensely,  and  the  protoplasm  is  very  densely  packed 
with  neutrophilic  granules.  The  iodin  reaction  affects  chiefly  these  cells 
(see  p.  634).  The  normal  number  of  polymorphonuclear  cells  is  about 
70  to  72  per  cent,  of  the  leukocytes — /.  e.,  4900  to  5040  per  cubic  mil- 
limeter. 

^  "  Nenere   Streitfragen   aus   dem    Gebiete   der   Hamatolosrie,"  Zeils.  f.  klin.  Med., 
vol.  xlvii.,  p.  3  and  4,  1902. 
41 


642  EXAMINATION  OF  THE  BLOOD. 

(e)  Hosinophilic  Cells. — These  resemble  the  polymorphonuclear 
neutrophilic  cells,  except  that  the  small  neutrophilic  granules  are  replaced 
by  coarse  oxyphilic  granules.  The  coarse  granules  refract  the  light  so 
strongly  that  these  cells  are  readily  recognized  without  staining.  When 
unstained,  however,  they  might  be  mistaken  for  mast  cells  (see  below), 
although  the  granules  of  the  latter  are  usually  much  coarser.  The 
eosinophiles  normally  furnish  between  2  to  4  per  cent,  of  the  leukocytes 
— i.  e.,  140  to  280  per  cubic  millimeter. 

(/)  Mast  cells  are  cells  of  the  polymorphonuclear  or  transitional 
type  with  marked  basophilic  granules,  which  are  quite  large,  uneven, 
and  irregularly  distributed  and  are  not  distinctly  stained  by  the  triple 
stain.  The  number  of  these  cells  in  normal  blood  is  about  0.5  per  cent» 
of  the  leukocytes — i.  e.,  35  per  cubic  millimeter. 

These  figures  for  the  proportions  of  the  various  kinds  of  leukocytes 
in  the  blood  should  be  modified  in  the  case  of  children  below  five  years 
of  age,  where  the  mononuclear  cells  predominate.  From  the  fifth  year 
on  the  polynuclear  cells  become  50  per  cent.^  There  is  as  yet  no  more 
accurate  information  regarding  the  occurrence  of  any  individual  type  of 
leukocyte  in  children  of  different  ages. 

II.    PATHOLOGIC    LEUKOCYTES. 

(a)  Mononuclear  Neutrophilic  Cells  {Myelocytes,  "Ehrlich's 
3IarkzeUen.^') — These  are  large  cells  with  a  large,  faintly  staining 
nucleus,  differing  from  the  large  mononuclear  cells  of  normal  blood 
by  the  presence  of  neutrophilic  granules  contained  in  the  proto- 
plasm. They  are  not  found  in  normal  blood,  or  if  so  they  are  so  scat- 
tered that  they  are  not  included  among  normal  leukocytes.  They  should 
be  considered  a  preliminary  or  transitional  stage  of  abnormal  polymor- 
phonuclear cells,  and  are  characteristic  of  the  blood  in  splenomyeloge- 
nous  leukemia.  They  may  be  found  under  other  pathologic  conditions  ; 
for  instance,  in  malignant  tumors  of  the  bone  marrow,  in  infantile  ane- 
mia, in  pseudoleukemia,  in  leukocytosis,  and  especially  in  diphtheria. 

The  presence  of  a  considerable  number  of  myelocytes  in  the  blood  always 
indicates  a  serious  change  in  the  bone  marrow.  When  associated  with  leuko- 
cytosis, their  occurrence  evidently  signifies  that  immature  elements  have  gained 
access  to  the  circulation  from  the  bone  marrow  through  chemotactic  influences, 
and  in  a  certain  sense  is  indicative  of  an  insufiiciency  of  the  bone  marrow.  Their 
occurrence  in  great  numbers  in  diphtheria  makes  the  prognosis  unfavorable.  In 
the  medullary  metastases  of  malignant  tumors,  the  appearance  of  myelocytes  in 
the  blood  is  of  great  diagnostic  importance. 

(b)  Mononuclear  Eosinophilic  Cells  (EhrUch's  and  Lazarus' 
Eosinophilic  Myelocytes.) — These  authors  consider  them  to  be  early  tran- 
sitional forms  of  abnormal  eosinophilic  cells,  bearing  the  same  relation 
to  these  cells  as  do  the  neutrophilic  myelocytes  to  the  neutrophilic  poly- 
morphonucleated  cells.  They  occur  especially  in  myelogenic  leukemia. 
Very  small  cells  of  this  sort  have  been  termed  eosinophilic  microcytes. 

(c)  Small    Neutrophilic    Pseudolymphocytes. — These   are 

^  Besredka,  Annales  Pasteur,  1898,  No.  5,  p.  327,  et  seq. 


OTHER  MORPHOLOGIC  RELATIONS  OF  THE  BLOOD.  643 

small  mononuclear  cells  with  a  deeply  staining  nucleus  and  neutrophilic 
granules.  They  are  very  rare.  Ehrlich  and  Lazarus  believe  that  they 
result  from  the  division  of  ordinary  polynuclear  cells. 

(d)  Irritation  Forms  (Tiirk). — These  are  mononuclear  cells  with- 
out granulation,  resembling  the  lymphocytes  in  size.  Their  protoplasm 
stains  dark  brown  with  the  triacid  mixture.  Tiirk  found  them  under 
conditions  similar  to  those  associated  with  myelocytes. 

With  the  exception  of  the  lymphocytes,  which  are  derived  from  the 
lymph  glands,  probably  all  normal  and  pathologic  leukocytes  are  derived 
from  the  bone  marrow.  Recent  investigations  show  that  the  spleen  does 
not  appear  to  play  an  important,  but  quite  a  secondary,  part  in  their 
formation.  This  source  may  nevertheless  give  origin  to  some  of  the 
lymphocytes.  The  pathologic  forms  originate  chiefly  in  the  bone  marrow, 
although  there  is  considerable  variation  under  different  pathologic  condi- 
tions. Sometimes  the  bone  marrow  is  actively  employed  in  the  production 
of  lymphocytes  (lymphoid  leukemia),  while  in  other  instances  there  is  a 
myeloid  metamorphosis  of  the  substance  of  the  lymphatic  glands  which 
furnishes  elements  such  as  those  which  normally  originate  only  in  the 
bone  marrow.  In  some  leukemias  the  spleen  may  also  take  part  in  the 
production  of  lymphocytes  and  liberate  them  into  the  blood,  or  throw 
elements  into  the  circulation  which  are  usually  of  myeloid  origin. 

From  Ms  investigations  of  the  bone  marrow  Niigeli  ^  has  recently  described, 
under  the  name  of  myeloblast,  a  new  type  of  cell.  This  is  a  collective  term  for 
bone-marrow  cells  without  granules,  and  is  especially  applicable  to  the  smaller 
type,  which  up  to  the  i^resent  time  have  been  included  in  the  bone  marrow  and 
in  the  blood  as  lymphocytes,  because  of  their  correspondence  in  size.  According 
to  Nageli,  they  have  a  reticular  nucleus  and  exhibit  different  staining  character- 
istics from  the  lymphocytes,  the  chief  of  which  is  that  in  specimens  stained  with 
the  triacid  mixture  the  nucleus  of  the  lymphocytes  is  dark,  and  that  of  the 
myeloblasts  considerably  lighter.  If,  on  the  other  hand,  the  slide  is  kept  in  an 
incubator  at  131°  C,  and  stained  with  pure  alcoholic  methylene-blue,  the  nuclei 
of  the  lymphocytes  will  appear  pale,  and  the  nuclei  of  the  myeloblasts  dark. 
The  reverse  is  true  for  the  protoplasm,  that  of  the  lymphocytes  staining  dark, 
and  that  of  the  myeloblasts  staining  lighter.  Myeloblasts,  as  contrasted  with, 
the  fully  developed  types,  are  found  in  increased  numbers  in  the  bone  marrow  in 
pernicious  anemia,  myelogenic  leukemia,  and  typhoid. 

It  remains  for  future  investigation  to  decide  how  much  of  Nageli' s  observa- 
tions will  be  corroborated,  and  to  determine  the  relation  of  the  myeloblasts  to  the 
above-mentioned  varieties  of  cells.  According  to  Nageli,  the  large  mononuclear 
cells  in  normal  blood  correspond  to  the  large  myeloblasts.  Nevertheless  the  small 
myeloblasts  (myeloblast  in  the  strictest  sense  of  the  word)  may  appear  in  the  blood 
under  pathologic  conditions  (leukemia,  pernicious  anemia,  and  typhoid),  and 
should  then  be  distinguished  from  the  lymphocytes,  with  which  they  have  been 
confounded  up  to  the  present  time.  This  may  be  done  by  the  above-named  charac- 
teristics, although  it  is  not  always  easy. 

DIFFERENTIAL  COUNTING  OF  LEUKOCYTES  AND  THEIR  PRO- 
PORTIONS UNDER  NORMAL  CONDITIONS. 

If  it  be  desired  to  differentiate  simply  the  mononuclear  and  poly- 
nuclear elements,  the  differential  count  may  be  made  from  blood  treated 
with  dilute  acetic  acid,  which  renders  the  nuclei  quite  distinct.     For 

1  Deutsch.  med.  Woch.,  1900,  No.  18. 


644  EXAMINATION  OF  THE  BLOOD. 

the  further  differentiation  of  the  several  varieties  of  leukocytes  (see 
p.  640),  dry  specimens  stained  with  eosin  hematoxylin  have  usually 
been  employed,  and  carefully  prepared  give  a  sufficient  idea  of  the 
numeric  ratios  of  the  individual  varieties.  Advantage  may  also  be 
taken  of  dry  preparations  stained  by  other  methods;  for  example,  by 
Ehrlich's  triacid  mixture  or  Jenner's  solution.  If  these  preparations 
have  been  carefully  prepared — i.  e.,  if  the  layer  is  thin  and  uniform — we 
can  form  some  opinion  of  the  proportion  of  the  different  varieties.  If 
a  movable  stage  is  used,  the  entire  preparation  may  be  counted.  The 
total  number  of  leukocytes  is  determined  in  the  ordinary  way. 

For  differential  counting,  Ehrlich  uses  an  ocular  made  by  Leitz,  by 
means  of  which  the  field  of  vision  is  made  rectangular  and  of  known 
size.  A  larger  or  smaller  field  is  employed,  according  to  the  abundance 
of  the  corpuscles  in  the  dry  preparation.  The  total  number  of  the 
white,  and  the  number  of  each  individual  kind,  can  be  conveniently 
counted  by  moving  the  preparation  so  that  different  parts  enter  the  field 
of  vision.  The  figures  thus  obtained  are  sufficiently  accurate.  Ehrlich 
also  employs  this  method  to  determine  the  proportion  of  white  and  red 
blood-cells. 

Our  knowledge  of  leukocytosis  was  at  first  considerably  restricted 
by  the  fact  that  attention  was  drawn  exclusively  to  the  determination 
of  the  quantitative  relation  between  the  white  and  the  red  corpuscles. 
Similarly,  the  limitation  of  the  investigation  to  the  determination  of  the 
quantitative  relations  of  the  various  leukocytes,  without  due  regard  to 
the  absolute  number  of  these  cells,  has  also  considerably  restricted  our 
knowledge  of  this  topic.  The  recent  literature,  however,  indicates  that 
the  importance  of  determining  the  absolute  numbers  has  been  recognized. 

ZoUikofer's '  method  of  staining  fresh  blood-preparations  in  the 
counting-chamber,  and  then  detei^mining  the  absolute  number  of  the 
different  kinds  of  leukocytes  present,  is  a  welcome  simplification. 

The  following  two  solutions  are  required  : 

I. 

Eosin,  w.  g.  (Griibler) 0.05 

Fonnalin  cone.  (40  percent.) 1.00 

AquiB  destillatae 100.00 

Filter.     ' 

II. 

Methylene-blue,  B.  X.  (Griibler)      0.05 

Formalin  cone 1.00 

Aquffi  destillatse 100.00 

Filter. 

Both  solutions  are  kept  in  dark  bottles,  and  before  using  are  mixed  in  about 
equal  quantities  with  a  medicine  dropper. 

The  blood  is  drawn  into  a  Thoma-Zeiss  leukocyte  counter,  and  diluted  twenty 
times  with  the  freshly  mixed  stain.  The  stain  after  being  mixed  must  be  used 
immediately,  because  a  precipitate  is  formed  if  it  stands  for  any  length  of  time. 
The  dilution  of  the  blood  with  the  stain   must  be  done  very  rapidly,  for  if  the 

^  Zeits.f.  mik.  Technik.,  1901. 


OTHER  MORPHOLOGIC  RELATIONS  OF  THE  BLOOD.         645 

blood  remains  in  the  capillary  tube  for  any  length  of  time,  it  is  hard  to  render  the 
red  blood-corpuscles  invisible. 

The  jjipet  is  shaken  for  about  five  minutes,  and  a  drop  then  placed  on  the 
counting-slide.  The  red  blood-corpuscles,  unless  nucleated,  are  invisible.  The 
leukocytes  are  preserved,  and  the  individual  kinds  can  be  distinguished.  The  a 
granules  are  stained  yellowish  to  carmin,  and  are  characterized  by  their  size. 
The  e  granules  are  grayish  violet,  often  filling  up  the  Sntire  body  of  the  leuko- 
cyte, but  in  rare  cases  scattered  only  in  the  protoplasm.  The  y  granules  remain 
unstained.  The  leukocytes  without  granulations  may  be  distinguished  by  the 
amount  of  protoplasm  and  the  size  of  the  nucleus.  They  are  lymphocytes  and 
large  mononuclear  cells.  The  nucleus  is  less  distinctly  stained  in  the  granular 
types,  and  for  this  reason  the  mononuclear  granulated  leukocytes  (myelocytes) 
cannot  be  accurately  separated  from  the  polynuclear.  The  blood-plates  are  of  a 
bluish-violet  tinge,  and  may  be  recognized  by  their  typical  grape-like  arrange- 
ment. 

The  proportion  of  the  eosin  to  the  methylene-blue  can  be  so  regulated  that 
neither  the  nuclei  nor  the  granules  predominate. 

The  same  mixture  can  be  used  in  dry  preparations  which  have  been  well 
fixed  at  120°  C.  They  should  be  stained  from  one-half  to  one  minute.  Besides 
differentiating  the  various  kinds  of  leukocytes,  it  stains  malarial  parasites,  bac- 
teria, and  the  basophilic  granules  of  the  erythrocytes,  and  shows  the  polychroma- 
tophilic  changes  of  the  red-cell  plasma. 

LEUKOCYTOSIS  AND  LEUKOPENIA. 

By  the  term  leukocytosis  is  understoood  the  state  of  the  blood,  occur- 
ring under  various  conditions,  in  which  there  is  an  increase  of  the  white 
corpuscles,  except  in  those  cases  where  such  an  increase  is  due  to  the 
specific  or  idiopathic  disease  of  the  blood,  leukemia.  Most  leukocytoses 
are  characterized,  in  contradistinction  to  leukemia,  by  an  increase  in  the 
polynuclear  neutrophiles,  which  are  derived  from  the  bone  marrow,  so 
that  the  term  leukocytosis,  used  without  qualification,  usually  means 
the  increase  of  this  kind  of  cell. 

An  unusual  form  of  leukocytosis,  except  when  it  is  associated  with 
leukemia,  is  characterized  by  an  increase  in  the  number  of  lymphocytes, 
the  so-called  lymphocytosis. 

Leukopeyiia  is  the  reverse  of  leukocytosis — i.  e.,  a  diminution  in  the 
number  of  leukocytes. 

Leukocytoses  are  either  physiologic  or  pathologic.  The  polynuclear 
elements  of  pathologic  leukocytoses  are  usually  neutrophilic,  so  that  a 
polynuclear  neutrophilic  leukocytosis  is  usually  pathologic.  There  is, 
however,  a  pathologic  eosinophilic  polynuclear  leukocytosis.  These 
pathologic  leukocytoses  are  explained  by  the  presence  of  chemotactic 
substances  in  the  blood-plasma,  most  of  which  exert  a  positive  influence 
on  the  neutrophilic,  and  but  little  on  the  eosinophilic,  cells.  A  leuko- 
cytosis in  which  the  third  kind  of  granular  cells,  the  mast  cells,  are 
increased  is  not  as  yet  known.  But  in  leukemia  these  cells  are  usually 
very  much  increased. 

PHYSIOLOGIC  LEUKOCYTOSES. 

To  this  group  belong  the  leukocytosis  of  digestion,  the  leukocytosis  after 
exertion  and  after  a  cold  bath,  the  leukocytosis  of  pregnancy  and  that  of  the 
newborn. 


646  EXAMINATION  OF  THE  BLOOD. 

The  leukocytosis  of  digestion  begins  about  one  hour  after  a  meal,  and 
reaches  its  maximum  (a  30  to  40  per  cent,  increase  of  the  white  cells)  in  about 
three  to  four  hours  (Rieder).  It  is  most  marked  after  food  rich  in  proteids. 
Considering  the  comparatively  slight  digestion  leukocytosis,  any  great  degree 
of  pathologic  leukocytosis  can  be  recognized  even  during  digestion.  The  lympho- 
cytes are  increased  in  this  type  of  leukocytosis. 

Very  little  definite  information  is  as  yet  at  hand  regarding  the  leukocytosis 
after  exertion  and  cold  bat/is.  It  is  not  yet  known  whether  there  is  an  actual 
increase  in  the  total  number  of  leukocytes,  or  whether  this  is  only  a  pseudo- 
leukocytosis — i.  e.,  one  produced  by  an  accumulation  of  leukocytes  in  the  skin 
vessels.  The  leukocytosis  of  pregnancy  may  amount  to  50  or  80  per  cent.,  is 
present  only  in  the  later  months  of  pregnancy,  and  disappears  rapidly  after 
delivery. 

Leukocytosis  of  the  Newborn. — The  white  count  is  two  to  three  times 
the  normal  during  the  first  day  of  life.  It  then  diminishes  to  normal,  and 
increases  again  after  the  first  week,  remaining  for  several  weeks  at  about  50  per 
cent,  above  the  normal. 

In  these  physiologic  leukocytoses  the  proportions  of  the  individual  types  of 
leukocytes  are  about  normal,  and  consequently  there  is  chiefly  an  increase  of 
polynuclear  neutrophilic  leukocytes;  but  in  the  leukocytosis  of  the  newborn  the 
mononuclear  cells  predominate. 

LEUKOCYTES  IN  THE  INFECTIOUS    DISEASES;    INFECTIOUS    LEUKOCYTOSIS 

AND  LEUKOPENIA.* 

Pneomonia. 
Pneumonia  is  usually  accomj^anied  by  a  pronounced  leukocytosis.  The 
degree  does  not  correspond  to  the  severity  of  the  infection,  nor  does  it  permit 
of  an  absolute  prognostic  conclusion.  The  leukocytes  usually  run  from  15,000 
to  30,000  per  cubic  millimeter.  A  sudden  drop  in  the  number  usually  comes 
on  the  day  of  the  crisis,  or  sometimes  on  the  day  before.  It  is  not,  however, 
usual  to  have  the  number  drop  below  the  normal  after  the  crisis.  The  leukocy- 
tosis of  pneumonia  is  composed  of  neutrophiles,  the  eosinophiles  disappearing 
during  the  course  of  the  disease.  The  reappearance  of  eosinophiles  indicates 
that  the  height  of  infection  has  been  passed,  and  is,  therefore,  more  or  less  indic- 
ative of  a  fevorable  prognosis.  It  usually  takes  place  on  the  day  of  the  crisis, 
but  sometimes  one  or  two  days  before.  Later  the  eosinophiles  may  be  increased 
beyond  the  normal  limits.  A  normal  leukocyte  count  with  a  relative  increase 
of  the  polynuclear  neutrophiles  indicates  a  severe  infection  and  reduced  resist- 
ance. Leukopenia  in  pneumonia  suggests  a  dubious  prognosis,  although  it  need 
not  necessarily  indicate  a  fatal  termination. 

Typhoid. 

Typhoid  difiers  sharply  from  pneumonia  in  being  usually  characterized  by 
leukopenia.  Nageli  continued  Rieder's  and  Tiirk's  investigations,  and  studied 
the  hematology  of  typhoid  more  minutely.  He  has  arrived  at  the  following 
conclusions  : 

In  the  first  stage  (ascending  fever  curve)  there  is  usually  a  neutrophilic  leu- 
kocytosis. This  may  be  inferred  from  the  condition  found  in  recurrences.  It 
soon  diminishes,  and  is  then  followed  by  a  diminution  in  the  neutrophiles.  The 
eosinophiles  disappear  entirely  or  very  nearly.  The  diminution  of  lymjahocytes 
is  moderate. 

^  Chiefly  compiled  from  Rieder,  Beitrdge  zur  Kenntnis  der  Leukocytose,  Leipzig, 
Vogel,  1882  ;  Tiirk,  Klinische  Untersuchungen  ilber  das  Verhalten  des  Blutes  hei  acuten  Infec- 
tionskrankheiten,  Wien  and  Leipzig,  1898  ;  O.  Nageli,  "  Ueber  die  Typhnsepidemie  in 
Oberbipp,  ein  Beitrag  znr  Aetiologie  and  Haematologie  des  Typhus  abdorainalis,"  Cor- 
respondenzhl.  f.  Schiveizer  Aerzte,  1899,  No.  18 ;  and  the  same,  "  Die  Leukocyten  beim 
Typhus  abdominalis,"  Deutsch.  Arch.  f.  klin.  Med.,  1900,  vol.  Ixvii.,  p.  279. 


OTHER  MORPHOLOGIC  RELATIONS  OF  THE  BLOOD.  647 

In  the  second  stage  (fastigium,  continued  fever)  the  number  of  neutrophiles 
and  lymphocytes  diminishes  still  further,  although  the  latter  may  be  somewhat 
increased  toward  the  end  of  this  period. 

In  the  third  stage  (period  of  remissions)  the  lymphocytes  are  frequently 
increased,  and  sometimes  decidedly  so.  The  neutrophiles  are  still  more  dimin- 
ished, and  the  eosinophiles  begin  to  reappear  at  the  end  of  this  jjeriod.  In 
adults  the  lymphocytes  may  remain  few  in  number. 

The  fourth  stage  (descending  fever  curve)  is  characterized  by  a  still  further 
■diminution  of  the  neutrophiles,  which  reaches  its  maximum  during  this  period. 
The  lymphocytes  are  considerably  increased,  and  may  be  much  more  numerous 
than  the  neutrophiles  (crossing  of  the  two  curves).  The  eosinophiles  begin  to 
increase  slowly  and  regularly. 

Soon  after  the  fever  disappears  the  neutrophiles  begin  to  increase.  The 
lymphocytes  are  very  abundant  and  the  eosinophiles  continue  to  increase.  A 
few  days  after  the  disease  has  run  its  course,  there  may  be  a  considerable  lympho- 
cytosis, a  marked  increase  of  eosinophiles,  and  normal  or  slightly  increased 
numbers  of  neutrophiles.  This  condition  is  most  pronounced  in  young  individ- 
uals, especially  two  or  three  months  after  defervesence.  In  adults  it  is  less 
marked,  and  usually  disappears  within  two  months  ;  but  in  children  it  persists 
considerably  longer. 

During  the  active  stage  of  the  disease  the  variations  in  the  leukocytes  are 
more  pronounced  in  children  than  in  adults,  especially  while  the  lymphocjiies 
are  increasing.  On  the  other  hand,  even  if  children  are  extremely  ill,  the  number 
of  leukocytes  is  rarely  as  low  as  in  adults  (apparently  due  to  a  less  severe  involve- 
ment of  the  bone  marrow  and  the  lymijhatic  apparatus). 

Complications,  of  course,  influence  the  number  of  neutrophiles.  They  are 
usually  increased,  but  generally  not  excessively,  by  suppuration,  cystitis,  paro- 
titis, pleuritis,  bronchopneumonia,  nephritis,  etc.  Absence  of  leukocytosis  in 
spite  of  complications  indicates  an  insufficiency  in  the  function  of  the  bone 
marrow.  This  is  a  very  dangerous  condition  (impossibility  of  forming  new  neu- 
trophiles). 

The  persistence  or  early  reaj^pearance  of  eosinophiles,  the  slight  diminution 
of  neutrophiles,  and  the  marked  and  early  increase  in  lymphocytes  all  favor  the 
prognosis.  Marked  diminution  of  all  kinds  of  leukocytes,  or  an  absence  of  leu- 
kocytosis despite  complications,  is  unfavorable.  In  the  recurrences  the  blood- 
picture  is  similar  in  all  respects  to  that  of  the  primary  attack. 

The  blood-findings  may  persist  long  after  the  disease  has  disppeared  ;  they 
are  very  characteristic,  and,  as  Nageli  has  shown,  may  prove  that  a  patient  has 
typhoid,  although  he  is  apparently  well,  often  with  even  greater  accuracy  than  is 
possible  with  Widal's  reaction,  a  fact  which  may  be  of  considerable  importance 
in  determining  the  beginning  of  an  epidemic  of  typhoid. 

Acute  Articular  Rheumatism. 

In  uncomplicated  cases  of  this  disease  there  is  usually  a  slight  polynuclear 
neutrophilic  leukocytosis  (about  15,000),  which  persists  so"  long  as  there  is  fever 
and  exudation  (Tiirk).  The  leukocytosis  increases  if  complications  occur 
(pleura,  pericardium).  Eosinophiles  are  absent  only  in  the  very  early  cases, 
before  there  has  been  any  amelioration  of  the  symptoms.  Later  they  usually 
reappear.  The  presence  of  eosinophiles  is  of  favorable  prognostic  importance 
in  this  disease  also. 

Meningitis. 

In  epidemic  cerebrospinal  meningitis  there  is  always  a  pronounced  polynu- 
clear neutrophylic  leukocytosis  of  varying  degree.  In  tubercular  meningitis  the 
leukocyte  count  may  be  normal  or  distinctly  increased  (up  to  20,000  and  more). 
Absence  of  leukocytosis,  then,  points  toward  tuberculous  disease,  but  its  presence 
does  not  exclude  this  disease.  The  blood-examination  in  cerebrospinal  meningitis 
furnishes  no  prognostic  data. 


648  EXAMINATION  OF  THE  BLOOD. 

Septicemia. 

In  this  disease  there  is  usually  a  polynuclear  neutrophilic  leukocytosis.  Indi- 
vidual cases,  usually  the  very  severe,  may  have  no  leukocytosis. 

Erysipelas. 

In  the  majority  of  the  cases  there  is  a  moderate  degree  of  polynuclear  neu- 
trophilic leukocytosis ;  in  others  the  leukocyte-count  may  be  normal  or  only 
slightly  increased.  The  degree  of  leukocytosis  is  of  no  prognostic  value,  except 
that  when  marked  it  suggests  the  formation  of  pus.  In  this  disease,  too,  the  num- 
ber of  eosinophiles  is  diminished  at  the  height  of  the  disease. 

Scarlet  Fever. 

Here,  too,  there  is  an  increase  of  polynuclear  neutrophiles.  The  character- 
istic feature  of  the  leukocytosis  of  this  disease  is  its  persistence,  for  it  does  not 
disappear  for  a  considerable  period  after  the  rash  and  the  fever  have  vanished,  a 
fact  which  can  be  made  use  of  for  diagnosis  after  the  disease  has  run  its  course. 
The  eosinophiles  are  diminished  during  the  early  stages  of  the  disease  ;  but  after 
the  rash  has  reached  its  climax  and  during  the  period  of  desquamation  they  may 
be  normal,  or  at  times  considerably  increased.  The  persistence  of  leukocytosis 
after  this  disease  has  run  its  course  may  possibly  have  some  prognostic  value  in 
regard  to  the  danger  of  late  nephritis. 

Measles. 

Uncomplicated  cases  in  adults  are  accompanied  by  a  diminution  of  leuko- 
cytes (leukopenia)  similar  to  that  in  typhoid.  This  is  most  decided  during  the 
l^eriod  of  eruption,  and  especially  when  the  latter  is  at  its  height.  The  ratio 
between  the  polynuclear  cells  and  the  lymphocytes  remains  undisturbed.  After 
the  rash  has  disappeared  the  total  number  of  leukocytes  increases  to  the  nor- 
mal, and  the  number  of  large  mononuclear  cells  may  be  above  the  normal. 
The  eosinophiles  up  to  the  height  of  the  disease  are  either  normal  or  dimin- 
ished, but  subsequently  they  become  slightly  increased.  A  subnormal  or  later 
a  normal  number  of  leukocytes  may  be  useful  in  the  diiferential  diagnosis  between 
measles  and  scarlet  fever.  A  marked  eosinophilia  and  leukocytosis  would  be  in 
favor  of  scarlet  fever  rather  than  measles. 

Varicella. 
In  this   disease   Erben   found   an   increase  of  the   mononuclear   leukocytes, 
although  the  total  number  of  leukocytes  was  normal. 

Pertussis. 
Pertussis  leads  to  an  increase  of  the  lymphocytes  and,  to  a  less  marked  degree, 
also  to  an  increase  of  the  polynuclear  leukocytes. 

Mumps. 
In  mumps,  even  with  high  fever,  F.  Pick  -  found  no  leukocytosis.     He  regards 
this  of  importance  in  the  differential  diagnosis  of  orchitis  due  to  mumps  from  that 
due  to  gonorrhea,  and  concludes  from  it  that  the  former  is  purely  a  serous  inflam- 
mation. 

Malaria. 
The  ordinary  benign  cases  of  malaria,   according  to  Tiirk,  regularly  show  a 
diminution  in  the  total  number  of  leukocytes  both  during  the  attacks  and  in  the 
interval.     During  the  attack  the  percentage  of  neutrophiles  is  relatively  increased 

^Wien.klin.  Rundschau,  1902,  No.  16. 


OTHER  MORPHOLOGIC  RELATIONS  OF  THE  BLOOD.         649 

at  the  expense  of  the  lymphocytes  and  eosinophiles.  Schindler  has  reached 
different  conclusions.  He  observed  a  diminution  of  the  leukocytes  and  an  in- 
crease of  the  mononuclear  cells  between  the  attacks,  with  a  reappearance  of  the 
normal  figures  at  the  height  of  the  attack.  Turk  has  counted  the  plasmodia  in 
connection  with  the  leukocytes  in  this  disease  (see  p.  656). 

Tuberculosis. 

This  disease  gives  rise  to  a  polynuclear  leukocytosis  if  it  is  associated  with 
suppuration.  In  acute  miliary  tuberculosis  the  number  of  leukocytes  is  usually 
normal. 

Infectious  Inflammationst   Tetanus,  Suppurations,  Perityphlitis,  Empyema,   etc. 

These  usually  produce  a  moderate  leukocytosis. 

In  infectious  inflammations  we  are  not  justified  in  diagnosing  suppuration  from 
the  degree  of  leukocytosis  obtained  by  a  single  examination  ;  but  if  we  carefully 
follow  the  blood-picture  during  the  course  of  a  perityphlitis,  as  recommended  by 
Curschmann,  we  may  obtain  valuable  diagnostic  aid.  The  majority  of  observers 
have  confirmed  Curschmann' s  statements  that  marked  leukocytosis  (above  15,000 
to  20,000  leukocytes  per  cubic  millimeter)  occurs  early  in  perityphlitis,  even  in  the 
benign  cases  which  recover  without  operation  ;  but  that  when  this  marked  leuko- 
cytosis continues  or  assumes  a  progressive  character,  reaching  30, 000  to  40, 000 
leukocytes,  we  have  evidence  in  favor  of  progressive  suppuration  and  an  indica- 
tion for  surgical  interference.  The  leukocytic  count  is  of  no  value  in  old 
encapsulated  abscesses,  since  it  may  be  perfectly  normal  under  these  conditions. 
It  is  probable  that  it  may  be  of  value  for  the  diagnosis  and  prognosis  of  pleural 
empyemata.     The  same  is  true  of  suppurative  affections  of  the  biliary  passages. 

OTHER  POLYNUCLEAR   NEUTROPHILIC  LEUKOCYTOSES. 

Toxic  and  Medicinal  Leukocytosis.— This  is  observed  chiefly  in  poisoning 
with  the  blood-poisons,  potassium  chlorate,  phenacetin,  and  arsenic,  after  chloro- 
form, and  in  hemoglobinuria.  These  conditions  have  not  been  especially  studied. 
The  drugs  which  produce  a  polynuclear  neutrophilic  leukocytosis  when  used  inter- 
nally are  autipyrin,  antifebrin,  and  others.  The  pilocarpin  leukocytosis  seems 
to  be  mainly  a  lymphocytosis. 

Anemic  Leukocytosis. — This  is  observed  chiefly  after  acute  loss  of  blood 
(posthemorrhagic  leukocytosis)  and  in  those  types  of  anemia  where  the  bone 
marrovt^  is  in  a  state  of  increased  regenerative  activity  (secondary  anemia).  The 
polynuclear  neutrophilic  cells  are  chiefly  aflfected.  The  leukocytosis  may  be  very 
marked.     It  disappears  when  the  loss  of  blood  has  been  replaced  by  regeneration. 

Cachectic  Leukocytosis. — This  is  polynuclear  and  neutrophilic,  and  is 
observed  chiefly  in  malignant  tumors,  carcinoma  and  sarcoma. 

Leukocytosis  of  Ag^ony. — This  has  been  observed  shortly  before  death 
from  various  diseases,  even  in  those  which  in  themselyes,  as  a  rule,  produce  no 
leukocytosis.  Ehrlich  and  Lazarus  do  not  regard  this  as  a  true  leukocytosis, 
but  claim  that  the  white  corpuscles  are  deposited  in  the  peripheral  vessels  on 
account  of  the  general  depression  of  the  circulation.  This  accumulation  affects 
chiefly  the  polynuclear  neutroj^hilic  cells. 

EOSINOPHILIC  LEUKOCYTOSIS,   OR  EOSINOPHILIA, 

Is  not  only  a  relative,  but  an  absolute,  increase  of  polynuclear  eosinophilic  leu- 
kocytes. The  number  of  eosinophiles  is  normally  140  to  280  per  cubic  milli- 
meter— i.  e.,  2  to  4  per  cent,  of  the  total  number  of  leukocytes.  They  may 
increase  up  to  5000.  It  must  be  borne  in  mind  in  estimating  the  degree  of 
eosinophilia  that  the  eosinophiles  are  more  numerous  in  children  than  in  adults. 
A' pathologic  eosinophilia  is  observed  : 

1.  In  bronchial  asthma,  where  the  eosinophiles  may  be  increased  to  about  20 
per  cent,  of  the  total  number  of  leukocytes. 


650  EXAMINATION  OF  THE  BLOOD. 

2.  In  pemphigus,  Zappert  found  4800  eosinopMles  in  a  cubic  millimeter. 

3.  In  various  other  cutaneous  diseases,  Lazarus  found  60  per  cent,  of  the  leu- 
kocytes to  be  eosinophiles  in  a  case  of  urticaria. 

4.  In  helminthiasis  or  uncinaria  (ankylostoma,  oxyuris,  bothriocephalus, 
tenia,  trichinosis,  and  perhaps  in  other  intestinal  parasites).  Eosinophilia  has 
been  observed  especially  when  Charcot's  crystals  are  present  in  the  stools.  The 
diagnostic  significance  of  this  condition  is  manifest.  In  cases  of  grave  anemia 
following  bothriocephalus  infection  the  eosinophiles  may  be  entirely  absent. 

5.  In  trichinosis,  since  eosinophilia  is  present  in  the  overwhelming  majority 
of  these  cases,  it  is  of  the  greatest  diagnostic  importance,^  especially  in  differ- 
entiating this  affection  from  typhoid  fever,  in  which  the  eosinophilic  cells 
entirely  disappear  at  the  height  of  the  disease.  In  trichinosis  the  number  of 
eosinophilic  leukocytes  after  the  fourteenth  day  may  be  increased  to  40  to  50  per 
cent,  of  the  total  number.  The  absolute  number  of  total  leukocytes  is  not 
always  increased. 

6.  After  the  disappearance  of  the  fever  in  some  infectious  diseases,  espe- 
cially if  accompanied  by  the  ordinary  neutrophilic  leukocytosis  (pneumonia, 
acute  rheumatism,  malaria).  In  scarlet  fever  the  eosinophiles  are  increased  not 
only  after  the  fever  has  vanished  but  during  the  fever  also.  After  injection  o*f 
tuberculin,  postfebrile  eosinophilia  has  been  observed. 

7.  In  malignant  tumors,  leading  to  cachexia. 

8.  After  removal  of  the  spleen  and  in  chronic  tumors  of  the  spleen, 

LYMPHOCYTOSIS. 

This  name  is  applied  to  those  conditions  of  the  blood  where  there  is 
an  increase  of  lymphocytes,  but  it  does  not  include  the  lymphocytosis 
of  lymphatic  leukemia,  which  is  sufficiently  characterized  as  an  inde- 
pendent disease.  We  know  very  little  as  yet  about  the  occurrence  of  a 
pure  lymphocytosis.  It  should  be  mentioned,  however,  that  in  some 
conditions  of  ordinary  polynuclear  leukocytosis — for  instance,  in  the 
digestion  leukocytosis — the  lymphocytes  may  also  be  increased,  and 
that  in  the  newborn  a  lymphocytosis  is  physiologic.  Pathologically,  a 
lymphocytosis  with  a  slight  polynuclear  leukocytosis  has  been  observed 
in  whooping-cough,  and  after  injection  of  tuberculin  and  pilocarpin.  A 
lymphocytosis  occurs  in  certain  stages  of  typhoid.  A  lymphocytosis  is 
of  an  entirely  different  clinical  significance  from  a  polynuclear  leuko- 
cytosis, not  only  because  the  former  cells  are  derived  from  the  lymphatic 
glands,  but  also  because,  on  account  of  their  slightly  developed  ameboid 
contractility,  their  origin  must  be  attributed,  according  to  Ehrlich  and 
his  school,  not  to  chemotactic  irritants  in  the  blood,  but  rather  to  a 
mechanical  washing  out  of  the  lymphocytes  from  the  lymphatic  glands, 
and  consequently  to  anatomic  changes  in  the  latter  structures.  In  con- 
tradistinction to  the  earlier  supposition,  it  should  be  noted  that  recent 
observations  indicate  that  the  lymphocytes  are  by  no  means  immobile. 

BLOOD-PLATES. 

Bizzozero  and  Hayem  have  recently  demonstrated  that  the  granules  and 
clumps  of  granules  visible  in  any  fresh  blood-preparation  are  postmortem  forma- 
tions which  owe  their  existence  to  rapid  disintegration  of  the  elements  called 
blood-plates  or  hematoblasts. 

'  See  Schleip,  75  Naturfoi-scherversammlung,  1903,  ref.  in  Berlin,  klin.  Woch.,  1903, 
No.  41,  p.  946,  and  Arch.f.  klin.  Med.,  vol.  Ixxx. 


OTHER  MORPHOLOGIC  RELATIONS  OF  THE  BLOOD.         651 

These  blood-plates  are  small,  circular  or  oval,  colorless  formations,  about 
3  IX  in  diameter.  They  disintegrate  very  easily,  and  adhere  very  readily  to  each 
other  and  to  the  other  elements  of  the  blood.  They  seem  to  play  an  important 
part  in  the  etiology  of  white  thrombi.  Their  number  is  variously  estimated  at 
from  200,000  to  500,000  per  cubic  millimeter. 

For  the  purpose  of  examining  blood-plates  before  they  are  destroyed,  it  is 
necessary  to  add  some  preservative  fluid  to  the  blood  the  moment  it  is  drawn. 
Hayem  recommends  the  following  : 

(1)  A  solution  of  1  part  of  methylene-violet  and  5000  parts  of  75  per  cent, 
(physiologic)  solution  of  sodium  chlorid. 

(2)  A  mixture  of  1  part  of  a  1  per  cent,  aqueous  solution  of  osmic  acid  and 
2  parts  of  0.75  per  cent,  solution  of  sodium  chlorid.  The  latter  fluid  fixes  the 
blood-plates  permanently,  whereas  the  former  stains  them.  Bizzozero  puts  a 
drop  of  one  of  these  solutions  on  the  finger-tip,  the  skin  of  which  has  been  care- 
fully cleansed.  The  skin  is  then  punctured  through  the  fluid,  so  that  the  ele- 
ments of  the  blood  come  in  immediate  contact  with  the  fluid.  This  blood- 
mixture  is  placed  under  the  microscope  ;  the  characteristic  blood-plates  are  then 
seen,  but  as  granules. 

Blood-plates  are  counted  in  a  very  similar  way  to  the  red  blood-corpuscles. 
Bizzozero,  however,  believes  that  if  this  method  of  counting  blood-plates  is  used, 
a  considerable  number  adhere  to  the  side  of  the  pipet.  He  therefore  advises 
that  the  blood  be  received  directly  in  a  14  per  cent,  solution  of  magnesium  sul- 
phate by  the  process  just  described.  The  blood-plates  are  a  little  deformed,  to  be 
sure,  but  this  solution  has  the  advantage  over  the  other  fluids  of  keeping  them 
isolated.  The  ratio  between  red  blood-corpuscles  and  blood-plates  can  then  be 
estimated  by  the  Thoma-Zeiss  counter,  the  number  of  red  blood-corpuscles 
determined  in  the  usual  way,  and  the  absolute  number  of  blood-plates  then 
reckoned.  Affanasiew  has  recommended  the  use  of  a  solution  consisting  of  0.6 
per  cent,  sodium  chlorid  with  0. 6  per  cent,  peptone  and  a  little  methylene-violet. 
The  number  of  blood-plates  may  also  be  found  by  a  determination  of  the  ratio 
between  it  and  the  number  of  the  leukocytes  in  a  dry  preparation  ;  the  disad- 
vantage of  this  method  is  that  the  blood-plates  are  found  continually  clumped. 

Little  is  as  yet  known  regarding  the  relation  of  blood-plates  to  physiologic 
and  pathologic  conditions.  According  to  Bizzozero,  they  are  increased  in  preg- 
nancy, after  the  loss  of  blood,  in  various  anemias  (chlorosis),  in  tuberculosis, 
cholera,  etc.  They  are  diminished  in  fever  and  acute  diseases,  but,  according  to 
Hayem,  increase  toward  the  end  of  a  fever.  Denys  observed  a  diminution  of 
blood-plates  in  purpura.  (Compare  p.  634  with  reference  to  the  lodin  Eeaction 
of  Blood-plates.) 

THE  SO-CALLED  CASTS  IN  THE  BLOOD. 

Litten  ^  first  called  attention  to  the  fact  that  peculiar  large  cylindric  forma- 
tions, moderately  refractile  to  light,  were  found  in  fresh  unstained  blood-prepa- 
rations both  from  healthy  and  from  diseased  individuals.  They  are  sometimes 
granular,  sometimes  homogeneous  and  flaky.  Litten  considers  theqi  artificial 
formations  due  to  the  preparation  of  the  slide.  He  maintains  that  if  the  cover- 
glass  is  dragged  a  little,  they  can  easily  be  formed  from  blood-plates  or  from  red 
corpuscles,  and  are  of  no  diagnostic  interest.  Buttersack  '^  considers  that  they 
are  formed  within  the  vessels,  and  represent  capillaiy  blood-plate  thrombi. 

MELANEMIA. 

By  melanemia  is  meant  the  presence  of  granular  brownish  or  black  pigment  in 

the  blood.     It  is  usually  found  in  the  interior  of  white  blood-corpuscles,  which 

are  often  irregular  in  shape,  and  less  frequently  as  free  plates  between  the  cellular 

elements  of  the  blood.     Melanemia  has  as  yet  been  found  only  following  long- 

1  Devtsch.  med.  WocL,  1896,  No.  15,  p.  230;  ibid.,  1898,  No.  18,  p.  188. 
"  Zeits.f.  klin.  Med.,  vol.  xxxiii. 


652 


EXAMINATION  OF  THE  BLOOD. 


continued  malarial  cachexia  and  in  recurrent  fever.  In  malaria  the  pigment 
derived  from  hemoglobin  may  show  all  shades  of  color.  Sometimes  it  may  even 
be  black.  The  presence  of  white  blood-corpuscles  with  pigment  or  of  free  pig- 
ment is  of  great  diagnostic  importance  in  those  cases  in  which  the  malarial 
parasites  are  not  readily  discoverable. 

LIPEMIA. 

Blood  always  contains  some  fat  under  physiologic  conditions.  More  marked 
lipemia  is  observed  physiologically  during  digestion,  and  pathologically  in  chronic 
alcoholism,  in  acute  phosphorus-poisoning,  in  severe  diabetes,  and  in  fracture  of 
bones,  which  may  lead  to  fat-emboli.  If  the  blood  contains  a  considerable  amount 
of  fat,  its  pallor  and  cloudiness  is  apparent  to  the  naked  eye.  Under  the  micro- 
scope the  fat  is  usually  seen  in  the  form  of  veiy  fine  granules,  just  as  in  chyle;  in 
embolic  lipemia  distinct  light-refracting  drops  may  be  seen.  They  are  stained 
black  by  osmic  acid,  and  red  by  Sudan  III. ,  and  dissolved  in  a  diy  preparation 
by  the  addition  of  ether,  i 

BACTERIA  IN  THE  BLOOD. 

To  demonstrate  bacteria  in  the  blood,  dry  preparations  are  spread  between 
two  cover-slips  in  the  usual  way.  The  slides  are  passed  through  the  flame  two 
or  three  times,  and  then  stained  like  specimens  of  sputum  (compare  p.  593). 

Since  the  staining  of  the  erythrocytes  and  of  the  dried  albumin  of  the  blood 
interferes  with  the  beauty  and  transparency  of  the  preparations,  the  procedure 
suggested  by  Giinther  may  be  followed  -  with  advantage,  as  by  it  the  hemoglobin 
and  part  of  the  albumin  are  removed  from  the  dried  sijecimen.     Giinther  fixes 


Fig  234.— Recurrence  spirillffi  in  blood.  Photo-       Fig.  235.— Anthrax  bacilli  in  blood,  unstained 
graph  by  Weiehselbaum  (x  1000).  (X  iSOj  CFrankeD. 

the  dried  blood  by  heat,  and  then  washes  it  for  ten  seconds  in  a  5  per  cent,  solu- 
tion of  acetic  acid.  The  cover-glass  is  then  dried,  and  for  several  seconds  the 
smeared  side  is  held  directly  over  an  open  bottle  of  ammonia,  which  has  been 
pre^^ously  well  shaken,  so  that  the  last  remains  of  the  acid  may  be  neutralized. 
The  cover-glass  is  now  immersed  in  the  staining  solution  for  a  short  time  and 
then  washed  in  water.  Since  the  tinctorial  characteristics  of  the  erythrocytes 
depend  upon  their  contained  hemoglobin,  these  structures  will  appear  colorless, 
and  any  bacteria  which  may  be  present  will  be  easy  of  recognition. 

The  spirilke  of  recurrent  fever  and  the  bacUli  of  anthrax  (Figs.  234  and  235) 

'  Eieder,  Arch.  f.  klw.  Mer}.,  vol.  lix.,  p.  444. 
2  Forii^chritie  de'r  Med.,  1885,  vol.  iii.,  p.  756. 


OTHER  MORPHOLOGIC  RELATIONS  OF  THE  BLOOD.         653 

are  pathognomonic  when  found  in  the  blood.  Both  of  these  micro-organisms 
may  be  recognized  in  unstained  specimens. 

Bacteria  are  more  easily  demonstrated  in  the  blood  by  cultures  than  by  a 
microscopic  examination — e.  g.,  the  streptococci  and  staphylococci  (compare 
Figs.  218  and  219)  found  in  septicopyemia.  The  number  of  mici'O-organisms 
found  in  the  blood  is  always  comparatively  small,  so  that  considerable  blood 
should  be  emjjloyed  to  inoculate  the  culture  medium.  For  this  purpose  a  suffi- 
cient quantity  of  blood  is  removed  from  some  vein  of  the  arm  with  the  aid  of  a 
small  syringe  fitted  with  an  asbestos  piston  and  thoroughly  sterilized.  This 
syringe  should  contain  about  5  c.c.  The  skin  should  be  first  carefully  disinfected 
with  alcohol  and  corrosive  sublimate.  About  1  c.c.  of  this  blood  is  added  to  a 
tube  of  agar  (liquefiable  at  40°  C.  at  the  most),  to  one  with  10  per  cent,  gelatin,  and 
to  two  bouillon  tubes.  The  fluids  are  carefully  shaken,  and  the  agar  and  the  gelatin 
tubes  are  plated.  The  agar  plates  and  the  bouillon  tubes  are  placed  in  the  incu- 
bator at  37°  C,  the  gelatin  plate  at  22°  C.  Sittmann  ^  found  pus  cocci  or 
staphylococci  in  the  blood  in  every  case  of  septic  pyemia  which  he  examined  in 
this  way.  The  bacteriologic  examination  of  the  blood  is  the  most  accurate  aid 
for  determining  pyemia. 

In  severe  cases  of  pneumonia  we  have  not  infrequently  been- able  to  demon- 
strate i)neumococci  in  the  blood  either  by  direct  microscopic  examination  or  by 
culture  methods.  This  shows  the  relationship  existing  between  pneumonia  of 
the  human  subject,  which  is  usually  regarded  as  a  purely  local  affection,  and  the 
pneumococcic  sepsis  of  laboratory  animals.  The  procedure  given  upon  j).  652  for 
the  removal  of  the  hemoglobin  with  acetic  acid  greatly  aids  the  demonstration  of 
the  capsules  of  the  pneumococci. 

Typhoid  bacilli  may  frequently  be  demonstrated  in  the  blood  of  typhoid  fever 
patients,  either  in  fresh  specimens  or  in  cultures,  and,  in  the  writer's  experience, 
may  even  be  found  in  cases  running  a  mild  course.  They  are  most  frequently 
found  in  the  first  week  of  the  disease. 

The  demonstration  of  joesi!  bacilli  (Fig.  228)  plays  an  important  role  in  the 
diagnosis  of  bubonic  plague.  (For  their  recognition  the  reader  is  referred  to  the 
section  upon  Examination  of  the  Sputum.) 

The  occurrence  of  the  bacillus  mallei  (p.  602)  in  the  blood  is  of  less  diagnostic 
importance. 

Tubercle  bacilli  (p.  593)  have  as  yet  been  found  in  the  blood  only  in  acute 
miliary  tuberculosis,  and  then  in  very  small  numbers. 

THE  BLOOD  IN  MALARIA;   MALARIAL  PLASMODIA. 

We  owe  our  knowledge  of  the  malarial  parasite,  first  of  all,  to  the  pioneer 
investigations  of  the  French  military  surgeon  Laveran.  Fui'ther  development  in 
the  study  of  the  etiology  of  malaria  has  been  accomplished  chiefly  by  Italian 
investigators,,  esjjecially  Golgi,  Marchiafava,  and  Celli,  and  recently  by  R.  Koch 
and  many  others.  Of  the  comprehensive  articles  upon  this  topic  may  be  cited 
the  monograph  of  Mannaberg,^  and  more  recently  those  of  Marchiafava,  Celli, 
Thayer,  and  others. 

Malarial  parasites,  ordinarily  called  plasmodia,  are  unicellular  organisms 
belonging  to  the  class  of  sporozoa,  subclass  hemosporidia,  which  are  on  the  border 
line  of  the  animal  and  the  vegetable  kingdoms.  They  consist  of  small  masses  of 
protoplasm,  the  diameters  of  which  vary  between  1  and  10  mm.,  according  to 
the  age  and  species  of  the  individuals.  The  younger  specimens  show  active 
ameboid  motion.  They  develop  in  the  interior  of  the  red  blood-cells,  destroying 
their  host  in  their  growth.  Most  varieties  alter  the  hemoglobin  of  the  blood- 
corpuscles  which  they  inhabit  to  a  brownish-black  pigment.     This  pigment  is 

^  Deutsch.  Arch.  f.  klin.  Med.,  vol.  liii.,  p.  327,  1894;  see  Petruschki,  ZeZ/.s.  /.  7%/. 
u.  Tvfection^r^krankhriten,  vol.  xvii.,  p.  59. 

^  Jill.  Maniialierg,  Die  Molar iapara.vlm,  Wien.  1893,  and  "Die  Malariakrank- 
heiten,"  in  yoUinuf/el' a  Spec.  Pathologie  u.  IVierapie,  1898. 


654  EXAM^ATION   OF  THE  BLOOD. 

genei'ally  visible  in  the  interior  of  tlie  parasite,  undergoing  active  dancing  motion, 
whicli  may  partly  depend  upon  the  intrinsic  motion  of  the  jjrotoijlasm,  and  should 
not  be  confounded  with  the  much  slower  ameboid  motion  of  the  organism.  After 
the  parasite  has  reached  a  certain  stage  of  development  within  the  red  blood-cell, 
and  has  more  or  less  completely  consumed  the  latter  (Plate  7,  Figs.  1  to  4  and 
11  to  13),  it  multiplies  by  sporulation  (Plate  7,  Figs.  5  to  8  and  16).  This  takes 
place  by  a  process  of  division,  varying  in  the  different  types,  but  always  in  such 
a  manner  that  nothing  remains  of  the  mother  organism  but  the  pigment.  The 
free  pigment  is  taken  up  by  the  white  blood-corpuscles,  and,  when  these  are  sub- 
sequently disintegrated,  is  deposited  in  the  organs  (melanemia).  The  young 
parasites  produced  by  subdi'S'ision  are  known  as  spores.  They  differ,  however, 
from  the  folly  developed  jaarasites  only  in  their  size.  They  penetrate  fresh  blood- 
corpuscles,  and  then  repeat  the  stages  of  development.  The  type  of  development 
of  the  quartan  malarial  parasite  is  represented  in  Plate  7,  Figs.  11  to  17  ;  of  the 
tertian  organism,  in  Figs.  1  to  10.  The  attacks  of  fever  so  characteristic  of  ma- 
laria are,  generally  speaking,  associated  with  sporulation  of  the  parasite.  These 
attacks  follow  at  regular  intervals  in  the  ordinary  types  of  malaria,  because  the 
time  for  the  cycle  of  development  of  one  generation  of  parasites  is  a  definite 
quantity  which  can  be  usually  expressed  in  terms  of  days — e.  g.,  tertian  and  quartan. 
Types  with  longer  periods  (quintan)  are  more  uncommon  and  not  so  thoroughly 
understood.  ]Most  quotidian  types,  at  least  in  regions  where  tertian  and  quartan 
fever  prevail,  represent  composite  forms  which  arise  by  different  generations 
of  tertian  or  quartan  parasites  developing  in  the  organism  on  succeeding  days, 
the  one  generation  being  a  day  older  than  the  other.  A  quotidian  type  of 
fever  will  be  observed  if  two  generations  of  tertian  or  three  generations  of  quartan 
parasites  complete  their  cycle  of  development  on  days  succeeding  each  other. 
This  view  of  quotidian  t\^es  was  prevalent  even  before  the  parasite  of  malaria  was 
discovered,  because  the  attacks  were  peculiarly  grouped  together  in  pairs  with 
reference  to  their  severity  and  other  symptoms  (tertiana  duplex,  quartiana  triplex). 
Besides  these  combined  quotidian  t^'pes,  a  true  quotidian  type  whose  cycle  of 
development  lasted  only  one  day  was  supposed  to  exist,  until  in  recent  times  the 
investigation  of  E.  Koch  (more  in  detail  later)  disproved  this  idea. 

Our  knowledge  of  the  morphologic  conditions  and  the  development  of  the 
malarial  parasites  is  at  the  present  time  so  complete,  thanks  to  the  work  of  the 
above-mentioned  Italian  authors,  that  a  physician  familiar  with  the  morphology 
of  the  jaarasites  is  able,  by  examining  the  blood,  not  only  to  recognize  the  presence 
of  malaria,  but  also  to  determine  the  form,  the  type,  and  the  clinical  course  of  the 
attack.     We  shall  refer  to  this  later. 

Two  other  kinds  of  parasites  have  been  observed  in  the  blood  in  malaria,  the 
so-called  crescents  of  the  testivo-autumnal  type  of  the  disease,  and  flagellate  bodies. 

Figs.  25  to  27,  Plate  7,  represent  types  of  the  crescent  series,  which  are 
peculiar  to  the  malignant  (tropic)  form  of  malaria.  They  differ  in  shape  from 
the  ordinary  plasmodia,  and  possess  a  double  capsule.  The  crescents  (Figs.  25  to 
27,  Plate  7)  develop  in  the  interior  of  the  red  blood-corpuscles,  as  indicated  by 
the  remnant  of  the  red  corpuscles  frequently  seen  attached  to  them.  Elongated 
cigar-shaped  and  spheric  formations  (ovals  and  spheres  of  the  testivo-autumnal 
crescents)  develop  from  the  crescents  by  changes  in  shajse  slow  enough  to  be 
observed  under  the  microscope.  These  forms  do  not  possess  any  ameboid 
motion  proper.  Mannaberg  believes  that  the  crescents  are  formed  by  approxi- 
mation and  fusion  of  two  plasmodia  in  the  interior  of  the  red  blood-cells,  and 
that  they  are  therefore  a  kind  of  copulation  type,  a  so-called  sjzygy  formation. 
The  crescents  may  divide  into  their  component  parts  by  subsequent  segmenta- 
tion. Clinical  conditions  seem  to  make  it  probable  that  the  crescents  are  more 
or  less  i^ermanent  forms,  which  produce  symptoms — i.  e.,  fever — only  after 
transformation  into  the  vegetative  type.  How  this  process  takes  place  is  still 
uncertain,  whether  the  crescents  segment  into  their  component  parts,  or  whether, 
as  Canalis  claims,  they  sporulate  also  directly  after  they  have  changed  to  the 
spheric  form.  At  any  rate,  the  crescents  seem  to  have  a  slow  stage  of  develop- 
ment.    Durino;  the  intermissions  of  eight  to  fourteen  davs  free  from  fever    in 


PLATE  7. 


JO 


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14 


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19 


20 


21 


22 


S3 


24- 


26 


27 


Various  Forms  of  Malarial  Parasites  (Thayer  and  Hewetson). 

Figs.  1  to  10  inclusive,  tertian  organisms;  Figs.  11  to  17  inclusive,  quartan  organisms ;  Figs. 
18  to  27  inclusive,  estivo-autumnal  organisms. 

Fig.  1.— Young  hyaline  form  ;  2,  hyaline  form  with  heginning  pigmentation  ;  3,  pigmented 
form  ;  4,  full-grown  pigmented  form  ;  5,  6,  7,  8,  segmenting  forms  ;  9,  extracellular  pigmented 
form  ;  10,  flagellate  form. 

Fig.  11.— Young  hyaline  form  :  12, 13,  pigmented  forms  ;  14,  fully-developed  pigmented  form; 
15,  16,  segmenting  forms;  17,  flagellate  form. 

Figs.  18, 19,  20.— Ring-like  and  cross-like  hyaline  forms  ;  21,  22,  pigmented  forms  ;  23,  24,  seg- 
menting forms  ;  25,  26,  27,  crescents. 


OTHER  MORPHOLOGIC  RELATIONS  OF  THE  BLOOD.  655 

the  severe  tropic  malaria,  which  is,  except  for  such  intermission,  quotidian, 
only  crescents  can  be  found  in  the  blood.  It  is  therefore  probable  that  these 
free  intervals  correspond  to  the  stage  of  development  of  the  crescents.  At  any 
rate,  both  the  crescents  themselves  and  the  secondary  types  developed  from  them 
(ovals  and  spheres)  are  not  independent  formations,  but  stages  in  the  develop- 
ment of  the  Plasmodia,  and  are  entirely  confined  to  the  malignant  types  of  malaria. 
In  the  tertian,  quartan,  and  composite  quotidian  types  of  the  temperate  zones  cres- 
cents have  never  been  observed. 

The  flagellate  bodies  are  found  in  all  kinds  of  malaria  (Plate  7,  Figs.  10  and 
17).  Under  the  microscope  they  may  be  seen  to  develop  from  adult  j^lasmodia 
which  have  destroyed  their  blood-corpuscle  and  have  not  sporulated  and  again 
from  the  spheres  of  the  crescent  series.  These  flagella  suddenly  appear  at  the 
margin  of  the  parasite  ;  they  move  very  quickly  and  lash  the  surrounding  blood- 
corpuscles  without,  as  a  rule,  causing  any  particular  motion  to  the  jjarasite 
itself.  Every  once  in  a  while  individual  flagella  will  tear  themselves  ofl^  and 
move  about  with  great  rapidity  in  the  field.  These  isolated  flagella  are  the  only 
formations  in  the  whole  cycle  of  development  of  malarial  parasites  which  have 
the  power  of  changing  their  position  to  any  great  extent.  Probably  the  flagellate 
forms  develop  only  in  microscopic  preparations  ;  Mannaberg  therefore  considers 
that  they  correspond  to  a  saproj^hytic  existence.  Recently,  however,  their  biologic 
significance  has  been  explained  in  a  very  interesting  and  probable  way,  which 
will  be  discussed  later. 

Unstained  blood-preparations  may  be  employed  to  detect  the  malarial  para- 
sites. They  should  be  especially  thin  (p.  631),  so  that  the  individual  blood-cor- 
puscles may  not  overlap  nor  stick  together  and  form  rouleaux.  The  preparations 
are  best  examined  with  an  oil  immersion.  Abbe's  condenser,  and  a  half-023en  iris. 
The  pigmented  forms,  the  crescents,  and  the  flagellate  types  can  be  very  easily 
detected,  but  the  hyaline  forms  are  not  so  easily  differentiated  from  the  endoglob- 
ular  types  of  degeneration  or  the  so-called  vacuoles  of  the  red  blood-corpuscles. 
Differences  of  light  refraction,  however,  cause  a  more  sharply  outlined  contour  in 
the  latter  than  in  the  plasmodia.  Ameboid  motion  is  common  to  both.  Doubt- 
ful cases  can  be  decided  by  examining  stained  preparations.  Where  so  few  plas- 
modia occur  as  to  be  difficult  to  demonstrate,  Tiirk  recommends  diluting  the 
blood  ten  times  with  a  \  per  cent,  solution  of  acetic  acid,  just  as  for  counting 
Plasmodia  and  leukocytes.  The  leukocytes  and  plasmodia  will  be  preserved  and 
the  red  blood-coi'jiuscles  destroyed. 

Malarial  blood  should  be  stained  as  indicated  on  p.  631.  Fixation  should  be 
accomplished  not  by  heating,  but  by  allowing  the  slides  to  remain  for  five  minutes 
in  absolute  alcohol.  They  are  then  placed  for  half  an  hour  in  a  half-concentrated 
and  freshly  filtered  aqueous  solution  of  methylene-blue,  or  else  stained  for  five  or 
six  minutes  in  the  following  (Plehn's  contrast  stain): 

■  Concentrated  aqueous  methylene-blue 40 

Two  per  cent,  solution  of  eosin,  60  per  cent,  alcohol    ...  80 

Water 40 

Twenty  per  cent,  potassic  hydroxid .  12  drops. 

The  endoglobular  degeneration  spots  remain  colorless,  but  the  plasmodia  stain 
well  with  methylene-blue  and  show  a  characteristic  structure — namely,  an  un- 
stained nucleus,  and  sometimes  a  stained  nucleolus.  This  structure,  esijecially 
the  stained  nucleolus,  enables  us  to  distinguish  blood-plates  and  granular  debris 
of  the  blood  from '  the  spores  of  malarial  parasites.  The  blood-plates  have  no 
nucleus  and  are  devoid  of  structure. 

Mannaberg  recommends  staining  the  plasmodia,  to  show  the  finer  structures, 
with  the  following : 

Concentrated  solution  of  aqueous  methylene-blue 24  parts. 

Five  per  cent,  borax  solution 16     " 

Water 28     " 

Filtered  after  twenty-four  hours. 


656  EXAMINATION  OF  THE  BLOOD. 

The  preparations  remain  twenty-four  hours  in  this  solution  and  are  then 
washed  with  water. 

R.  Koch  has  recently  recommended  a  similar  solution  of  borax-methylene- 
blue  for  rapid  staining.  An  aqueous  solution  of  2  per  cent,  methylene-blue  and 
5  per  cent,  borax  is  diluted  with  water  before  being  used  until  a  layer  1  cm.  thick 
begins  to  become  transparent.  The  dry  specimen  is  once  passed  through  the 
flame,  placed  in  alcohol  for  twenty  minutes,  dried,  and  then  dipped  into  this  solu- 
tion several  times,  and  washed  with  water  until  it  has  become  of  a  slightly  greenish 
tinge.  It  is  then  dried  with  filtered  paper  and  mounted  in  cedar  oil.  The 
malarial  parasites  will  be  stained  intensely  blue,  the  blood-corpuscles  pale  green, 
and  the  nuclei  of  the  leukocytes  darker  than  the  plasmodia. 

Homanowski'  s  method  of  staining  can  be  heartily  recommended  to  show  the 
finer  structure  of  the  malarial  parasites.  The  technic  is  as  follows :  The  slides 
are  fixed  either  in  alcohol  or  by  heating  to  105°  or  115°  C.  for  half  an  hour. 
They  are  then  allowed  to  float  in  a  solution  of  1  part  of  concentrated  aqueous 
methylene-blue  and  2  parts  of  1  per  cent,  aqueous  eosin  for  two  to  three  hours. 
They  are  next  washed  in  water,  and,  if  overstained,  in  alcohol.  The  stock  solu- 
tions may  be  preserved  for  a  long  time.  The  eosin  solution  must  be  free  from 
mold,  whereas  the  solution  of  methylene-blue  is  said  to  be  better  after  a  little 
mold  has  developed  on  its  surface.  The  required  quantity  of  each  solution  is 
filtered  off"  before  using.  When  they  are  mixed,  a  considerable  precipitate 
develops,  which  should  not  be  filtered  off".  Romonowski  claims  that  a  new  neu- 
tral color  is  formed  in  the  mixture,  which  is  supposed  to  stain  the  chromatin  of 
the  malarial  parasites  particularly  intensely.  The  plasma  of  the  parasite  is 
stained  blue,  and  the  chromatin  of  the  nucleus  is  violet  carmin.  The  success  of 
the  stain  seems  to  depend  considerably  upon  the  quality  of  the  coloring  matter. 
Hochster's  medicinal  methylene-blue  and  eosin  are  the  best  dyes.  Sometimes  the 
proportions  of  the  solutions  must  be  modified.  ^ 

To  find  malarial  plasmodia  quickly  when  they  are  but  sparingly  present, 
R.  Ruge  ^  recommends  employing  a  thick  layer  of  blood  from  which  the  hemo- 
globin has  been  removed  before  staining,  in  a  similar  manner  to  the  method 
described  upon  p.  652.  A  cover-glass  is  thickly  smeared  with  blood,  dried,  and 
then  laid  with  the  smeared  surface  down  in  a  watch  glass  containing  2  per 
cent,  formaldehyd  and  a  J  to  1  per  cent,  acetic  acid.  A  few  minutes  suffices  to 
fix  the  specimen  and  also  to  extract  its  hemoglobin.  It  is  now  stained  with 
methylene-blue  in  the  ordinary  manner,  and  the  plasmodia  may  be  readily  found, 
even  though  there  be  a  number  of  layers  of  erythrocytes.  This  procedure  has 
the  advantage  of  employing  more  than  twenty  times  the  volume  of  blood  utilized 
in  the  usual  cover-glass  smear.  Ruge  admits,  however,  that  there  is  always  a 
greater  or  less  amount  of  precipitate,  which  an  inexperienced  observer  might 
differentiate  fi-om  plasmodia  with  difficulty.  He  also  calls  attention  to  the  fact 
that  the  ring  forms  of  the  young  malarial  plasmodia  (p.  657)  are  beautifully  shown 
by  this  procedure. 

Counting  the  plasmodia  gives  more  or  less  information  as  to  the  severity  of  a 
malarial  infection.  Turk  counts  them  in  the  same  way  as  leukocytes,  in  a  J  per 
cent,  solution  of  acetic  acid,  a  method  available  only  for  the  pigment  forms. 
The  time  of  counting  should  therefore  be  immediately  before  the  attack — e.  g., 
in  tertian  fever,  the  evening  before  the  day  of  fever.  Turk's  figures  vary  between 
6700  and  16,800  per  cubic  millimeter. 

The  diagnostic  significance  of  malarial  parasites  in  the  blood  is  absolute.  The 
presence  of  one  single  parasite  is  sufficient  for  a  diagnosis  of  malaria  (the  pig- 
mented forms  and  the  crescents  cannot  be  mistaken).  Negative  results  are  not  so 
certain,  because  many  cases  of  malaria  require  a  long  search  before  a  single  para- 
site is  seen.  The  blood  should  be  examined  both  during  and  between  the  attacks. 
Even  the  most  expert  investigators  have  been  sometimes  compelled  to  make  the 
diagnosis  of  malaria  without  finding  the  parasite.     In  these  cases  the  parasites 

1  Deuhch.  med.  Woch.,  1903,  No.  12,  p.  205. 

^  See  Mannaberg  in  Nothnucjel'»  Spec.  Pathologie  u.  I'herapie,  1899,  p.  34. 


OTHER  MORPHOLOGIC  RELATIONS  OF  THE  BLOOD.         657 

are  either  very  few  in  number  or  else  develop  in  the  tissues  rather  than  in  the 
blood  (hypothetic).  An  inexperienced  examiner  should  always  mistrust  a  negative 
result  and  repeat  his  search.  In  case  of  repeated  negative  blood-examination, 
suspicion  should  be  directed  to  the  presence  of  one  or  more  diseases  which  are 
easily  confounded  with  malaria  clinically — e.  g.,  acute  sepsis,  irregular  chole- 
lithiasis, ulcerative  endocarditis,  etc. 

The  blood  of  severe  malaria  shows  in  addition  the  characteristics  of  anemic 
blood — namely,  the  diminution  of  hemoglobin  and  of  the  number  of  red  cells. 
Poikilocytosis  is  by  no  means  uncommon.  There  is  usually  no  leukocytosis,  but 
rather  a  leukopenia.  The  presence  of  pigment  in  the  white  blood-corpuscles  or 
pigment  floating  free  in  the  blood  is  of  considerable  diagnostic  imjiortance  if  the 
parasites  cannot  be  found.  The  red  blood-cells  which  are  invaded  by  the  para- 
sites may  be  altered  in  various  ways.  The  ordinary  types  usually  decolorize 
the  cells  gradually,  until  finally  all  that  is  left  is  an  indistinct  stroma  sur- 
rounding the  parasite.  The  blood-corpuscles  may  be  considerably  enlarged 
by  the  tertian  parasites,  which  differ  from  the  quartan  variety  in  this  respect. 
In  the  malignant  types  the  infected  blood-corpuscles  shrink  and  become 
darker,  and,  according  to  Mannaberg,  resemble  the  color  of  old  brass  (brassy 
bodies. 

The  majority  of  investigators  have  concluded  that  the  various  forms  of  mala- 
rial parasites  found  in  the  blood  represent  various  developmental  phases  not  only 
of  the  same,  but  also  of  different  species.  Each  type  of  malaria  which  is  char- 
acterized clinically  and  endemiologically  represents  a  separate  species  of  parasites 
with  a  definite  cycle  of  development.  The  reasons  for  these  views  may  be  found 
in  Mannaberg' s  monograph.  He  describes  the  following  five  species  of  para- 
sites : 

1.  The  parasites  of  quartan  fever. 

2.  The  parasites  of  the  common  tertian  fever. 

3.  Pigmented  quotidian  parasites. 

4.  Non-pigmented  quotidian  joarasites. 

5.  Malignant  tertian  parasites. 

Those  of  3,  4,  and  5  are  malignant  varieties  with  crescents,  which  probably 
explains  the  difiiculty  with  which  these  cases  are  influenced  by  quinin. 

R.  Koch,  on  the  other  hand,  considers  these  three  groups  of  parasites  as  one 
species,  which  is  to  blame  for  the  malignant  summer  fevers  (aestivo-autumnal) 
of  southern  Europe,  especially  of  Italy,  and  of  the  tropics.  Koch  therefore  dis- 
tinguishes only  the  jjarasites  of  quartan,  tertian,  and  tropic  fever.  He  shows 
that  a  fresh  infection  of  the  parasite  of  tropic  fever  always  produces  attacks  of  a 
pronounced  tertian  tyjje  (corresj^onding  to  m^Jignant  tertian  j^arasites).  When 
the  disease  has  persisted  for  some  time  and  the  natural  course  has  been  more  or 
less  influenced  by  treatjnent  with  quinin,  there  may  develop  from  the  tertian  tyj^e 
either  a  quotidian  type,  an  irregularly  remitting,  or  a  continued  fever.  Accord- 
ing to  this  view  there  is  no  true  quotidian  parasite.  Koch's  simplified  classifica- 
tion is  based  inore  or  less  upon  his  view  that  the  difference  in  the  j^igment  which 
gives  rise  to  the  distinction  between  the  so-called  pigmented  and  non-pigmented 
quotidian  parasites  is  an  artificial  condition  depending  upon  the  method  of  prepara- 
tion. When  dry  preparations  were  made  skilfully  and  rapidly  he  found  that  the 
young  parasites  of  tropic  fever  were,  as  a  rule,  without  pigment  or  had  only  very 
fine  granules,  and,  at  any  rate,  were  free  from  lumps  of  pigment,  even  when  the  fine 
pigment  lent  a  brownish  diffuse  hue ;  lumps  of  pigment  were  found  only  when  the 
parasite  underwent  subdivision  or  death.  If  a  wet  preparation  was  allowed  to  stand 
for  any  length  of  time,  lumps  of  j^igment  were  apt  to  develop.  Koch  therefore 
maintains  that  the  only  correct  method  of  examination  is  by  properly  prepared 
dry  slides.  He  considers  that  the  ring-shaped  young  parasites  found  with  this 
method  (quartan  and  tertian  as  well  as  tropic  fever)  represent  the  correct  mor- 
phologic conditions.  Other  investigators  have  observed  these  ring  forms,  to  be 
sure,  but  have  considered  them  partly  as  artificial  j^roducts,  partly  as  the  result 
of  the  circular  arrangement  of  the  stained  substance  and  not  of  the  whole  jjroto- 
plasm. 

42 


658  EXAMINATION  OF  THE  BLOOD. 

.  For  determining  tlie  various  varieties,  Koch  lays  special  stress  upon  tlie  size 
of  the  parasite,  and  the  presence  of  crescents  so  characteristic  of  the  tropic 
fevers.  He  makes  the  following  statements  in  regard  to  this  matter  :  The  young 
circular  parasites  of  tertian  and  quartan  fever  have  a  diameter  of  about  one- 
quarter  to  one-third  that  of  the  red  blood-cells.  In  size  and  shape  they  resemble 
the  fully  developed  parasite  of  tropic  malaria  so  completely  that  they  cannot  be 
differentiated.  But,  as  a  rule,  in  tertian  and  quartan  fever  scattered  large  pig- 
mented parasites  are  found  in  addition  to  the  small  circular  ones,  which  makes 
the  diagnosis  easy.  If  the  latter  should  be  absent,  the  determination  of  the  body 
temperature  at  the  time  of  examination  will  furnish  sufficient  explanation  of  the 
significance  of  the  preparation.  If  the  temperature  is  low  and  the  fever  has 
ceased,  the  parasites  must  have  completed  their  cycle  of  development.  The  small 
types  found  must,  therefore,  represent  the  fully  developed  smaller  parasites  of 
the  tropic  malaria.  If,  on  the  other  hand,  the  temperature  is  high  and  the  patient 
is  in  the  early  stages  of  an  attack,  then  these  small  ring  bodies  must  be  young 
parasites  of  the  tertian  and  quartan  groups  which  have  not  yet  reached  their  full 
size. 

The  variations  of  sporulation  also  serve  to  distinguish  the  individual  varieties. 
This  is  seen  in  Plate  7  better  than  it  can  be  described.  It  is  of  some  clinical 
interest  to  be  able  to  tell  the  time  of  an  attack  merely  from  the  period  of  sporu- 
lation (Figs.  5  to  8  and  16).  It  usually  takes  place  three  to  five  hours  after  the 
spore  forms  have  appeared. 

The  crescents  are  said  to  be  formed  in  the  blood  eight  days  after  infection. 
If  these  persist  in  the  blood  along  with  the  other  forms  of  the  parasite,  after 
cessation  of  fever,  recurrences  may  be  expected.  There  is  ordinarily  no  fever 
when  only  crescent  forms  are  present. 

The  significance  of  the  so-called  flagellate  forms  has  recently  been  explained. 
The  investigations  of  Eoss,  MacCallum,  SakharoflT,  Koch,  et  al.,  with  the  hemo- 
sporidia  species  halteridimn  and  proteosoma,  which  occur  in  birds'  blood  and 
which  are  closely  related  to  the  malarial  parasites  of  human  blood,  have  shown 
that,  besides  the  endogenic  cycle  of  development  culminating  in  sporulation, 
there  is  a  second  sexual  cycle  of  development.  Koch  divides  this  into  the  follow- 
ing stages  :  1.  Separation  of  the  parasite  from  the  red  blood-corpuscle.  Differen- 
tiation into  male  and  female  elements.  The  thread-like  formations  which  were 
formerly  considered  flagella  develop  from  the  interior  of  the  male.  They  sepa- 
rate, propel  themselves  independently,  and  play  the  part  of  spermatozoa.  2. 
Fructuation  by  penetration  of  the  spermatozoa  into  the  female  plasmodia.  This 
takes  place  in  the  stomach  of  a  mosquito  which  has  sucked  the  blood  from  some 
infected  bird.  3.  Change  of  the  impregnated  female  parasites  into  worm-like 
bodies.  4.  Penetration  of  the  stomach-wall  of  the  mosquito  by  the  latter  and 
their  change  to  coccidia-like  spheres.  5.  Formation  of  sickle-shaped  bodies  in 
these  spheres.  6.  Deposit  of  these,  fully  developed  and  liberated,  in  the  poison 
and  salivary  glands  and  perhaps  in  the  other  organs  of  the  mosquito.  7.  Trans- 
mission of  young  parasites  again  to  birds  by  fresh  bites  of  the  mosquito. 

It  has  been  shown  that  these  biologic  facts  are  also  true  for  the  parasites  of 
human  malaria,  especially  since  the  transmission  of  the  disease  by  mosquito  bites, 
an  old  and  popular  belief,  has  recently  been  definitely  proved  experimentally. 

It  is  of  considerable  pathologic  interest  to  know  that  the  action  of  quinin 
results  in  a  necrosis  of  the  parasite.  This  may  be  recognized  in  stained  prepara- 
tions by  the-  disappearance  of  the  nucleus.  Very  young  parasites  are  more 
susceptible  to  its  action,  which  accounts  for  the  rule  that  it  is  best  to  give  quinin 
three  or  four  hours  before  an  attack  is  expected.  The  crescents  are  almost 
immune  to  the  direct  action  of  quinin,  as  shown  by  microscopic  examination,  so 
that  the  action  of  repeated  doses  of  quinin  in  malignant  types  resembles  more  or 
less  a  process  of  fractional  sterilization.  The  crescents  themselves  are  not  dis- 
turbed, but  the  Plasmodia  developing  from  them  are  killed  by  the  repeated  doses. 
In  exceptional  cases,  however,  the  crescents  are  not  so  resistant. 


CONDITION  OF  BLOOD  IN  MOST  IMPORTANT  BLOOD-DISEASES.   659 

PARASITIC  WORMS  IN  THE  BLOOD. 

Of  the  two  helminthes  inhabiting  the  human  blood  in  the  tropics,  Distomum 
haematobium  (Bilharzia  heematobia)  and  Filaria  sanguinis,  only  the  latter  is  of 
diagnostic  importance  in  blood-examinations.  The  blood  of  patients  infected 
with  filaria  (tropic  chyluria)  contains  numerous  small  thread-like  worms,  the 
filaria  embryos,  0.21  to' 0.36  mm.  long  and  0.004  to  0.0075  mm,  broad  (Fig.  205). 
Strange  to  say,  they  are  usually  found  only  at  night. 

CONDITION  OF  THE  BLOOD  IN  THE  MOST  IMPORTANT 

BLOOD-DISEASES* 

THE  ANEMIAS. 

The  condition  ordinarily  called  anemia  really  should  more  correctly  be  termed 
oligochromemia;  either  merely  the  quantity  of  hemoglobin  in  the  blood  may  be 
decreased,  or  the  number  of  erythrocytes  may  also  be  simultaneously  diminished. 
An  actual  loss  of  blood,  and  then  probably  merely  for  a  short  time,  occurs  only 
when  the  anemia  is  produced  by  hemorrhage.  In  all  anemias  undeveloped 
erythrocytes  may  be  present  in  the  blood,  as  the  result  either  of  a  disturbed  or  of 
an  incomplete  development.  The  subdivisions  of  anemia  vary  considerably.  The 
following  arrangement  would  seem  to  correspond  best  to  the  actual  conditions : 

THE  SO-CALLED  PRIMARY  ANEMIAS. 

Chlorosis. — The  chief  characteristic  of  the  blood  in  chlorosis  is  a  diminution 
in  the  amount  of  hemoglobin.  This  is  not  infi-equently  as  low  as  20  per  cent. 
The  number  of  red  blood-corpuscles  is  also  usually  diminished,  and  sometimes 
very  considerably  (1,500,000);  but  it  is  more  or  less  characteristic  that  the  dimi- 
nution of  hemoglobin  in  chlorosis  is  more  marked  than  the  diminution  of  the 
number  of  red  cells. 

The  color  index  (blood-corpuscle  quotient  of  value)  is  therefore  less  than  1. 
The  pallor  of  an  individual  blood-corpuscle  may  sometimes  be  recognized  micro- 
scopically. Severe  cases  of  chlorosis  exhibit  poikilocytosis,  microcytes,  nucleated 
red  cells,  and  the  disintegrating  forms  of  red  blood-cells  described  by  Maragliano. 
Granular  degeneration  and  polychromatophilic  changes  in  the  erythrocytes  are 
absent.  The  number  of  white  corj^uscles  and  of  blood-plates  is  usually  within 
normal  figures.  A  diagnosis  of  chlorosis  cannot  always  be  made  from  an  exami- 
nation of  the  blood  alone,  as  in  many  cases  it  depends  considerably  upon  the 
clinical  picture.  Chlorosis  is  a  disease  occurring  during  the  period  of  develop- 
ment, especially  in  women,  and  is  probably  to  be  explained  by  the  fact  that 
the  amount  of  blood  formed  is  not  sufficient  for  the  demands  of  the  growing 
organism.  1 

The  iirine  of  chlorotics  is  pale  and  contains  but  little  urobilin.  This  favors 
the  theory  just  given,  and  indicates  that  the  destruction  of  red  blood-corpuscles  is 
limited,  for  in  some  other  types  of  anemia,  especially  in  so-called  pernicious 
anemia,  the  increased  destruction  of  red  cells  is  manifested  clinically  in  a  dark 
urine,  which  contains  a  good  deal  of  urobilin.  The  patient  is  usually  well  nour- 
ished, and  may  even  be  increased  in  weight.  This  makes  the  peculiar  clinical 
picture  of  chlorosis. 

V.  Noorden  demonstrated  that  this  abundance  of  fat  in  chlorotics  is  not  due 
to  the  diminution  of  the  oxygen  content  of  the  organism  from  deficiency  in  the 

*  The  greater  frequency  of  chlorosis  in  women  must  be  associated  with  the  peculi- 
arities of  the  female  sex.  Apparently,  disturbances  somewhere  in  the  generative  organs 
inhibit  the  stimuli  which  affect  the  blood-forming  organs,  upon  which  is  deijendent  the 
normal  blood-formation  of  the  female.  The  conception  that  blood-formation  is  intimately 
connected  with  the  female  sexual  organs  has  much  in  its  favor,  as  it  is  reasonable  to 
assume  that  the  female  body,  which  loses  blood  during  menstruation,  a  process  peculiar 
to  the  sex,  must  have  an  adaptive  mechanism  in  the  genitalia  which  serves  to  stimulate 
blood-formation. 


660  EXAMINATION  OF  THE  BLOOD. 

hemoglobin  of  the  blood,  but  to  the  relatively  diminished  exercise  enforced  upon 
the  patient  by  the  disease. 

Simple  Primary  Anemia. — Under  this  term  we  may  include  all  cases, 
except  chlorosis  and  so-called  i^ernicious  anemia,  where  there  is  a  diminution  of 
the  hemoglobin  or  red  cells,  either  of  one  or  both  at  the  same  time,  and  where  no 
other  disease  is  present  which  can  cause  the  conditions.  Simple  primary  anemia, 
like  chlorosis,  can  be  considered  a  disease  of  the  blood-forming  organs  ;  it  differs 
from  chlorosis  in  that  it  does  not  affect  growing  individuals,  and  is  not,  therefore, 
a  disease  of  development.  The  fact  that  the  condition  of  the  blood  in  simple 
primary  anemia  is  identical  with  that  of  chlorosis  supports  this  view. 

To  distinguish  simple  primary  anemias  from  pernicious  anemia,  see  below. 

So-called  Pernicious  Anemia. — As  indicated  by  its  name,  this  disease  is 
malignant,  and  is  associated  with  an  unfavorable  prognosis.  This  view,  however, 
does  not  entirely  explain  the  situation,  for  the  severity  of  the  symptoms  is  a  rela- 
tive affair,  and  undoubtedly  many  cases  of  so-called  pernicious  anemia  have 
recovered.  It  would  seem  more  appropriate  to  consider  the  characteristic  feature 
of  the  clinical  picture  to  be  not  only  the  inusfiicient  blood-formation,  but  also  the 
abnormal  destruction  of  blood-cells,  which  does  not  occur  in  chlorosis  and  in  the 
so-called  simple  anemias.  This  jjeculiarity  must  ultimately  depend  upon  some 
especially  severe  disturbance  of  blood-formation,  not  only  quantitative  but  qualita- 
tive, as  is  evident  from  the  peculiar  condition  of  the  bone  marrow  (megaloblastic), 
and  the  j^resence  of  megaloblasts  in  the  blood.  At  the  present  time  an  effort  is 
being  made  to  explain  j^ernicious  anemia  as  a  megaloblastic  degeneration  of  the 
bone  marrow.  The  cases  to  be  mentioned  further  on  do  not,  however,  support 
this  view,  because  megaloblasts  were  absent  in  the  bone  marrow,  although  all  the 
other  clinical  signs  of  pernicious  anemia  were  present.  The  destructibility  of  red 
blood-corpuscles  in  pernicious  anemia  is  usually  indicated  clinically  by  the  marked 
poikilocytosis,  the  presence  of  basophilic  degeneration  of  the  red  cells,  and  the 
presence  of  urobilinuria  and  icterus.  Anatomically,  there  is  a  deposit  of  iron  in 
the  liver  and  kidneys,  as  shown  by  Quincke.  The  granular  basophiles  and  the 
polychromatophilic  changes  in  the  red  cells  (see  p.  637  et  seq.)  which  occur  so 
frequently  in  this  disease  can  -no  longer,  as  formerly,  be  considered  as  degenerative 
changes.  There  are,  to  be  sure,  less  severe  signs  of  red-cell  degeneration  in  other 
types  of  anemia  ;  for  instance,  in  severe  chlorosis. 

The  number  of  red  cells  is  usually  considerably  more  diminished  in  i^ernicious 
anemia  than  in  chlorosis  and  simple  primary  anemia.  This  diminution  is  generally 
more  marked  than  the  reduction  of  the  hemoglobin,  which  probably  means  that  a 
portion  of  the  hemoglobin  of  the  destroyed  blood-cells  or  the  superfluous  material 
for  the  formation  of  hemoglobin  is  made  use  of  by  the  remaining  blood-cells  (or 
is  present  free  in  the  plasma).  On  account  of  this  relation  between  the  amount 
of  hemoglobin  and  the  number  of  red  cells,  the  color  index  is  above  1.  This  is 
partly  due  to  the  intense  coloring  and  partly  to  the  increase  in  size  of  the  individ- 
ual blood-cells.  In  a  case  reported  by  Quincke  the  number  of  red  blood-cells 
sank  to  143,000  per  cubic  millimeter. 

Micro-  and  macrocytes  and  poikilocytes  are  found  in  great  numbers.  It  is 
usually  possible  to  find  granular  erythrocytes,  although  in  very  small  numbers  ; 
and  red  cells  with  polychi'omatophilic  changes  are  more  or  less  abundant.  The 
presence  of  megaloblasts  in  the  blood,  however,  is  specially  characteristic  of  per- 
nicious anemia.  They  are  usually  very  scanty  and  require  patient  searching. 
They  are  found  only  exceptionally  in  large  numbers,  and  then  only  in  the  agony 
of  death.     Normoblasts  may  also  be  found. 

The  number  of  leukocytes  is  usually  diminished  in  pernicious  anemia.  As 
the  function  of  the  bone  marrow  is  diminished,  this  decrease  is  at  the  expense  of 
the  polynuclear  leukocytes,  so  that  the  lymphocytes  seem  to  be  relatively 
increased.  According  to  Ehrlich  and  Lazarus,  they  may  constitute  62  per  cent, 
of  the  total  number.     Strauss '  regards  the  decrease  of  the  polynuclear  leukocytes 

^  Strauss  and  Rohnstein,  Die  Blutzusammensetzuiuj  in  den  verschiedenen  Andmien, 
Berlin,  1901. 


CONDITION  OF  BLOOD  IN  MOST  IMPORTANT  BLOOD-DISEASES.   661 


as  characteristic  of  true  liernicious  anemia,  as  compared  with  anemia  following 
carcinoma,  in  which  the  percentage  of  the  polynuclear  cells  is  usually  greater  than 
that  of  the  mononuclear,  and  in  which  there  is  frequently  present  a  pronounced 
polynuclear  leukocytosis.  The  latter  peculiarity,  however,  is  not  always  present 
in  the  anemia  of  carcinoma,  and  may  sometimes  be  observed  during  a  temporary 
improvement  in  pernicious  anemia.  In  pernicious  anemia  the  blood-plates  are 
diminished  in  number. 

Individual  cases  have  been  observed  where,  clinically,  the  megaloblasts  have 
been  absent  from  the  blood  and  the  bone  marrow  has  not  been  found  red  at  the 
autopsy  (aplastic  type  of  pernicious  anemia).  It  is  not  quite  clear  yet  whether 
these  cases  belong  properly  to  megaloblastic  pernicious  anemia.  The  etiology  of 
this  disease  is  by  no  means  uniform ;  it  has  been  known  to  occur  after  repeated 
severe  loss  of  blood,  from  carcinoma  of  the  stomach,  from  bothriocephalus,  and 
from  absolutely  unfathomable  causes,  so  the  difficulty  of  sharply  distinguishing  it 
is  plain. 

This  fact  suggests  that  pernicious  anemia  may  possibly  be  due  to  a  gradual 
increase  in  severity  of  an  ordinary  secondary  anemia.     The  fact  that  the  blood  in 


Fig.  236— Pseudoleukeiiiiii  (New  York  City  Hospital). 


these  cases  is  of  megaloblastic  type  certainly  indicates  that  the  ordinary  influences,, 
or  possibly  their  increased  action,  exert  some  specific  action  on  the  bone  marrow 
which  is  not  yet  understood. 

Pseudoleukemia. — This  is  the  designation  given  to  those  cases  of  general 
lymphomatosis  in  which,  as  a  result  of  a  general  proliferation  of  the  lymphatic 
apparatus,  there  is  an  enlargement  of  the  spleen  and  lymphatic  glands  analogous 
to  those  found  in  true  lymphoid  leukemia,  and  in  which  the  blood  shows  changes, 
but  not  the  characteristic  changes  of  lymphoid  leukemia.  The  most  striking  and 
best-known  change  in  the  blood  in  these  conditions  is  oligochromemia,  although 
this  may  be  absent.  A  more  important  characteristic  is  the  relation  of  the  leuko- 
cytes. The  number  is  normal  or  slightly  increased,  but  there  is  a  relative  increase 
of  the  lymphocytes — i.  e.,  there  is  a  slight  degree  of  absolute  lymphocytosis. 
This  leukocytic  finding  is  indicative  of  what  Tiirk  fittingly  designates  as  a  sub- 
lymphemic  condition  of  the  blood.  He  differentiates  pseudoleukemia  from  lym- 
phoid leukemia,  in  which  the  lympliocytosis  is  so  marked  that  the  total  number 
of  leukocytes  seems  to  be  considerably  increased,   and  an  actual   lymphemia  is 


662  EXAMINATION  OF  THE  BLOOD. 

brought  about  by  the  flooding  of  the  blood  with  lymphocytes.  It  cannot  be  said, 
however,  that  a  sharp  boundary  exists  between  pseudoleukemia  and  lymphoid 
leukemia,  for  the  former  may  pass  into  the  latter.  When  the  chief  enlargement 
was  in  the  spleen,  we  formerly  spoke  of  pseudoleukemia  lienalis  or  anaemic 
splenica;  while  if  the  increase  in  size  mainly  affected  the  lymphatic  glands,  we 
referred  to  the  disease  as  lymphatic  pseudoleukemia,  malignant  lymphoma, 
Hodgkin's  disease,  or  ansemia  lymphatica.  It  would  be  wise  to  drop  these  names, 
since  they  refer  to  immaterial  differences  and  do  not  characterize  the  particular 
affection.  It  seems  best  to  the  author  to  classify  everv^  case  of  lymphomatosis,  as 
advised  by  Tiirk,  according  to  its  acuteness,  its  anatomic  malignancy  or  benign- 
ancy,  and  the  alymphemic,  sublymphemic,  or  lymphemic  condition  of  the  blood, 
and  to  tabulate  it  according  to  the  following  scheme  without  giving  it  a  name, 
since  names  frequently  do  more  harm  than  good  in  pathology. 

A  Classificatiox  of  the  Lymphomatoses 
(From  Tiirk,  with  slight  modification).  ^ 

Chronic  Malignant-  Growth 
Chronic  Benign-  Groivth.  Acute  growth.  vnthout  blood-changes. 

1.  Alymphemic     (so-called      a.  Benign.     6.  Partly  malignant,     g  S  S    1.  General  (lymphosarco- 

malignant  Ij-mphoma.  1.  Alymphemic.      Alymphemic.    ■)'5'S§  matosis). 

2.  Sublymphemic   (pseudo-  2.  Sublymphemic.  Sublymphemic.  yZ~  g   2.  Regional  or  local  lym- 

leukemia).  3.  Lymphemic.       Lymphemic.      J  2  c~  phosarcoma. 

3.  Lymphemic  (chronic  E-i-^o 

lymphoid  leukemia). 

Clinical  experience,  particularly  that  of  Tiirk,  indicates  that  all  of  the  clinical 
conditions  in  this  classification  pa.ss  over  into  each  other,  so  that  the  differences 
between  them  are  sim^^ly  those  of  gradation. 

This  classification  of  the  lymphomatoses  probably  also  includes  the  splenome- 
galies, Banti'  s  disease,  and  (according  to  Bleichroder  ^)  certain  forms  of  cirrhosis 
of  the  liver. 

From  a  practical  standpoint,  it  is  still  difiicult  to  differentiate  the  alymphemic 
lymphomatoses  of  chronic  benign  growth,  which  were  previously  designated  as 
malignant  lymphomata,  from  similar  conditions  dependent  ujion  tuberculosis.  A 
rather  plausible  conception  of  these  tubercular  cases  assumes  that  they  are  combi- 
nations of  tuberculosis  with  lymphomatosis  or  with  malignant  lymphoma.  If  this 
be  true,  the  question  is  not  that  of  differentiating  the  so-called  malignant  lym- 
phoma from  tuberculosis,  but  of  discovering  some  sign  by  which  we  may  know 
that  the  malignant  lymphoma  has  become  combined  with  tuberculosis. 

SECONDARY  ANEMIAS. 

These  include  all  anemias  which  can  be  traced  definitely  to  some  other  defi- 
nite disease — that  is,  all  the  anemic  conditions  in  diseases  which  produce  cachexia, 
disturbances  of  nutrition  or  loss  of  blood  (phthisis,  cancer,  ulcer  of  the  stomach, 
ankylo.stomiasis,  bothriocephalus).  We  cannot  sharply  separate  secondary  from 
primary  anemias,  as  we  do  not  yet  definitely  know  the  cause  of  the  disturbance  in 
the  blood-making  organs  which  is  assumed  to  be  responsible  for  the  primary 
anemias.  The  knowledge  gained  concerning  the  production  of  the  typical  pict- 
ure of  pernicious  anemia  by  the  bothriocephalus  indicates  that  perhaps  other 
cases  of  pernicious  anemia  may  be  secondary  to  other  disorders.  For  instance, 
the  severe  anemia  so  frequent  in  carcinoma  of  the  stomach  has  not  yet  been 
definitely  distinguished  from  iDcrnicious  anemia,  although,  as  a  general  rule,  the 
megaloblasts  usually  present  in  pernicious  anemia  are  absent  in  the  anemia  of 
carcinoma,  and  a  polynuclear  leukocytosis  is  the  rule.     Nevertheless,   in  some 

1  Wien.  Min.  Woch.,  190.3,  p.  .39. 

^  The  terms  benign  and  malignant  are  used  here  in  a  pathologico-anatomic  .sense,  and 
refer  to  aggressive  growths  which  proliferate  into  and  destroy  the  neighboring  tissues. 
^  Virchow's  Archiv,  vol.  clxxvii.,  1904. 


CONDITION  OF  BLOOD  IN  MOST  IMPORTANT  BLOOD-DISEASES.  663 

cases  of  carcinoma  both  megaloblasts  and  leukopenia  have  been  found,  just  as  in 
pernicious  anemia.  We  have  little  accurate  information  as  yet  in  regard  to  the 
real  condition  of  the  blood  in  the  secondary  anemias.  A  pale  ajjpearance  does 
not  constitute  an  anemia  at  all,  as  we  have  already  mentioned,  for  the  percentage 
of  hemoglobin  and  red  blood-corpuscles  may  be  normal. 

Anemias  Following  the  Loss  of  Blood. 

This  type  of  anemia  is  the  only  one  which  has  been  accurately  studied. 

Acute  Loss  of  Blood. — After  an  acute  hemorrhage  the  blood  becomes 
rapidly  diluted,  owing  to  the  absorption  of  lymph  and  water.  Although  the 
hemoglobin  and  the  number  of  blood-corpuscles  may  be  normal  immediately  after 
a  hemorrhage,  all  the  characteristics  of  oligochromemia  soon  appear,  and  persist 
until  a  normal  condition  has  again  been  reached.  The  oligochromemia  reaches 
its  maximum  within  a  few  hours  after  a  slight  hemorrhage,  but  after  severe  hemor- 
rhages not  until  about  nine  days.  Evidence  of  a  regeneration  of  the  blood-cor- 
puscles can  be  found  almost  as  soon  as  the  plasma  begins  to  be  replaced.  Accord- 
ing to  the  investigations  of  Ott  and  Laache,  the  number  of  red  blood-corpuscles 
is  normal  much  sooner  than  the  percentage  of  hemoglobin.  This  produces  a 
condition  similar  to  chlorosis.  Normoblasts  may  be  found  from  the  second  to 
the  third  day  on.  The  regeneration  is  associated  with  an  active  posthemorrhagic 
leukocytosis,  chiefly  jjolynuclear.  The  number  of  blood-plates  is  increased  and 
the  coagulation  hastened  after  acute  losses  of  blood.  Mikulicz  considers  that 
major  surgical  operations  will  not  prove  successful  if  the  hemoglobin  sinks  below 
30  per  cent.  This  assumption  is  rather  arbitrary,  and  the  percentage  of  hemo- 
globin which  would  justify  an  operation  might  very  well  be  placed  a  little  higher, 
especially  if  the  narcosis  is  to  be  a  prolonged  one,  as  narcosis  exercises  some 
detrimental  influence  upon  the  composition  of  the  blood. 

Chronic  Loss  of  Blood  (Hemorrhoids,  Menorrhagia,  Chronic  Gastric  Ulcer, 
Carcinoma,  Ankylostomiasis,  etc.). — Generally  speaking,  the  condition  of  the 
blood  here  is  very  similar  to  that  several  days  after  an  acute  loss.  The  number 
of  red  blood-corpuscles  is,  as  a  rule,  not  diminished  to  so  great  an  extent  as  the 
hemoglobin,  probably  on  account  of  the  processes  of  regeneration.  The  anemia 
following  chronic  loss  of  blood  differs  from  that  caused  by  acute  loss  of  blood  in 
that  the  former,  provided  it  is  severe  and  prolonged,  presents  a  poikilocytosis, 
just  as  does  pernicious  anemia.  This  is  in  all  probability  due  to  the  continued 
loss  of  plasma  and  the  permanent  hydremic  nature  of  the  blood-plasma.  Another 
difference  is  that  the  leukocytes  are  not  increased  in  the  severe  cases  of  anemia 
following  chronic  hemorrhages,  and  so  the  picture  approaches  more  and  more 
that  of  pernicious  anemia.  The  number  of  polynuclear  leukocytes  is  an  approxi- 
mate measure  of  the  regenerative  activity  of  the  bone  marrow  in  the  anemias 
following  hemorrhage.  The  presence  of  nucleated  blood-corpuscles,  which  gen- 
erally belong  to  the  normoblastic  type,  is  another  index. 

ERYTHEMIA  OR   POLYCYTHEMIA. 

Numerous  descriptions  have  recently  appeared,  the  first  coming  from  French 
authors,  1  of  a  peculiar  affection  which  consists  essentially  of  a  more  or  less  marked 
increase  of  the  erythrocytes,  associated  with  splenic  enlargement,  and,  further, 
is  characterized  clinically  by  a  marked  redness  or  cyanosis  of  the  face,  headache, 
attacks  of  vomiting,  slight  albuminuria  with  casts,  and  the  presence  of  blood  in 
the  sputum,  vomitus,  and  feces.  The  autopsy  findings  indicate  that  in  addition  to 
the  increased  number  of  erythrocytes  there  is  also  a  true  plethora,  since  all  jjarts 
of  the  body  seem  to  contain  an  excessive  quantity  of  blood.  The  heart  is  normal 
or  somewhat  enlarged.  In  several  cases  the  blood-pressure  was  found  to  be 
increased.  The  disease  appears  in  middle  life  and  lasts  for  many  years.  As  yet 
there  is  no  accurate  information  as  to  any  change  in  the  bone  marrow.     Careful 

^  Rendu  et  Widal,  Bull,  et  mem.  de  la  .soc.  med.  des  hop.,  vol.  iii.,  Ser.  1899,  p.  528. 
Further  references  in  Turk's  article,  Wien.  klin.  Woch.,  1904,  Nos.  6  and  7. 


664  EXAMINATION  OF  THE  BLOOD. 

examinations  of  the  blood  in  these  cases  show  that  the  number  of  erythrocytes 
may  be  increased  to  12,000,000  per  cubic  millimeter,  and  the  hemoglobin  to  200 
per  cent.  The  number  of  leukocytes  varies.  Tiirk  always  found  leukocytosis  in 
his  cases.  In  one  case  myelocytes  were  observed.  The  specific  gravity  of  the 
blood  is  increased.  It  is  still  doubtful  whether  all  cases  answering  to  this  descrip- 
tion are  one  and  the  same  affection.  Tiirk  believes  that,  in  some  of  the  cases  at 
least,  there  is  a  primary  hyperplasia  of  the  erythroblastic  bone  marrow  with  func- 
tional hypertrophy.  In  favor  of  this  conception  is  the  frequently  occurring  leuko- 
cytosis and  the  finding  of  myelocytes.  Tiirk  has  suggested  the  name  of  erythe- 
mia  or  erythrocythemia  for  this  disease,  and  contrasts  it  with  myeloid  leukemia. 

LEUKEMIA.. 

The  chief  characteristic  of  leukemia  is  a  considerable  and  permanent  pathologic 
increase  of  the  mononuclear  leukocytes  in  patients  who  do  not  exhibit,  aside 
from  the  changes  in  the  blood-forming  organs  (the  bone  marrow,  spleen,  and 
lymph  nodes),  any  other  lesions  which  may  be  considered  primary. 

Formerly  leukocytosis  was  separated  from  leukemia  in  a  very  arbitrary  way 
according  to  the  degree  of  increase  of  the  white  blood-corpuscles.  If  the  pro- 
portion of  white  to  red  cells  reached  from  1  :  50  to  1  :  20,  the  affection  was  called 
leukemia.  This  method  of  differentiation  was  shown  to  be  useless  in  the  early 
periods  of  leukemia  and  in  cases  of  severe  leukocytosis  associated  with  marked 
anemia.  When  Ehrlich  emphasized  the  freqviency  of  the  eosinophilic  leukocyte 
in  leukemic  blood,  it  was  at  first  believed  that  he  had  found  a  reliable  point  of 
differentiation  between  leukemia  and  leukocytosis,  but  it  did  not  prove  to  be  a 
correct  one.  Since  the  morphology  of  leukocytes  has  been  more  accurately 
studied,  we  have  found  that  the  difference  between  leukemia  and  leukocytosis  is 
neither  one  of  gradation  nor  one  depending  upon  the  tinctorial  properties  of  the 
leukocytic  granules  ;  but  that  the  true  difference  lies  in  the  fact  that  in  leukemia 
the  increase  is  chiefly  in  the  mononuclear  type  of  leukocytes,  which  are  always 
in  excess  of  the  polynuclear  tj'pe,  except  in  the  rare  and  transitory  conditions 
which  will  be  mentioned  later,  while  in  the  different  varieties  of  leukocytosis, 
except  in  a  few  cases  to  be  subsequently  mentioned  (p.  666),  the  polynuclear  cells 
predominate,  as  in  the  normal.  Thus,  it  is  usually  easy  even  in  early  cases  to 
distinguish  leukemia. 

The  other  characteristics  of  the  blood  in  leukemia  are  as  follows :  In  very 
advanced  cases  the  blood-drop  is  peculiarly  whitish,  clay-colored,  or  milky,  and 
upon  coagulation  a  thick  grayish-white  film  is  deposited  above  the  layer  of  red 
blood-corpuscles  (the  so-called  buffy  coat  containing  the  white  blood-corpuscles).- 
Coagulation  is  considerably  retarded,  and  in  advanced  cases  the  clot  is  of  a  soft, 
jelly-like  consistence.  The  specific  gravity  of  the  blood  is  diminished  and  the 
amount  of  water  contained  increased.  The  blood  feels  peculiarly  sticky.  The 
number  of  red  cells  is  frequently  diminished,  as  is  the  percentage  of  hemoglobin. 
These  latter  conditions  are  not  constant,  especially  in  the  early  stages — e.  g.,  leu- 
kemic blood  is  not  always  pale.  Where  the  hemoglobin  is  considerably  dimin- 
ished, poikilocytosis  and  nucleated  red  blood-coi-puscles  are  found  (normo-  and 
megaloblasts).  The  white  cells  are  usually  very  considerably  increased,  not 
uncommonly  to  500,000  per  cubic  millimeter.  All  the  normal  types  of  leuko- 
cytes are  present,  as  well  as  the  pathologic  variety  described  on  p.  642. 

Leukemia  was  formerly  divided  into  splenic,  myelogenous,  lymphatic,  and 
intermediate  or  mixed  types,  according  to  the  changes  in  the  organs.  To-day 
the  condition  of  the  blood  decides  to  which  type  a  given  case  belongs. 

The  changes  in  the  viscera  cannot  be  sharply  separated  ;  hence  the  associated 
alterations  of  these  organs  is  of  no  particular  value  for  properly  classifying  the 
disease.  For  instance,  in  a  lymphatic  leukemia,  when  the  enlargement  of  the 
lymph  glands  controls  the  clinical  picture,  it  is  very  common  to  have  similar 
changes  in  the  spleen  and  bone  marrow  without  the  corresponding  blood-changes 
even  when  the  spleen  is  considerably  enlarged.  Purely  splenic  leukemia  is 
equally  hard  to  distinguish.     According  to  modern  investigations,  the  spleen  has 


Ar' 


«r9 


PLATE  8. 


A 


\ 


C 


.  o^ 


f^O^^O^^L^-^Oo-^Q.-O 


y<»^o  ^» 


o 


^' 


Normal  blood.  In  the  field  of  vision  a 
lymphocyte,  a  polynuclear  cell,  and  an  eosino- 
phile  one.  The  nuclei  of  all  the  white  cells 
dark  blue,  the  eosinophile  granulations  a  bril- 
liant red  (Rieder). 


Inflammatory  leukocytosis.  Marked  in- 
crease of  polynuclear  leukocytes.  Represen- 
tation of  their  neutrophile  granules  (Rieder). 


Heart-disease  cells  from  fresh  sputum-preparation  (Jakob). 


Lymphatic  leukemia.  Almost  all  the  white 
blood-corpuscles  uninuclear  (lymphocytes) ; 
most  of  them  very  small  (Rieder). 


Lienomyelogenic  leukemia.  Most  of  the 
white  cells  are  uninuclear ;  many  are  strik- 
ingly large,  with  large,  plump  nucleus.  Sev 
eral  eosinophile  cells.  One  nucleus  contains 
red  blood-corpuscles  (Rieder). 


CONDITION  OF  BLOOD  IN  MOST  IMPORTANT  BLOOD-DISEASES.  665 

little  or  nothing  to  do  with  the  formation  of  blood.  Besides,  in  certain  leuke- 
mias  with  enormous  tumors  of  the  spleen,  apjjarently  justifying  the  term  splenic 
leukemia,  not  only  has  the  bone  marrow  been  found  altered,  but  the  increased 
leukocytes  present  in  the  blood  are  similar  morphologically  to  those  derived  from 
the  marrow.  Finally  it  had  been  demonstrated  that  the  so-called  splenic  leu- 
kemia is  also  myelogenous  ;  hence  the  separation  of  myelogenous  leukemia,  in 
the  old  sense  of  the  word,  has  no  foundation. 

Ehrlich  and  Lazarus  recommend  subdividing  leukemia  into  two  types  based 
upon  the  blood-examination  :  lymphatic  leukemia  or  lymphemia  and  myelog- 
enous leukemia  or  myelemia.  The  associated  changes  in  the  organs  may  be 
described  in  connection  with  these  terms ;  for  instance,  a  lymphemia  with 
splenic  tumor,  or  a  myelemia  with  a  splenic  tumor  and  swelling  of  the  lymph 
nodes.  The  characteristics  of  the  blood  in  lymphemia  and  myelemia  are  repre- 
sented in  Plate  8,  Figs.  4  and  5,  after  Rieder. 

The  finding  of  protozoa  in  the  leukocytes  in  leukemia  by  Lowit  and  Manna- 
berg  '  has  not  yet  been  generally  confirmed,  and  for  this  reason  cannot  be  dis- 
cussed in  detail. 

There  has  recently  been  a  growing  tendency  among  hematologists  to  give  up 
the  sharp  distinction  between  the  so-called  lymphatic  and  myelogenous  leuke- 
mias.  This  seems  to  be  justified,  since,  on  the  one  hand,  the  bone  marrow 
doubtless  also  contains  lymphatic  constituents,  and  consequently  forms  lympho- 
cytes ;  and,  on  the  other,  the  lymphatic  glands  in  myelogenous  leukemia  have 
frequently  been  found  undergoing  myeloid  transformation,  so  that  it  must  be 
assumed  that  they  are  also  implicated  in  the  production  of  the  blood-picture  in 
myelogenous  leukemia.  The  majority  of  authors,  moreover,  assume  that 
lymphatic  leukemia  occurs  only  when  there  are  also  anatomic  changes  in  the 
bone  marrow,  and  that  when  these  are  absent  the  disease  remains  in  the  stage 
of  pseudoleukemia  (p.  661).  In  this  connection  Pappenheim  suggests  employ- 
ing the  expressions  lymphatic  and  myelogenous  to  denote  the  place  of  origin, 
and  characterizing  the  blood-picture  as  lymjDhoid  or  myeloid  according  to  the 
predominance  of  lymphocytes  or  the  specific  elements  of  the  bone  marrow.  The 
question  of  terminology  is  a  most  difiicult  one,  owing  to  the  occurrence  of 
transition  forms  and  to  the  fact  that  it  is  frequently  impossible  to  determine 
whether  certain  elements  originate  in  the  lymphatic  glands  or  in  the  bone 
marrow.  For  this  reason  the  old  subdivision  of  leukemia  into  lymphemia 
(lymphoid  or  lymphatic  leukemia)  and  myelemia  (myelogenous  or  myeloid  leu- 
kemia) will  be  retained  here. 

LYMPHEMIA  (LYMPHATIC  LEUKEMIA;   LYMPHOID  LEUKEMIA). 

Chronic  lymphatic  leukemia  is  characterized  by  a  more  or  less  marked 
increase  of  leukocytes,  usually  over  100,000,  and  lay  a  predominance  of  the 
lymphocytes,-  especially  the  smaller  variety.  In  a  few  instances,  however,  the 
large  lymphocytes  are  more  abundant.  Both  are  as  normally  devoid  of  gran- 
ules. The  relative  number  of  lymphocytes  may  reach  99  per  cent,  of  the  total 
number  of  leukocytes.  The  other  leukocytes  are,  of  course,  always  diminished 
relatively  as  compared  to  the  total  number,  and  they  may  even  be  absolutely 
diminished.  The  blood  usually  contains  a  number  of  eosinophiles  and  mast  cells, 
but  the  myelocytes  which  are  characteristic  of  myelemia  are  very  rarely  present. 
As  in  myelemia,  the  number  of  red  blood-corpuscles  may  remain  normal  for  a 
considerable  length  of  time,  but  later  there  is  generally  a  moderate  decrease. 
Nucleated  erythrocytes  (normoblasts)  are  found  only  in  small  numbers.  The 
percentage  of  hemoglobin  corresponds  approximately  to  the  number  of  erythro- 
cytes. As  death  approaches  the  number  of  lymphocytes  may  increase  consider- 
ably. If  the  condition  is  complicated  by  an  acute  infectious  disease,  a  polynuclear 
leukocytosis  may  temporarily  take  the  place  of  the  lymphemia.     The   lymph 

^  The  findings  of  Mannaberg  refer  to  lymphemia,  those  of  Lowit  to  both  forms  of 
leukemia. 


6Q6  EXAMINATION  OF  THE  BLOOD. 

glands  are  usually  more  or  less  swollen,  although  the  spleen  and  the  liver  may 
also  be  enlarged  and  the  bone  marrow  aifected.  Lymphatic  leukemia  needs  to 
be  studied  more  accurately.  It  is  much  less  common  than  myelemia,  and  is 
still  little  understood  hematologically. 

The  cases  of  acute  leukemia  are  usually  grouped  with  the  lymphatic  type. 
This  peculiar  clinical  picture  presents  the  signs  of  a  very  acute  anemia  accom- 
panied by  hemorrhagic  diathesis.  The  disease  generally  runs  a  very  acute  and 
lethal  course.  Large  numbers  of  cells  like  large  lymphocytes  are  found  in  the 
blood.  They  are  noticeably  different  from  the  ordinary  large  lymphocytes,  how- 
ever, especially  on  account  of  the  marked  lack  of  chromatin  in  the  nucleus,  so 
that  it  is  possible  that  they  may  be  undeveloped  bone-marrow  cells  (Nageli's 
myeloblasts).  In  some  instances  small  lymphocytes  predominate.  As  a  rule,  the 
number  of  red  blood-corpuscles  and  the  percentage  of  hemoglobin  are  consider- 
ably diminished.  Nucleated  red  blood-cells  are  found  only  in  small  numbers. 
Cases  of  acute  leukemia  are  not  common,  and  but  few  have  been  investigated 
from  the  standpoint  of  modern  hematology. 

Cases  of  acute  myelemia  or  myeloid  leukemia  have  recently  been  described 
(see  p.  667),  a  fact  which  must  be  borne  in  mind  in  making  a  ditferential  diag- 
nosis of  acute  cases. 

MYELEMIA   (MYELOGENOUS    LEUKEMIA;    MIXED  LEUKEMIA;    MYELOID 

LEUKEMIA). 

This  variety  of  leukemia  (Plate  8,  Fig.  5,  and  Plate  6,  Fig.  2)  has  been  much 
more  extensively  studied  than  lymphemia.  The  only  constant  visceral  changes  are 
alterations  in  the  bone  marrow.  The  spleen  is  usually  considerably  increased  in  size 
(compare  Fig.  112).  The  lymph  glands  and  the  liver  are  usually  enlarged.  The 
blood-picture  is  very  characteristic,  and  in  itself  diagnostic  and  positive.  Ehrlich 
and  Lazarus  mention  the  following  anomalous  conditions  as  determinative  for  the 
diagnosis  : 

1.  Not  only  polynuclear  cells,  but  also  their  early  developmental  stages,  the 
mononuclear  granular  leukocytes,  must  be  found  in  considerable  numbers  in  the 
blood. 

2.  All  three  types  of  granular  cells — the  neutrophiles,  eosinophiles,  and  mast 
cells — ^but  chiefly  the  first,  must  be  increased. 

3.  Atypical  cells  must  be  found  ;  for  instance,  dwarf  types  of  the  different 
varieties  of  white  blood-corpuscles,  and  leukocytes  with  mitoses. 

4.  Lastly,  the  blood  must  contain  nucleated  red  blood-corpuscles,  chiefly 
of  the  normoblastic  type. 

The  name  ' '  mixed  leukemia ' '  is  preferred  by  some  authors  because  the 
lymphocytes  are  also  increased  in  this  form,  and  even  in  those  cases  in  which 
there  are  no  changes  in  the  lymphatic  glands.  This  fact  at  once  becomes  intelligi- 
ble if  we  assume  with  Pappenheim  that  the  bone  marrow  also  forms  lymphocytes. 

The  mononuclear  neutrophilic  granular  cells  are  the  main  characteristic  of 
myelemic  blood — the  "  Markzellen, "  marrow  cells  or  myelocytes,  as  they  were 
named  by  Ehrlich.  It  is  not  uncommon  to  find  100,000  myelocytes  per  cubic 
millimeter  in  a  case  of  myelemia.  In  jjronounced  cases  these  cells,  as  a  rule, 
predominate,  although  the  polynuclear  cells  are  also  increased.  All  other  varie- 
ties of  the  Avhite  cells  appear  in  insignificant  numbers,  compared  with  the 
myelocytes.  In  certain  stages  of  the  disease,  however,  the  myelocytes  may  be 
numerically  less  than  the  polynuclear  neutrophiles,  so  that  the  blood  resembles 
that  of  a  leukocytosis  plus  myelocytes.  This  reverse  of  the  typical  picture  of 
the  blood  is  observed  chiefly  with  intercurrent  febrile  diseases,  and  may  easily 
give  rise  to  diagnostic  and  prognostic  errors,  especially  as  the  total  number  of 
leukocytes  may  be  considerably  diminished.  We  have  seen  the  blood-picture  of 
a  myelemia  temporarily  change  to  that  of  a  pronounced  leukopenia  XN^thout  any 
known  cause — i.  e.,  without  intercurrent  disease. 

However,  in  all  of  these  conditions,  which  probably  represent  but  transitory 
episodes  in  leukemia,  the  absolute  number  of  myelocytes  is  still  considerably 


CONDITION  OF  BLOOD  IN  MOST  IMPORTANT  BLOOD-DISEASES.   667 

increased  ;  and  even  if  the  blood-j^icture  does  resemble  a  simple  neutrophilic 
leukocytosis,  the  number  of  the  myelocytes  is  much  more  significant  than  in 
leukocytosis,  where,  according  to  Tiirk,  they  hardly  ever  exceed  1000  per  cubic 
millimeter.  In  such  exceptional  cases  an  absolute  increase  of  the  other  granular 
leukocytes,  esi^ecially  the  eosinophiles  and  mast  cells,  will  decide  the  diagnosis 
in  favor  of  myelemia.  The  percentage  of  eosinophiles  and  mast  cells  need  not 
be  increased,  so  that  it  is  necessary  to  consider  the  absolute  numbers.  Myelemia, 
even  in  atypical  cases,  does  therefore  differ  very  decidedly  from  neutrophilic 
leukocytosis.  It  also  diflfers  from  the  eosinophilic  leukocytosis  described  upon 
p.  649.  The  total  number  of  leukocytes  in  eosinophilic  leukocytosis  is  only 
moderately  increased  ;  the  eosinophiles  are  exclusively  polynuclear  ;  both  mast 
cells  and  neutrophilic  myelocytes  are  practically  absent.  The  normal  figures 
(see  p.  640)  will  enable  one  to  judge  of  any  increase  in  the  individual  types 
of  leukocytes. 

In  some  few  cases  the  neutrophilic  granules  of  the  mark  cells  and  of  the 
polynuclear  leukocytes  are  either  very  slightly  developed  or  even  for  the  time 
being  almost  entirely  absent.  In  cases  of  this  sort  reported  in  recent  literature,  ^  the 
examinations  were  made  shortly  before  death.  We  observed  the  same  condition 
temporarily  in  a  case  which  was  at  the  time  improving  considerably  under  arsenic. 

In  leukemic  blood  which  has  been  kept  moist  for  some  time  Charcot's  crys- 
tals (Fig.  211,  e)  appear  quite  regularly.  This  condition  is  probably  connected 
in  some  way  with  the  abundance  of  eosinophilic  cells  in  myelemia,  Charcot's 
crystals  being  supposed  to  be  derived  from  these  cells. 

After  Jolly  demonstrated  ameboid  movement  in  mononuclear  leukocytes, 
Ehrlich  and  Lazarus  concluded  that  myelemia,  like  leukocytosis,  depends  upon 
some  chemotactic  influence  which  produces  an  emigration  of  undeveloped  ele- 
ments from  the  bone  marrow.  As  against  this  view,  which  places  leukemia  and 
leukocytosis  in  close  relationship,  we  know  that  myelemic  metastases  are  found 
in  the  spleen,  in  the  liver,  and  in  many  other  organs,  a  fact  which  would  seem 
to  indicate  rather  that  the  changes  in  the  bone  marrow  are  more  or  less  analo- 
gous to  tumors,  and  to  suggest  the  idea  that  the  cells  are  washed  out  mechanically 
from  the  bone  marrow. 

In  reference  to  the  occurrence  of  acute  myelemia,  the  clinical  picture  of 
which  practically  agrees  with  that  of  the  chronic  form,  the  reader  is  referred  to 
the  monograph  of  Fr.  Billings  and  J.  A.  Capps.^ 

THE    SO-CALLED    LEUKANEMIA. 

Under  this  name  Leube,^  and  subsequently  Leube  and  Arneth,*  and  Luces  have 
described  blood-aifections  in  which  the  phenomena  of  myelogenous  leukemia  and 
pernicious  anemia  occurred  simultaneously  (myelocytes,  megaloblasts,  red  meta- 
plasia of  the  bone  marrow).  There  is  no  doubt  that  these  cases  should  be 
regarded  as  a  species  of  myelogenous  leukemia. 

OSMOTIC     PRESSURE    OR    MOLECULAR    CONCENTRATION    OF   THE    BLOOD- 

In  contrast  to  cryoscopy  of  the  urine,  which  received  a  rather  adverse  criti- 
cism upon  p.  548  et  seq.,  we  possess  in  cryoscopy  of  the  blood  an  extremely 
valuable  method  of  examination.  It  furnishes  important  conclusions,  particu- 
larly in  the  diagnosis  of  fiinctional  diseases  of  the  kidneys.  It  cannot  be  re- 
placed by  the  determination  of  the  specific  gravity  of  the  blood-serum,  since  to 
get  results  analogous  to  those  obtained  from  the  osmotic  pressure,  the  albumin 
must  be  removed   from  the  blood-serum,   and  the  complete  removal  of  such  a 

'  Ehrlich  and  Lazarus,  "Die  Andmie,"  imrt  1,  in  Nothnaoel's  Spec.  Palholoqie  u.  Ther- 
apie,  1898,  p.  126. 

"^  Amer.  Jour.  Med.  ScL,  September,  1903. 
^  Leube,  Deut^ch.  Klinik,  1902,  No.  42. 

*  Leube  and  Arneth,  Deulsch.  Arch.  f.  klin.  Med.,  vol.  Ixix. 

*  Luce,  ihid.,  vol.  Ixxvii,  parts  3  and  4. 


668  EXAMINATION  OF  THE  BLOOD. 

large  quantity  of  albumin  is  possible  only  after  a  preceding  dilution.  Moreover, 
in  view  of  the  small  quantities  of  blood  usually  at  our  disposal,  the  specific 
gravity  must  be  determined  by  the  rather  troublesome  capillary-pyknometric 
method  of  Hammerschlag  (see  p.  612). 

The  nature  of  the  osmotic  pressure  and  its  measurement  by  determinations 
of  the  freezing-point,  or  cryoscopic  examination,  have  been  explained  on  p.  545 
et  seq.  In  reference  to  the  method  of  determining  the  freezing-point,  the  reader 
is  also  referred  to  what  has  jjreviously  been  stated  in  detail  (p.  546  et  seq.).  Only 
those  features  which  are  peculiar  to  the  cryoscoj)y  of  the  blood  will  now  be  dis- 
cussed. 

The  determination  of  the  fi-eezing-point  of  the  blood  is  usually  carried  out 
by  withdrawing  rather  a  large  quantity  of  blood  (usually  about  20  c.c.)  from  the 
patient  by  venesection  (see  p.  610)  and  allowing  it  to  coagulate.  The  separation 
of  the  serum  from  the  coagulum  may  be  accelerated  by  loosening  the  latter  from 
the  sides  of  the  vessel.  This  serum  is  then  employed  for  the  examination.  The 
fi-eezing-point,  or  osmotic  pressure,  of  the  serum  is  practically  equal  to  that  of  the 
plasma,  since  the  fibrin,  in  consequence  of  its  great  molecular  weight  and  of  the 
small  percentage  present,  exerts  practically  no  influence  upon  the  lowering  of  the 
freezing-point.  Since  the  osmotic  pressure  of  the  serum  is  equal  to  that  of  the 
plasma,  it  must  also  be  equal  to  that  of  the  whole  blood  or  of  the  defibrinated 
blood,  since  the  blood-corpuscles  must  necessarily  j)Ossess  the  same  osmotic  press- 
ure as  that  of  the  plasma.  It  consequently  follows  that  the  osmotic  pressures 
of  the  serum,  of  the  plasma,  of  the  whole  blood,  and  of  the  defibrinated  blood 
are  identical.  Nevertheless,  we  do  not  recommend  the  employment  of  the  whole 
blood,  because  it  can  be  used  only  in  a  coagulated  condition,  and  with  this 
semi-solid  mass,  even  though  it  be  stirred,  we  have  no  guarantee  that  the  tempera- 
ture is  absolutely  homogeneous.  It  is  only  when  a  sufficient  quantity  of  serum 
cannot  be  obtained  that  the  coagulated  whole  blood  may  be  employed,  and  then 
it  should  be  well  broken  up  by  the  platinum  stirrer  after  its  introduction  into  the 
fi-eezing-apparatus  and  before  the  determination  is  made.  It  would  be  better 
previously  to  defibrinate  the  blood.  This  may  readily  be  accomplished  immedi- 
ately after  its  withdrawal  by  stirring  it  in  a  glass  vessel  for  some  time  with  the 
platinum  stirrer  belonging  to  the  fi-eezing-apparatus.  In  every  case  all  of  the 
hemoglobin  should  be  changed  into  oxyhemoglobin  before  coagulation  and  sepa- 
ration of  the  serum,  since  the  blood  obtained  by  venesection  always  contains  a 
large  quantity  of  CO^,  and  since  the  variable  quantities  of  CO^  found  combined 
or  free  in  the  blood  are  dependent  upon  the  degree  of  oxidation  of  the  hemo- 
globin, so  that  this  naturally  has  some  influence  ujion  the  osmotic  pressure.  Con- 
stant results  will  be  obtained  only  when  the  blood  employed  is  saturated  with 
oxygen.  This  saturation  with  oxygen  is  most  easily  insured  by  allowing  the 
blood  from  the  cannula  to  trickle  in  a  thin  layer  along  the  sides  of  the  receiving 
vessel.  The  contact  of  the  blood  with  atmospheric  air  is  sufficient  to  convert  all 
of  its  hemoglobin  into  oxyhemoglobin  ;  the  area  of  contact  may  be  increased  by 
catching  the  blood  in  a  funnel  introduced  into  the  mouth  of  the  receiving  vessel, 
and  then  markedly  tilting  the  funnel  so  that  the  blood  will  spread  out  in  a  thin 
layer  upon  its  inner  surface  and  slowly  trickle  into  the  receptacle.  Where  the 
blood  has  been  defibrinated,  the  requisite  stirring  is  sufficient  to  convert  the 
reduced  hemoglobin  into  oxyhemoglobin.  Some  investigators  also  pass  oxygen 
into  the  blood,  but  this  seems  to  the  writer  to  be  superfluous  and  too  complicated 
for  clinical  purposes.  It  might  also  be  noted  that  it  does  not  matter  whether 
or  not  some  of  the  erythrocytes  remain  in  the  serum  (as  frequently  happens),  since 
defibrinated  blood  and  serum  have  the  same  freezing-point. 

The  normal  freezing-point  of  the  blood  is  — 0.56°  C. 

The  most  important  result  of  the  determination  -of  the  freezing-point  of  the 
blood  is  that  it  gives  definite  information  in  reference  to  the  sufficiency  or 
insufficiency  of  the  elimination  of  urinary  solids  by  the  kidneys.  When  the 
method  is  accurately  carried  out  with  due  regard  to  the  previously  mentioned 
precautions,  among  which  the  writer  would  lay  special  stress  upon  the  saturation 
of  the  blood  with  oxygen,   an  elevation  of  the  freezing-point  amounting  to 


CONDITION  OF  BLOOD  IN  MOST  IMPORTANT  BLOOD-DISEASES.   669 

0.01°  to  0.02°  must  be  regarded  as  pathologic.  Considerable  elevations  of  the 
osmotic  pressure  of  the  blood  are  most  frequently  encountered  in  uremic  con- 
ditions, when  freezing-points  of  —0.65°  and  —0.7°  C.  are  by  no  means  rare. 
This  evident  disturbance  of  the  elimination  of  urinary  solids  undoubtedly  has 
some  relation  to  uremia  ;  but  the  idea  that  an  elevation  of  the  osmotic  press- 
ure is  constantly  present  in  uremia  is  incorrect,  as  is  also  the  converse — that 
uremic  symptoms  must  be  present  when  the  osmotic  pressure  is  increased. 
From  this  it  follows  that  uremia  is  not  dependent  upon  the  elevation  of  the 
osmotic  pressure  alone,  but  must  be  due  to  the  retention  of  some  special  sub- 
stances. ^  This  retention  cannot  be  recognized  from  the  freezing-point  of  the 
blood  when  the  retained  substance  is  compensated  for,  from  an  osmotic  stand- 
point, by  the  elimination  of  other  solids.  Disregarding  the  question  of  uremia, 
the  determination  of  the  freezing-point  of  the  blood  furnishes  the  most  important 
data  for  the  estimation  of  the  work  done  by  the  kidneys  in  a  given  case  of 
nephritis,  and  consequently  justifies  important  conclusions  in  reference  to  treat- 
ment. The  author  would  call  special  attention  to  the  fact  that,  while  all  con- 
clusions in  reference  to  the  renal  function  based  upon  cryoscopic  examination  of 
the  urine  are  inaccurate  except  in  extreme  cases,  a  renal  insufiiciency  may  be 
surely  concluded  from  a  distinct  elevation  of  the  osmotic  pressure  of  the  blood, 
which,  for  example,  would  contra-indicate  the  extirpation  of  one  of  the  kidneys. 

Very  considerable  elevations  of  the  osmotic  pressure  of  the  blood  have  also 
been  observed  in  cardiac  cases  Avith  broken  compensation.  ^  Since  uremic  symp- 
toms, in  the  ordinary  sense  of  the  word,  are  scarcely  ever  present  in  these  cases, 
it  follows  that  uremia  does  not  essentially  depend  upon  the  elevation  of  the 
osmotic  pressure  of  the  blood. 

The  osmotic  pressure  of  the  blood  may  be  lowered  in  the  retention  of  w^ater 
as  the  result  of  nephritis,  in  case  this  retention  is  not  compensated  for  from  an 
osmotic  standpoint  by  the  simultaneous  retention  of  urinary  solids,  as  is  usually 
the  case.  If  the  loss  of  osmotic  pressure  be  more  than  compensated,  cryoscopy  is 
of  no  value  for  the  recognition  of  hydremic  plethora,  and  we  must  then  employ 
what  is  really  the  best  method  for  this  purpose,  the  determination  of  the  relative 
quantity  of  hemoglobin  in  the  blood. 

The  lowering  of  the  osmotic  pressure  of  the  blood,  indicative  of  the  retention 
of  water  in  febrile  diseases,  is  also  of  general  pathologic  interest.^ 

INVESTIGATION  OF  THE  VISCOSITY  OR  OF   THE    INTERNAL   FRICTION    OF 

THE  BLOOD. 

From  the  physico-chemical  investigations  of  Ostwald*  and  the  physiologic 
study  of  the  question  by  Hiithle,*  C.  Hirsch  and  C.  Beck «  have  worked  out 
a  clinical  method  for  determining  at  the  bedside  the  viscosity  or  internal  resist- 
ance of  the  blood.  The  apparatus  employed  is  illustrated  in  Fig.  237.  The 
method  depends  upon  measuring  the  time  required  by  a  known  quantity  of  blood 
to  flow  through  a  capillary  tube  under  a  definite  pressure.  The  experiment  must 
be  carried  out  with  a  constant  temperature,  since  the  temperature  influences  the 
viscosity.  The  apparatus  is  constructed  as  follows  :  It  consists  of  the  hand- 
bulb  A,  of  the  calcium  chlorid  tube  B,  of  the  pressure  flask  C,  which  is  protected 
against  heat  conduction  and  radiation  by  a  felt  jacket ;  of  the  manometer  D,  which 
is  rendered  more  sensitive  by  being  filled  with  benzol  ;  of  the  water  bath  E,  and 
of  the  actual  measuring  apparatus  F.  This  measuring  apparatus  consists  of  a 
U-shaped  tube,  XV,  which  is  dilated  at  G,  below  which  it  becomes  capillary,  to 
dilate  again  at  the  bendZZ,  and  pass  into  the  ampulla  M,  in  which  the  closed  tube  V 
is  inserted  by  means  of  a  ground  joint.  There  is  a  mark  both  above  and 
below  the  dihitation  at  G.     The  capacity  of  G  is  about  l  c.c,  and  the  diameters 

'  From  tlie  constant  findings  of  Strauss  in  his  analyses  of  the  blood  in  uremia,  these 
retained  substances  are  nitrogenous,  and  consist  largely  of  urea. 

2  Landau,  Arch.  f.  kiln.  Med.,  vol.  Ixxviii.,  1904.  •■*  See  Landau,  ibid. 

*  Physifo-clieniical  measurements. 

^  Fflu(^er\^  Archir,  vol.  Ixxxii.,  parts  9  and  10.         ^  Munch,  med.  Woeh.,  1900,  No.  49. 


670 


EXAMINATION  OF  THE  BLOOD. 


of  the  diflferent  capillary  tubes  vary  between  0.25  and  0.35  mm.  During  the 
course  of  the  experiment  this  measuring  apparatus  is  held  by  a  support,  as  indi- 
cated in  the  figure,  immersed  in  a  water  bath  at  a  temperature  of  88°  C,  and 
connected  by  the  T-tube  T  and  tubing  with  the  pressure  flask  G,  the  calcium 
chlorid  tube  B,  the  hand  bulb  A,  and  the  manometer  B,  as  indicated  in 
the  illustration.  The  upper  end  of  the  closed  tube  of  the  measuring  apparatus 
projects  into  the  air  above  the  level  of  the  water.  Before  commencing  the 
experiment,  the  measuring  apparatus  should  be  kept  for  some  time  in  air  at 
a  temperature  of  38°  C,  so  that  we  may  be  certain  that  its  temperature  is 
38°  C.  immediately  after  its  immersion  in  the  water.  Beside  the  apparatus  is  a 
chronometer  which  registers  fifths  of  a  second.  The  experiment  now  proceeds 
as  follows :  The  connection  is  broken  at  P;  the  tube  leading  to  the  pressure 


Fig.  237.— Apparatus  of  C.  Hirsch  and  C.  Beck  for  the  determination  of  the  viscosity  of  the  blood. 

flask  is  closed  by  a  stopcock,  and  the  desired  pressure  of  400  mm.  of  water, 
equal  to  452  mm.  of  benzol,  is  obtained  in  the  pressure  flask  by  means  of  the 
hand  bulb.  The  U-shaped  lower  portion  of  the  measuring  apparatus  is  now 
filled  to  the  upper  end  of  the  ampulla  (i¥)  with  blood,  which  is  obtained  fresh 
from  an  exposed  vein  in  the  arm  by  means  of  a  pointed  and  bent  glass  cannula. 
The  closed  tube  V  is  now  quickly  inserted.  Suction  is  then  made  at  Z  until 
the  blood  is  just  above  the  mark  X.  The  measuring  apparatus  is  now  con- 
nected with  the  pressure  flask  by  the  glass  tube  Z  P.  The  stopcock  is  opened, 
so  that  the  pressure  forces  the  blood  downward  through  the  capillary  tube. 
The  chronometer  is  set  going  as  soon  as  the  upper  level  of  the  blood-column 
passes  the  upper  mark  X,  and  is  stopped  at  the  moment  when  it  reaches  the 
lower  mark  X.  The  experimenter  notes  the  elapsed  time,  convinces  himself 
that  the  pressure  has  remained  constant,  and  immediately  repeats  the  measure- 


CHEMICAL  EXAMINATION  OF  THE  BLOOD.  671 

ment.  In  this  manner  from  two  to  six  measurements  may  be  made  with  the 
same  blood.  The  manipulation  must  be  done  very  quickly,  so  that  it  may  not 
be  interfered  with  by  coagulation.  According  to  Jakoby/  blood  may  be 
employed  which  has  been  rendered  non-coagulable  by  the  addition  of  leech 
extract  or  hirudin.  This  does  not  influence  the  result,  while  defibrinated  blood 
exhibits  a  diminished  viscosity.  The  apparatus  is  cleansed  with  soda  solution 
and  distilled  water  and  kept  in  a  dry  place. 

The  necessary  calculation  is  made  by  the  formula 

St 

in  which  r/  is  the  desired  coefficient  of  the  internal  friction  of  the  blood,  s  the 
specific  gravity  of  the  blood,  r/^  the  coefficient  of  the  internal  friction  of  the  fluid 
with  which  the  blood  is  compared,  Sj  the  specific  gravity  of  this  fluid,  and  /  and 
f^  the  flowing  times  of  the  two  fluids.  Freshly  distilled  anilin  is  selected  for 
comparison,  since  its  specific  gravity  is  so  close  to  that  of  the  blood  that  it 
may  be  assumed  to  be  equal  to  it.     This  simplifies  the  formula  so,  that 

t 

rj^,  the  coefficient  of  viscosity  of  anilin  as  compared  with  that  of  water 
(which  serves  as  the  unit  in  these  investigations),  is  determined  once  for  all,  and 
it  consequently  follows  that,  in  order  to  calculate  jj,  we  must  simply  determine 
the  flowing-time  of  anilin  =  f^  We  then  know  the  value  of  n^  and  t^,  and,  as 
we  have  determined  t  for  the  blood,  the  formula  gives  us  the  value  n  ;  that  is,  the 
coefficient  of  the  viscosity  of  the  blood  as  compared  with  water.  Since  interest 
centers  chiefly  in  relative  values,  it  is  still  simpler  for  clinical  purposes  to  select 
the  viscosity  of  anilin  as  the  unit.     This  gives  us 

t 

The  most  important  conclusion  arrived  at  by  Hirsch  and  Beck  in  a  large 
number  of  investigations  ^  is  that  it  is  incorrect  to  suppose  that  the  cardiac  hyper- 
trophy in  cases  of  nephritis  is  due  to  an  increase  in  the  viscosity  of  the  blood. 
Still  further  results  may  be  expected.  In  all  events,  the  viscosity  of  the  blood  is 
of  great  clinical  interest,  since,  according  to  the  laws  of  capillary  currents  as 
stated  by  Poiseuille  and  Hagenbach,  it  is  an  essential  factor  in  the  velocity  of  the 
blood-stream. 

CHEMICAL   EXAMINATION   OF  THE  BLOOD. 

(Percentage  of  hemoglobin,  compare  p.  616.  Eeaction  of  the  blood,  com- 
pare p.  613.  Removal  of  the  blood  for  the  purpose  of  chemical  examination, 
compare  p.  610.) 

IRON  TESTS  FOR  THE  BLOOD  WITH  JOLLES'  FERROMETER. 

A.  Jolles  '■'•  has  recently  succeeded  in  devising  a  method  for  determining  tbe 
amount  of  iron  in  the  blood  by  means  of  an  instrument  called  a  ferrometer.  The 
method  is  of  some  value  clinically,  for  it  requires  only  small  amounts  (0.05  c.c.) 
of  blood.  Its  principle  is,  briefly,  as  follows  :  A  measured  quantity  of  blood 
(0.05  c.c.)  is  removed  with  a  special  capillary  pipet  (such  as  is  used  in  Gowers' 

'"Sitzung  der  medic.    Gesellsch.  in  Gottingen,"   am   10.   Jiinner,    1901.     Eef.  in 
Deutsch.  med.  WocL,  1901,  No.  8. 
^  See  Arch.  f.  klin.  Med.,  vol.  Ixix. 
3  TJeutsch.  med.  Wock,  1897,  No.  10;  ibid.,  1898,  No.  7,  and  PjiiUjer's  Archiv.,  vol.  Ixv. 


672 


EXAMINATION  OF  THE  BLOOD. 


hemoglobin  examination).  It  is  reduced  to  ashes  in  a  platinum  dish,  0. 1  of  acid 
sulphate  of  potash  is  added,  and  the  combination  is  heated  and  evaj^orated  to 
dryness.  The  residue  contains  the  iron  of  the  blood  in  the  form  of  an  oxid  of 
iron.  This  is  dissolved  in  10  c.c.  of  hot  water  and  1  c.c.  of  diluted  hydrochloric 
acid  (1  :  3),  and  4  c.c.  of  ammonium  sulphocyanid  solution  (7.5  :  1000)  added,  so 
that  the  total  quantity  is  1 5  c.c.  This  gives  a  red  solution  of  sulphocyanid  of 
iron,  whose  composition  can  be  determined  colorimetrically  by  comparing  it  with 
a  solution  containing  a  known  quantity  of  iron.  The  latter  is  prepared  in  such  a 
way  that  each  cubic  centimeter  contains  exactly  0.00005  of  iron.^  One  c.c.  of 
this  standard  solution  is  diluted  to  10  c.c.  with  water,  and  then  1  c.c.  of  dilute 
hydrochloric  acid  and  4  c.c.  of  ammonium  suljihocyanid  solution  are  added  just 
as  above.  The  resulting  solution  is  then,  by  means  of  the  apjjaratus  pictured  in 
Fig.  238,  compared  colorimetrically  with  the  sulphocyanid  of  iron  solution 
derived  from  the  blood.  This  ai3paratus  consists  of  two  glass  cylinders,  C  and  C'', 
of  exactly  equal  caliber,  C  containing  accurately  15  c.c,  and  C^  about  16  c.c. 
Both  cylinders  are  subdivided  into  0.1  c.c,  and  both  are  closed  at  the  bottom 
with   glass    plates,   through    which   light    is    reflected   from  the  plaster-of-Paris 

reflector,  J\,  in  the  direction  of  their  axes. 
The  sulphocyanid  of  iron  solution  prepared 
from  the  blood  is  exactly  15  c.c,  and  so  just 
fills  the  cylinder  C,  which  is  then  covered 
with  a  glass  disk,  care  being  taken  to  avoid 
the  formation  of  air  bubbles.  Fifteen  cubic 
centimeters  of  the  sulphocyanid  of  iron  solu- 
tion (prepared  from  the  stock  solution)  are 
placed  in  cylinder  C^  for  comparison.  To 
avoid  the  development  of  a  meniscus,  which 
will  disturb  the  reading,  a  floating  stopper, 
made  of  aluminum  and  closed  at  both  ends 
with  parallel  glass  plates,  is  placed  on  the 
surface  of  the  fluid  in  cylinder  C^,  avoiding 
air  bubbles.  A  flat  fluid  surface  is  thus  ob- 
tained. This  contrivance  always  displaces  a 
slight  amount  of  fluid,  which  is  the  reason 
why  cylinder  C*'  must  be  made  somewhat 
taller  than  C.  Cylinder  C*'  is  provided  with 
a  lateral  escape  stopcock,  II.  Both  cylinders 
can  be  easily  removed  from  the  base  of  the 
instrument  for  cleansing  or  filling.  The  tin 
jacket  .surrounding  the  cylinders  shuts  out 
any  lateral  illumination.  The  colorimetric 
comparison  is  made  as  follows  :  Both  cylin- 
ders are  filled  as  just  described,  and  then  the 
fluid  in  C^  is  allowed  to  escape  through  the  stopcock  i/ into  the  vessel  A  until  the 
contents  of  both  tubes,  as  seen  from  above  by  transmitted  light,  present  exactly 
the  same  shade.  When  this  point  is  reached,  cylinder  (7  is  removed  and  the 
level  of  the  fluid  noted.  If  the  amount  of  fluid  remaining  in  C^  to  the  base  of 
the  floating  cork  were  exactly  15  c.c,  the  amount  of  blood  used  (0.05  c.c) 
would  contain  0.00005  of  iron — i.  e.,  1  liter  of  blood  would  contain  1  gm.  of 
iron.  If,  however,  when  the  color  in  the  two  cylinders  is  alike,  O'  contains 
only  7.5  c.c.  of  fluid,  the  amount  of  iron"  contained  is  only  half  as  much — /.  e., 
0.5  gm.  per  liter  of  blood.  A  table  to  calculate  the  percentage  of  iron  contained 
in  the  blood  has  been  prepared  by  Jolles,  and  is  included  with  the  instrument. 
It  takes  about  ten  to  fifteen  minutes  to  calculate  the  amount  of  iron  with  Jolles' 
ferrometer. 

The  same  maker  (Reichert)  has  recently  placed  upon  the  market  an  instru- 
ment Avhich  may  be  used  either  as  a  Fleischl-Miescher  hemometer  or  as  a  Jolles' 

^  For  the  exact  steps  see  above  reference. 


Fig.  238.— Jolles'  ferrometer. 


CHEMICAL  EXAMINATION  OF  THE  BLOOD.  673 

ferrometer,  since  the  intensity  of  the  color  of  the  sulphocyanid  of  iron  solution 
is  estimated  by  means  of  the  glass  wedge  of  the  hemometer/ 

Jolles  believed  at  first  that  his  method  was  an  accurate  means  of  determining 
the  amount  of  hemoglobin  indirectly,  for  he  assumed  that  hemoglobin  contained 
0.42  per  cent,  of  iron,  and  that  all  the  iron  present  was  contained  in  the  hemo- 
globin. But  in  more  recent  communications  ^  he  has  abandoned  this  theory, 
as  his  investigations  have  led  him  to  conclude  that  the  blood  contains  con- 
siderable quantities  of  iron,  probably  in  the  shape  of  nuclein,  outside  of  the 
hemoglobin.  This  idea  corresjionds  to  the  views  of  Biernatzki  and  Jellinek. 
Moreover,  it  is  likely  that  hemoglobin  itself  does  not  always  contain  a  constant 
amount  of  iron.  The  great  variations  (which  have  been  reported  in  literature) 
as  the  results  of  analyses  of  hemoglobin  crystals  in  one  and  the  same  animal 
.species  would  seem  to  suggest  this. 

Although  these  statements  might  give  rise  to  the  thought  that  the  estimation 
of  the  iron  in  the  blood  might  acquire  a  clinical  significance  independent  of  that 
of  the  estimation  of  the  hemoglobin,  the  investigations  of  Kruss  ^  and  Schwenk- 
enbecher*  would  make  this  seem  very  doubtful,  since  these  authors  reached 
the  conclusion  that  the  double  sulphocyanid  of  iron  producing  the  red  color  in 
Jolles'  method  becomes  so  markedly  dissociated  by  dilution  that  the  red  color 
decreases  in  intensity  more  rapidly  than  does  the  quantity  of  iron  in  the  solu- 
tion. In  other  words,  iron  cannot  be  accurately  estimated  by  this  colorimetric 
method. 

THE  BLOOD   IN    CARBON    DIOXID    POISONING. 

In  marked  cases  of  carbon  dioxid  poisoning  the  naked  eye  can  prob- 
ably appreciate  the  change  of  color  in  the  blood.  It  is  noticeably  bright 
red,  and  almost  fails  to  exhibit  the  difference  between  venons  and  arte- 
rial blood.  The  presence  of  carbon  dioxid  in  the  blood  is  demonstrated 
usually  by  means  of  the  spectroscope.  If  a  few  drops  of  blood  con- 
taining carbon  dioxid  are  diluted  with  water,  the  mixture  will  show  in 
the  spectroscope  two  bands,  between  the  green  and  yellow,  very  much 
like  those  of  oxyhemoglobin  (Fig.  167,  1).  They  are,  however,  very 
slightly  displaced  toward  the  violet  end  of  the  spectrum.  They  differ 
from  the  oxyhemoglobin  bands  by  not  disappearing  upon  the  addition 
of  ammonium  sulphid,  whereas  the  oxyhemoglobin  bands  are  replaced 
by  a  simple  band  of  reduced  hemoglobin  (Fig.  167,  2).  Oxyhemoglobin 
bands  disappear  very  slowly  after  adding  ammonium  sulphid  to  the 
blood,  and  may  be  temporarily  reproduced  if  the  liquid  is  shaken  with 
air,  owing  to  the  concentrated  action  of  the  oxygen. 

Another  test  for  carbon  dioxid  in  the  blood  consists  in  adding  a  little 
10  per  cent,  caustic  soda  or  potash  solution  to  the  blood  contained  in  a 
porcelain  dish,  and  then  gently  warming.  If  carbon  dioxid  is  present 
in  any  appreciable  quantity,  the  mixture  will  become  very  brilliant  red, 
while  normal  blood  will  turn  to  a  dirty  greenisli  brown. 

It  is  advisable  to  perform  both  spectroscopic  and  chemical  tests  and 
compare  them  with  the  normal  blood  for  a  control,  because  when  only  a 
slight  amount  of  carbon  dioxid  is  present  in  the  blood,  quantitative  dif- 
ferences are  iniportant  in  forming  an  opinion. 

1  S.  Jolles,  Berlin,  klin.  Wock,  1899,  No.  44,  p.  965.  ^  Lnc.  ci(. 

^  Colorimetrie  und  quantitative  Spectralanalyse  in  ihrer  Anwendung  auf  die  Cliemie, 
Hamburg  and  Leipzig,  1891,  p.  176. 

^  Arch.  f.  klin.  Med.,  vol.  Ixxv.,  parts  3-5. 

43 


674  EXAMINATION  OF  THE  BLOOD. 

We  must  not  overrate  the  diagnostic  value  of  these  investigations^ 
The  human  body  reacts  so  intensely  to  carbon  dioxid  gas  that  symptoms 
of  poisoning  may  be  very  pronounced  without  its  being  possible  to 
demonstrate  the  presence  of  this  poison  in  the  blood  either  chemically 
or  spectroscopically. 

THE   BLOOD   IN    METHEMOGLOBINEMIA. 
The  blood  contains  methemoglobin  in  various  types  of  poisoning, 
especially  from    chlorate    of   potash    and    antifebrin.     Its  presence  is 
demonstrated  by  means  of  the  spectroscope  after  sufficiently  diluting  the 
blood  with  water  (see  Fig.  167,  3). 

THE   BLOOD   IN   HYDROGEN   SULPHID   POISONING. 
In  severe  cases  the  color  may  be  a  dirty  green,  and  may  show  the 
characteristic  bands  of   sulphohemoglobin  besides    the  oxyhemoglobin 
bands.     The  former  resemble  the  bands  of  methemoglobin,  but  are  sit- 
uated a  little  more  toward  the  violet  end  of  the  spectrum  (Fig.  167,  3)» 

THE   BLOOD    IN   HEMOGLOBINURIA. 

Hemoglobinuria  may  appear  independently  as  the  so-called  periodic 
hemoglobinuria  (Lichtheim),  or  especially  in  certain  kinds  of  poisoning 
and  after  burns.  It  is  always  produced  by  the  red  blood-corpuscles 
becoming  dissolved  within  the  vascular  system.  Hemoglobinuria  is 
therefore  always  associated  with  hemoglobinemia  or  methemoglobinemia. 
Free  hemoglobin  and  methemoglobin  can  be  readily  demonstrated  in  the 
blood  by  allowing  several  cubic  centimeters  of  blood  to  coagulate. 
Under  normal  conditions  the  serum  will  only  be  stained  slightly  yellow 
(lutein),  provided  that  the  blood-clot  has  not  been  interfered  with 
mechanically.  In  hemoglobinuria,  on  the  other  hand,  the  serum  will 
be  more  or  less  of  a  ruby  red,  owing  to  the  presence  of  hemoglobin  in 
solution  ;  or  brown,  if  methemoglobin  is  present.  The  serum,  however, 
must  be  absolutely  clear,  for  if  it  is  cloudy  the  color  may  be  due  to  an 
admixture  of  blood-corpuscles  with  the  serum,  from  some  disturbance 
during  coagulation.  In  doubtful  cases  the  microscope  will  decide  the 
question.  The  stained  serum  will  give  the  characteristic  bands  of  oxy- 
or  methemoglobin,  one  or  both,  in  the  spectroscope  (Fig.  167).  In 
periodic  hemoglobinuria  the  blood  shows  during  the  attack  a  peculiarity 
first  described  by  Hayem,  and  subsequently  corroborated  by  Chvostek.^ 
It  coagulates  very  rapidly,  but  the  clot  dissolves  again  after  some  little 
time.  In  fresh  preparations  disintegrated,  deformed,  or  decolorized 
blood-corpuscles  may  be  found  under  the  microscope  (shadows,  p.  638). 

PRESENCE   OF   URIC   AQD   IN   THE   BLOOD. 

Physiologically,  the  blood  does  not  contain  any  appreciable  quantity 
of  uric  acid.     In  chronic  nephritis  and  acute  articular  rheumatism  mere 
traces  only  have  been  found ;  but  in  gout,  at  least  in  the  early  stage  of 
^  TJeher  das  Wesen  der  paroxysmcden  Haemoglobinuria,  F.  Deuticke,  1894. 


WIDAL'S  SEBUM  TEST  IN  TYPHOID  FEVEE.  675 

the  attack,  the  amount  of  uric  acid  contained  in  the  blood  is  so  consid- 
erable that  Garrod  devised  a  comparatively  simple  method,  the  so-called 
thread  test,  to  demonstrate  its  presence. 

According  to  Garrod,  30  to  35  c.c.  of  blood  are  allowed  to  coagu- 
late ;  10  c.c.  of  the  serum  which  accumulates  during  the  next  few  hours 
over  the  clot  is  mixed  with  100  c.c.  of  acetic  acid.  A  fine  linen  thread  * 
is  placed  in  the  mixture,  which  is  then  covered  so  as  to  prevent  evapora- 
tion, and  allowed  to  stand. 

If  the  blood  contains  at  least  0.0025  per  cent,  of  uric  acid,  character- 
istic crystals  (Fig.  186)  will  appear  on  the  thread  in  the  course  of  one 
or  two  days.  In  doubtful  cases  the  murexid  test  (p.  556)  may  be 
applied  to  these  crystals. 

Garrod  indirectly  demonstrates  an  increase  of  uric  acid  in  the  blood 
in  gout  by  performing  this  test  with  the  serum  of  an  artificially  pro- 
duced blister. 

WIDAL'S  SERUM  TEST  IN  TYPHOID  FEVER, 

This  test  has  its  origin  in  the  fact  that  the  blood-serum  of  patients  Avho  are 
convalescing  from  typhoid,  or  of  animals  immunized  to  typhoid,  according  to  the 
investigations  of  Griiber,  Durham,  and  Pfeiffer,  influences  the  typhoid  bacilli  in  a 
test  tube  in  such  a  way  that  the  latter  lose  their  motility  and  form  conglomerations 
which  may  be  recognized  microscopically.  A  similar  phenomenon  is  observed 
when  cholera-immune  sera  are  added  to  cultures  of  cholera  bacilli.  This  phe- 
nomenon has  been  attributed  to  the  presence  of  peculiar  hypothetic  substances  in 
the  immunized  serum,  which  have  been  called  agglutinin  or  glabrificin  by  Griiber, 
and  paralysin  by  Pfeiffer.  These  substances  are  not  identical  with  the  bactericidal 
nor  immunizing  substances  of  immune  serum. 

Based  upon  this  observation,  Widal  devised  a  peculiar  diagnostic  method  for 
recognizing  typhoid,  for  he  noticed  that  this  peculiarity  is  shown  not  only  by 
the  serum  of  convalescents,  but  also  by  the  serum  taken  during  the  disease,  and 
even  quite  early  in  the  attack.  He  projjosed  '■*  two  methods  for  testing  the  serum 
reaction  of  the  questionable  typhoid  cases,  the  so-called  microscopic  and  macro- 
scopic methods.  To  prevent  evaporation,  a  few  drops  of  freshly  drawn  blood  are 
put  into  a  closed  tube  of  narrow  caliber,  in  which  the  blood  may  be  preserved 
for  days.  The  serum  which  separates  by  spontaneous  coagulation  is  employed. 
In  the  beginning  Widal  demonstrated  the  reaction  microscopically  by  simply 
adding  a  drop  of  the  serum  to  a  drop  of  typhoid  broth  culture,  of  not  more  than 
twelve  to  twenty-four  hours'  growth,  upon  a  slide.  Under  the  microscope  the 
bacilli  in  the  broth  culture  must  be  very  active.  If  the  reaction  is  positive,  the 
bacilli  will  cease  to  move  within  from  a  few  minutes  to  half  an  hour  and  become 
conglomerated,  while  the  intervening  fluid  will  be  free  from  bacilli.  The  second 
method  depends  upon  the  macroscopic  appearance  of  a  typhoid  broth  culture  to 
which  the  serum  of  the  patient  in  question  has  been  added.  The  controlled 
culture  is  evenly  clouded  ;  but  a  culture  to  which  a  moderate  amount  of  typhoid 
serum  has  been  added  will  clear  up,  on  account  of  the  agglutinated  bacilli  settling- 
to  the  bottom  of  the  tube. 

It  has,  however,  been  demonstrated  in  the  Bern  Clinic  that  this  macroscopic 
serum  reaction  is  not  nearly  so  reliable  as  the  microscopic  test. 

^  It  is  better  not  to  use  a  thread,  but  to  separate  from  it  one  of  the  elementary  fibers 
of  which  it  is  composed. 

^  See  La  Semaine  MM.,  1896,  No.  33,  p.  259;  also  numerous  tests  of  the  metliod 
quoted  in  the  same  vear  of  this  periodical ;  also  tests  bv  the  Germans:  Stern,  Centralbl. 
f.  inn.  Med.,  }m\  *No.  49;  Breuer-Lichtheim,  Berlin.' kiln.  WocL,  1896,  Nos.  47  and 
48;  also  M.  F.  Widal  and  M.  A.  Sicard,  Ann.  de  I'institul  Pasteur,  1897,  vol.  xi..  No.  5. 


676  EXAMINATION  OF  THE  BLOOD. 

To  obtain  reliable  results,  the  microscopic  reaction  had  to  be  modified,  since 
it  was  found  necessary  to  take  into  account  the  dilution  of  the  serum.  For  it  was 
soon  discovered  that  in  low  dilutions  the  serum  of  some  people  not  suffering  from 
typhoid  had  a  moderate  power  of  agglutinating  typhoid  cultures.  It  was  there- 
fore found  necessary  to  determine  that  a  certain  very  small  quantity  of  the  serum 
would  exert  this  action  in  order  to  consider  the  test  positive  for  the  diagnosis  of 
typhoid. 

Widal's  reaction  is  performed  quantitatively  in  the  Bern  Clinic  as  follows, 
a  convenient  and  reliable  method  :  In  4  or  5  glass  staining  dishes  we  place  10,  20, 
50,  70  or  100  drops  respectively  of  a  typhoid  culture  not  over  twelve  or  fourteen 
hours  old,  by  means  of  a  glass  pipet  with  a  long,  fine  point.  But  1  drop  is 
allowed  to  escape  at  a  time.  The  bacilli  of  the  culture  must  be  known  to  be 
very  active.  A  drop  of  the  suspected  serum  is  added  to  each  dish  from  the  same 
pipet  (after  it  has  been  washed).  The  culture  and  the  serum  are  now  thor- 
oughly mixed  in  the  dish  with  a  platinum  wire.  The  serum  dilution  is  therefore 
1:10,  1 :  20,  1 :  50,  1 :  70,  etc.  A  microscopic  preparation  from  each  of  these 
mixtures  and  from  the  typhoid  culture  for  the  purpose  of  control  are  examined 
immediately  and  after  a  known  interval  with  an  oil-immersion  lens.  The  more 
concentrated  specimens  are,  of  course,  examined  first.  In  some  cases  of  .typhoid 
the  agglutinating  action  of  the  serum  may  be  so  marked  that  even  Avith  a  dilu- 
tion of  1 :  100  the  typhoid  bacilli  will  lose  their  power  of  motion  and  will  adhere 
in  clumps  immediately  after  the  addition  of  the  serum.  When  the  agglutination 
is  less  vigorous,  the  reaction  may  not  be  manifest  for  a  considerable  time,  or  it 
may  occur  only  in  the  more  concentrated  dilutions.  Before  an  absolute  diagno- 
sis of  typhoid  fever  is  made  from  the  serum  action  alone,  agglutination  should 
take  place  within  an  hour  with  a  dilution  of  the  serum  of  1  :  50.  The  sooner 
clumping  occurs,  the  safer  one  is  in  expressing  an  opinion.  It  is  useless  to  extend 
observations  beyond  an  hour,  because  by  using  the  more  concentrated  solutions  we 
can  get  sufficient  information  regarding  the  less  pronounced  agglutination  power 
in  less  than  an  hour.  If  the  period  of  observation  is  limited  in  this  way,  the 
microscopic  preparations  may  be  left  to  themselves  without  fear  of  having  them 
dry  up.  In  case  of  any  doubt,  it  is  always  easy  to  make  fresh  slides  from  the 
staining  dishes. 

Different  typhoid  cultures  vary  in  their  susceptibility  to  clumping,  so  that 
each  observer  should  make  himself  familiar  with  the  peculiarities  of  his  own 
cultures.     This  explains  variable  results  reported. 

In  this  connection  the  author  will  record  what  he  believes  to  be  a  new  obser- 
vation, made  in  his  clinic  during  an  epidemic  of  typhoid  fever.  Early  in  the 
disease  the  serum  of  the  patients  produced  more  marked  agglutination  in  weaker 
than  in  stronger  concentrations ;  but  this  condition  was  reversed  during  the 
course  of  the  disease.  This  indicates  that,  in  addition  to  the  agglutinative  effect 
of  the  serum,  there  is  a  counteraction  against  agglutination  early  in  the  disease, 
w^hich  may  be  overcome  by  the  more  marked  dilutions.  Since  agglutination  is 
doubtless  indicative  of  an  inj\uy  to  the  typhoid  bacilli,  this  phenomenon  is  to  be 
regarded  as  an  expression  of  a  favorable  influence  of  the  serum  upon  the  growth 
of  the  bacilli,  which  disappears  during  the  course  of  the  disease,  and  which  may 
be  overcome  by  the  more  marked  dilutions.  Further  investigations  are  now 
under  way  in  order  to  determine  whether  these  differences  between  the  effects  of 
concentrated  and  dilute  serum  mixtures  are  of  value  from  a  prognostic  stand- 
point. At  all  events,  the  observation  is  of  practical  importance,  since  it  demon- 
strates that  a  negative  result  should  neter  be  assumed  simply  because  agglu- 
tination is  not  obtained  by  a  concentrated  serum,  but  that  an  opinion  should  be 
withheld  until  the  test  has  been  made  with  a  much  diluted  serum.  It  also  shows 
the  necessity  of  tiying  the  different  concentrations  in  every  case. 

In  order  to  have  fresh  typhoid  cultures  always  at  hand,  it  is  best  to  trans- 
fer the  glycerin-agar  cultures  every  eight  or  fourteen  days,  as  otherwise  the 
cultures  will  degenerate  and  die  off.  A  bouillon  culture  is  prepared  from  the 
water  of  condensation  of  the  agar  culture  twelve  to  fourteen  hours  before  perform- 
ing the  test  and  placed  in  an  incubator.     The  water  of  condensation  always 


EXAMINATION  OF  THE  MOUTH  AND  PHARYNX.  677 

contains  very  active  bacilli.  Stock  cultures,  after  being  grown  for  a  little  while, 
are  best  preserved  at  the  temperature  of  the  room.  Authentic  typhoid  cultures 
are  best  obtained  from  the  spleen  of  a  fresh  typhoid  corpse  (with  the  ordinary 
precaution  to  avoid  contamination — i.  e.,  singeing  the  surface). 

Attempts  have  recently  been  made  to  substitute  for  the  original  Widal  reaction 
analogous  reactions  with  dead  preserved  typhoid  bacilli,  and  also  reactions  of 
precipitation  with  chemical  extracts  of  cultures  of  typhoid  bacilli.  Until  the 
results  obtained  are  shown  to  be  as  reliable  as  those  obtained  from  the  original 
procedure,  they  will  not  be  described  in  detail  in  this  work.  These  modifications 
would  certainly  have  the  advantage  of  rendering  the  procedure  more  accessible 
to  the  practising  physician. 


EXAMINATION   OF  THE  MOUTH  AND   PHARYNX. 

Inspection  is  the  most  important  method  for  examining  the  mouth 
and  pharynx.  For  proper  inspection  tlie  patient  should  open  his  mouth 
as  wide  as  possible,  and  then  retract  the  tongue  from  the  place  to  be 
examined.  The  pharynx  and  soft  palate  are  usually  seen  best  if  the 
base  of  the  protruded  tongue  is  depressed  with  a  spatula,  with  the  handle 
of  a  spoon,  or  with  the  finger  of  one  hand,  while  the  examiner  steadies 
the  patient's  head  at  the  same  time  with  his  other  hand.  Care  must  be 
taken  not  to  apply  the  depressor  too  far  back,  for  if  the  posterior  portion 
of  the  base  of  the  tongue  or  the  pharynx  is  touched,  gagging  results  and 
renders  the  examination  difficult.  The  posterior  wall  of  the  pharynx 
can  be  seen  better  when  the  patient  says  "Ah,"  and  so  elevates  the  soft 
palate.  It  is  sometimes  very  difficult  indeed  to  examine  patients' 
mouths  if  their  consciousness  is  at  all  disturbed,  and  it  is  almost  impos- 
sible to  examine  the  mouths  of  unruly  children.  Sometimes  closing  the 
nostrils  will  make  such  patients  open  the  mouth,  while  at  other  times 
we  have  to  forcibly  separate  the  jaws  with  a  spoon,  a  depressor,  or  a 
month  gag.  With  children,  whether  we  employ  the  aid  of  a  depressor 
or  not,  we  should  look  quickly  the  moment  the  child  opens  his  mouth 
to  cry. 

Palpation  with  the  finger  often  assists  in  determining  the  condition 
of  portions  of  the  mouth  which,  are  situated  farther  back.  Palpation 
of  the  nasopharynx  or  of  the  entrance  to  the  esophagus  to  hunt  for  for- 
eign bodies,  retropharyngeal  abscesses,  or  adenoids  must  be  done  very 
quickly,  because  it  is  very  disagreeable  to  the  patient  and  can  be  borne 
but  a  short  time.^  Unruly  patients  and  children  are  apt  to  bite  the 
examiner's  finger  unless  the  cheek  is  pressed  in  between  the  patient's 
teeth  with  the  free  hand.  This  is  a  better  method  than  to  employ  appli- 
ances for  protecting  the  fingers.  The  forefinger  is  better  adapted  for 
palpating  adults,  and  the  little  finger  for  small  children.  The  introduced 
finger  is  hooked  upward  or  downward,  according  to  the  region  to  be 

^  [The  application  of  a  sohition  of  cocain  ( 2  to  4  per  cent. )  to  the  back  of  the  pharynx 
will  deaden  the  sensibility  of  the  parts  and  allow  a  more  careful  digital  examination. — 
Eo.'] 


678 


EXAMINATION  OF  THE  MOUTH  AND  PHARYNX. 


explored.     The  entire  pharyngeal  cavity  can  be  palpated  from  the  top 
of  the  larynx  below  to  the  nasopharyngeal  space  above. 

I/ips. — The  examiner  should  notice  their  color  (pallor,  cyanosis), 


Fig.  239. 


"^^'T^^^P' 


Fig.  240. 


Fig.  239.— Hutchinson's  teeth  in  hereditary  syphilis:  Two  upper  middle  incisors  (second  denti- 
tion) with  deep  transverse  and  longitudinal  grooves ;  also  concave  edge  of  middle  incisors.  The 
length  of  the  teetli  is  normal,  but  tlie  width  is  diminished ;  hence,  broad  interspace  in  middle. 

Fig.  240.— Upper  middle  incisors  (second  dentition)  immediately  after  eruption  ;  also  four  lower 
incisors.  Lower  surface  of  upper  incisors  is  rough,  due  to  prominent  points  of  dentin.  Upper 
teeth  short  and  directed  away  from  each  other,  forming  a  broad  interspace.  On  the  four  lower 
teeth  are  numerous  excrescences,  due  to  deficient  formation  of  enamel.  Base  of  excrescences 
everywhere  at  same  level. 

the  presence  of  aphthous  patches,  mucous  patches,  fissures  (rhagades), 
or  their  scars,  which  leave  diverging  folds  at  the  corners  of  the  mouth 
(children  with  hereditary  syphilis),  and  herpes  labialis. 


Fig.  241.— Hutchinson's  teeth  :  The  upper  middle  incisors  (second  dentition)  and  all  four  lower 
incisors  are  characteristic  enough.  The  photograph  was  talcen  from  a  colored  child,  six  years  of 
age,  who  had  been  under  Dr.  McConnell's  observation  at  the  Vanderbilt  Clinic  for  a  year.  She 
has  sabre  shins,  and  when  first  brought  to  the  clinic  presented  a  rash.  An  older  sister  has  similar 
teeth.  The  mother  has  had  two  miscarriages  since  the  birth  of  her  last  child.  The  original  of 
this  photograph  has  improved  upon  biniodid  of  mercury. 

Teeth. — The   condition   and   the  time   of  appearance  of  the  first 
and  second   sots   are  important  in  childhood.^     In    adults   we   should 
notice  the  state  of  preservation  of  the  teeth.     Poor  teeth  not  infre- 
^  [Note  irregular  dentition  as  indicating  nasal  deformity  and  former  adenoids. — Ed.] 


TEETH. 


679 


quently  cause  digestive  disturbances.      They  are  quite  commonly  due 
to   some   general  disturbance.      Special    attention    should   be  paid  to 


Fig.  242.— AU  four  upper  incisors  approach  the  type  of  Hutchinson's  teeth.  The  lower  incisors 
are  practically  normal.  In  this  case  the  upper  middle  incisors  are  not  characteristically  peg- 
shaped,  but  the  groove  upon  the  cutting  edge  is  a  significant  feature.  No  other  facts  relating 
to  this  case  are  known.    It  is  probable  that  the  teeth  should  be  classified  as  Hutchinson's  teeth. 

so-called  "  rachitic  teeth."  They  are  characterized  chiefly  by  transverse 
and  longitudinal  grooves  with  uneven  enamel,  which  rapidly  wears  off 
on  account  of  its  irregular  distribution.     These  changes  are  most  marked 


Fig.  243.— Irret,Milar  teetli  siinuliitiii!,'-  Hutcliinsou's  teetli  in  a  patient  at  the  New  York  City 
Hospital,  who  exhibited  at  the  time  this  photograph  was  taken  a  well-marked  secondary  syph- 
ilitic eruption. 

in  the  incisors.  In  hereditary  syphilis  the  teeth  are  often  deformed  very 
much  as  in  rachitis.  Some  of  the  teeth  formations  Avhich  are  observed 
in  this  disease  are  by  no  means  characteristic  of  syphilis  alone,  but  occur 


680  EXAMINATION  OF  THE  MOUTH  AND  PHARYNX. 


Fig.  244.— Irregular  teeth  in  a  young  boy  with  a  high-arched  palate.  Although  the  two  upper 
middle  incisors  are  slightly  wedge-shaped,  there  is  not  sufficient  ground  for  considering  them  of 
the  Hutchinson  type.  The  irregularities  are  probably  due  to  an  iuflammation  of  the  gums  during 
the  second  dentition  (Dr.  W.  L.  Stowell,  Randall's  Island  Hospital). 

also  in  rachitis  and  other  general  disturbances,  or  even  when  the  teeth 
buds  have  been  damaged  by  stomatitis.     Hutchinson  considers  the  type 


Fig.  245. — Irregular  teeth,  not  Hutchinson's  teeth  (New  York  City  Hospital). 

of  teeth  shown  in  Figs.  239,  240  as  ])athognomonic  of  hereditary  syphilis.^ 
Other  authors  consider  the  concave  dents  (notches)  in  the  lower  margin 

^  "  Hutchinson's  Teeth." — These  were  first  described  in  the  Transactions  of  the  Path- 
ologic. Society  of  London,  July,  1858.  In  the  original  description  he  says:  "There  is  a 
peculiar  condition  of  the  teeth  resulting  from  hereditary  syphilis,  the  most  frequent  con- 
ditions being  the  following : 

"  («)  Smallness. — They  are  small,  stand  apart,  are  rounded  and  peggy. 

"  (6)  Notching. — They  usually  exhibit  at  the  border  a  broad,  shallow  notch  (some- 
times two  or  three  serrations). 

"  (c)  Color. — They  have  a  dirty-grayish  surface  without  polish,  and  are  rarely 
smooth. 

"  (cZ)  Wearing  Doum. — They  are  deficient  in  enamel  and  are  soft,  and  therefore  liable 
to  premature  Avearing  down. 

"  (fi)  These  signs  almost  exclusively  apply  to  the  incisors  and  canines." — [Ed.] 


GUMS.  •  681 

of  the  upper  middle  incisors  the  characteristic  feature  (Fig.  239,  a). 
The  term  "  Hutchinsonian  teeth  "  should  be  applied  more  especially  to 
those  showing  this  peculiarity.  These  are  observed  chiefly  in  the  second 
dentition.  After  the  twenty-fifth  year  this  concavity  is  usually  worn 
away. 

It  is  important  to  be  familiar  with  the  normal  periods  of  the  appearance  of 
teeth,  so  as  to  be  able  to  recognize  anomalies  in  the  formation  of  teeth  and  to 
attach  a  proper  significance  to  the  symptoms  oftentimes  connected  with  their 
eruption  in  early  childhood. 

A.  Vogel  makes  the  following  statements  (Fig.  246): 

FIRST  DENTITION. 

First  Group :  The  two  lower  middle  incisors  appear  almost  simultaneously 
between  the  seventh  and  the  ninth  month. 

Interval  of  three  to  nine  weeks. 

Second  Group :  The  four  upper  incisors  appear  between  the  eighth  and  the 
ninth  month,  and  follow  one  another  rapidly  within  a  few  weeks,  first  the  middle 
and  then  the  lateral  ones. 

Interval  of  six  to  twelve  weeks. 

Third  Group :  Six  teeth  appear  almost  at  the  same  time  between  the  twelfth 


„  1^2322^3   - 

b  Jt^rrrrrnrKTA^ 


Fig.  246.— Sequences  of  teeth  with  first  dentition  (A.  Vogel). 

and  the  fifteenth  month.  These  are  the  first  four  molars  and  the  two  lower  lateral 
incisors.  Usually  the  anterior  molars  of  the  upper  jaw  appear  first,  then  the 
lower  lateral  incisors,  and  finally  the  anterior  lower  molars. 

Interval  to  the  eighteenth  month. 

Fourth  Group :  The  four  canines  appear  between  the  eighteenth  and  the 
twenty-fourth  month. 

Interval  of  two  to  three  months. 

Fifth  Group :  The  four  second  molars  appear  between  the  twentieth  and  the 
thirtieth  month.  This  ends  the  first  dentition,  and  the  child  then  has  the 
twenty  "milk  teeth." 

SECOND    DENTITION. 

During  this  period  the  milk  teeth  are  supplanted  by  permanent  teeth,  and 
the  three  posterior  molars  in  each  jaw  appear.  The  latter  are  not  present  during 
first  dentition.  A  permanent  set  of  thirty-two  teeth  then  takes  the  place  of  the 
twenty  milk  teeth.  Second  dentition  begins  in  the  fifth  or  sixth  year  of  life  with 
the  appearance  of  the  first  molar  teeth  in  each  side  of  the  jaw.  The  milk  teeth 
now  begin  to  fall  out  in  the  same  order  that  they  appeared.  Each  tooth  as  it  fiills 
out  is  supplanted  immediately,  or  very  soon,  by  the  corresponding  second  tooth. 
The  second  molars  appear  during  the  twelfth  year,  and  the  third  molars,  or 
wi.sdom  teeth,  appear  fi-om  the  sixteenth  to  the  twenty-fourth  year,  or  sometimes 
still  later. 

Gums. — The  gums  are  swollen  and  bleed  easily  in  acute  and  chronic 
mercury-poisoning,  after  the  use  of  iodids  and  bromids,  and  in  scurvy. 


682 


EXAMINATION  OF  THE  MOUTH  AND  PHARYNX. 


The  bluish-gray  "  lead  line  "  on  the  gums,  due  to  a  deposit  of  sulphid 
of  lead  in  the  mucous  membrane,  is  of  great  diagnostic  importance  in 
chronic  lead-poisoning.  This  line  should  not  be  confused  with  a  discol- 
oration of  the  teeth  themselves  at  the  junction  of  the  gums.  The 
latter  is  not  uncommon  in  careless  individuals  and  those  who  smoke  a 
great  deal.  This  discoloration  is  visible  up  to  the  margin  of  the  gum, 
and  may  simulate  the  blue  appearance  of  a  lead  line  very  accurately. 
It  is  very  easy  to  tell  these  conditions  apart  by  pushing  the  corner  of  a 
stiff  piece  of  paper  beneath  the  margin  of  the  gum.  A  true  lead  line 
will  become  more  distinct  than  ever,  but  the  other  will  disappear  entirely. 
A  bluish  discoloration  sometimes  appears  at  the  margin  of  the  gums, 
due  to  venous  congestion,  not  only  in  general  circulatory  disturbances, 


Fig.  247.— Lead  line:  Note  the  interrupted  fringe-like  line  just  at  the  edge  of  the  gum  (photo- 
graphed from  a  water-color  drawing;  kindness  of  Dr.  R.  C.  Cabot). 

but  in  some  local  inflammations  of  the  gums,  and  may  lead  to  error. 
Employing  the  piece  of  paper  as  above  directed  makes  the  gum  anemic 
by  the  pressure  exerted  and  renders  the  distinction  easy. 

Tongrue. — The  way  the  tongue  is  protruded  is  sometimes  more  or 
less  characteristic.  Very  ill  or  stupefied  patients  push  it  out  with  a 
trembling,  and  leave  it  out  until  told  to  withdraw  it.  Injuries  or  scars 
on  the  tongue  from  biting  are  of  great  diagnostic  importance  in  epilepsy. 

We  should  examine  the  tongue  of  patients  with  bulbar  symptoms 
very  closely  for  any  noticeable  atrophy.  This  atrophy  may  become  very 
marked  indeed  in  progressive  bulbar  paralysis,  and  the  tongue  may 
exhibit  pronounced  fibrillary  contractions.  Some  healthy  individuals 
present  a  slight  fibrillary  twitching  of  the  tongue. 


TONGUE.  683 

The  so-called  "  coat "  of  the  tongue  is  of  some  diagnostic  inipor- 
iauce.  The  tongue  is  covered  in  all  dyspeptic  conditions  and  in  fever. 
This  coating  is  usually  associated  with  some  disturbance  in  the  appetite. 
However,  some  healthy  individuals  with  a  good  appetite  always  have  a 
coated  tongue.  Acute  and  chronic  gastric  catarrh  is  almost  always  asso- 
ciated with  a  coated  tongue ;  but  in  ulcer  of  the  stomach  the  tongue  is 
often  not  coated  and  there  is  no  disturbance  in  the  appetite.  The  cause 
of  the  coat  is  an  overgrowth  of  epithelium  of  the  mucous  membrane 
of  the  tongue,  but  it  is  not  yet  fully  understood.  It  is  very  often 
explained  as  being  due  to  the  fact  that  in  people  who  do  not  eat,  the 
lingual  epithelium  is  not  removed  in  a  normal  way  by  friction.  This 
explanation,  however,  does  not  correspond  to  clinical  experience.  Prob- 
ably some  trophic  disturbance  of  the  mucous  membrane  of  the  tongue 
is  produced  by  the  condition  of  the  digestive  organs. 

Frequently  in  patients  with  high  fever  the  tongue  is  not  only  coated, 
but  dry,  on  account  of  the  diminished  secretion  of  saliva.  Small  fis- 
sures of  the  mucous  membrane  are  rather  common  in  these  cases  and 
may  cause  some  bleeding.  The  blood-crusts  which  form  in  this  way, 
combined  with  the  dried  brownish  epithelium  of  the  tongue,  produce 
a  dark-brown  or  blackish  coating.  This  always  indicates  that  the 
patient's  condition  is  serious.  It  may  be  found  on  the  lips  at  the 
same  time. 

The  coating  of  the  tongue  is  often  stained  by  certain  foodstuifs, 
drinks  or  medicines  (milk,  red  wine,  coffee,  cocoa,  chocolate,  licorice, 
fruit,  tobacco,  etc.). 

The  presence  of  fungi  must  not  be  confused  with  an  ordinary  coat- 
ing of  the  tongue.  Fungi  may  be  found  on  the  tongue,  as  well  as  else- 
where on  the  mucous  membrane  of  the  mouth,  and  occur  in  the  form 
of  large  thick  patches.  Fresh  patches  are  easily  recognized  by  their 
snow-white  color  and  round  margins.  The  older  patches  often  lose  this 
white  color,  and  are  of  a  peculiar  dirty-gray  appearance.  The  situation 
of  these  mycotic  patches  on  the  margin  of  the  tongue  and  their  abundance 
in  other  parts  of  the  mouth  distinguish  them  from  a  simple  coated  tongue. 
Fig.  223  represents  the  microscopic  appearance  of  thrush. 

The  tongue  should  be  examined  for  aphthous  patches  and  syphilitic 
sores.  The  peculiar  circular  thickenings  of  the  epithelium,  with  slight 
inflammatory  signs,  so-called  "  leiikojylacia  buccatis,''  must  not  be  con- 
founded with  either  of  them.  Leukoplacia,  sometimes  called  ^'psoriasis 
linguce"  is  much  more  extensive.  Its  nature  is  not  as  yet  well  known. 
Whitish,  thickened  spots  of  epithelium,  produced  by  the  irritation  of 
bad  teeth  or  of  too  much  smoking,  may  resemble  very  closely  syphilitic 
mucous  patches. 

The  nature  of  the  so-called  black  hairy  tongue  is  utterly  unknown. 

The  erythematous  tongue  of  scarlet  fever,  with  its  red  and  swollen 
papillje,  is  very  characteristic.  It  is  familiarly  known  as  the  "straw- 
berry tongue.'' 

[Virchow's  smooth  atrophy  of  the  base  of  the  tongue  may  be  of 
some  value  in  diagnosing  late  syphilis.     It  consists  of  an  atrophy  of 


684 


EXAMINATION  OF  THE  MOUTH  AND  PHARYNX. 


the  lingual  tonsillar  tissue,  and  can  be  appreciated  by  palpation  better 
than  by  inspection. — Ed.] 

Soft  Palate  ;  Tonsils  ;  Pharynx, — The  various  kinds  of  acute 
angina  are  to  be  considered  in  this  connection  (angina  simplex.,  lacunaris, 
necrotica,  phlegmonosa,  and  diphtheritiGa) ;  furthermore,  the  different 
varieties  of  chronic  pharyngitis  (pharyngitis  sicca,  granulosa,  etc.).  (See 
text-books  of  Special  Pathology.) 

Examination  for  Diphtheria  Bacilli. — In  doubtful  diphtheric  membranes 
only  a  microscopic  demonstration  of  Loffler's  bacilli  (see  Fig.  248)  will  prove  the 
existence  of  true  diphtheria.     These  bacilli  are  sometimes  found  in  the  membrane 

of  true  diphtheria  in  great  numbers.  Dry 
preparations  may  be  made  from  the  mem- 
brane in  the  same  manner  as  described  for 
the  sputum,  and  then  stained  with  the  or- 
dinary anilin  stains,  preferably  by  Gram' s 
method.  But  cultures  are  generally  neces- 
sary. According  to  the  investigations  of 
the  Bacteriologic  Institute  at  Bern,^  Lof- 
fler'  s  horse-serum  and  glycerin-agar  (7  per 
cent,  glycerin)  tubes  are  the  best  media  for 
growing  diphtheria  bacilli. 

The  media  can  be  inoculated  from  the 
surface  of  the  affected  region  of  the  phar- 
ynx by  means  of  a  sterile  platinum  loop 
or  swab.  The  round  colonies  of  diphtheria 
bacilli,  transparent  at  first,  gradually  be- 
come opaque.  They  may  be  seen  after 
the  tube  has  remained  in  an  incubator 
about  twelve  hours.  The  colonies  must 
be  identified  by  preparing  and  examining 
microscopic  slides,  as  macroscoj)ically  they 
may  be  confounded  with  those  of  other  bacteria,  especially  streptococci.  It  is  diag- 
nostically  important  to  remember  that  diphtheria  bacilli  are  generally  present  in 
the  pharynx  in  cases  of  laryngeal  diphtheria,  even  when  the  pharynx  itself  is  not 
visiblv  affected. 


Fig.  248— Diphtheria  bacilli  (X  1000)  (after 
Weichselbaum.  Culture). 


THE  PRACTICAL  VALUE  OF  THE  BACTERIOLOGIC  EXAMINATION 

FOR  DIPHTHERIA. 

Diphtheria  may  be  recognized  clinically  with  a  considerable  degree  of  accuracy 
in  the  vast  majority  of  cases.  At  times,  however,  demonstrating  the  presence  of 
diphtheria  bacilli  may  be  very  important.'^  Where  there  are  clinical  reasons  for 
making  a  diagnosis  of  diphtheria  (epidemics),  w^e  should  not  rely  absolutely  upon 
the  result  of  a  single  negative  bacteriologic  examination  (even  when  Loffler's 
modified  serum  is  used). 

Negative  results  may  easily  be  due  to  accidental  conditions  in  inoculating  the 

^  G.  Michel,  "  Das  Wachsthum  der  Diphtheriebacillen  auf  vei-schiedenem  Sera  und 
Glycevinagar,"  .J.  D.,  Bern,  1897  {Centralhl.  f.  Bakteriologie).  The  author  concludes  that 
Loffler's  modified  horse  serum  is  the  best  medium  of  the  five  he  examined,  and  that 
glycerin-agar  is  next.  Loffler's  ox  serum  and  the  pure  ox  or  pure  horse  serum  without 
any  addition  are  considerably  inferior.  These  results  suggest  that  many  statements  in 
literature  regarding  false  diplitheria  ai'e  doubtful.  Lofflei-'s  modified  horse  serum  fre- 
quently gives  a  negative  result,  whereas  from  the  same  case  diphtheria  bacilli  grew  on 
one  or  the  other  inferior  medium.  Perhaps  the  most  logic  conclusion  is  that  one  negative 
examination  does  not  prove  anything. 

^  "Deucher  (Bern),  ZurKlin.  Diagnose  der Diphtherie,"  Correspondenzbl.  f.  Sehweizer 
Aerzte,  1895,  No.  IG,  p.  485. 


TONGUE.        ,  685 

medium  ;  or,  in  case  the  specimen  is  sent  to  a  central  laboratory,  the  bacilli  may- 
have  become  less  virile  from  drying.  Again,  other  bacteria  may  easily  outgrow 
the  diphtheric  in  the  culture  tube.  The  use  of  antiseptics  (gargling,  swabbing) 
in  diphtheria  is  often  responsible  for  a  negative  culture.  Finally,  for  unknown 
reasons,  certain  diphtheria  bacilli  (discovered  in  the  Bacteriologic  Institute  at  Bern) 
refuse  to  grow  well  upon  the  media  which  are  generally  supposed  to  be  best.  Con- 
trol examples  have  proved  beyond  doubt  that  these  factors  may  influence  the  result 
of  bacteriologic  examination.  A  physician  may  err  if  he  relies  absolutely  upon 
the  bacteriologic  examination,  especially  if  attempted  only  once.  Since  the  intro- 
duction of  serum  treatment  this  is  a  serious  matter,  from  a  therapeutic  standpoint, 
and  it  may  be  still  more  disastrous  from  a  prophylactic  one. 

A  positive  result  must  also  be  carefully  interpreted,  for  we  know  that  virulent 
diphtheria  bacilli  are  not  infrequently  found  in  perfectly  healthy  people,  in  ordi- 
nary cases  of  mild  coryza  and  rhinitis,  and  in  cases  of  pharyngitis  which  do  not 
even  produce  a  rise  in  temperature.  It  is  hardly  justifiable  to  administer  antitoxic 
serum  to  these  cases,  because,  as  is  well  known,  the  serum  does  not  remove  the 
bacilli.  It  is  perfectly  possible  that  at  some  later  date  a  severe  case  of  diphtheria 
may  develop  in  the  individual.  A  logical  and  practical  deduction  is  that  the 
serum  treatment  should  not  be  confined  to  cases  where  the  bacteriologic  examina- 
tion is  positive,  but  should  be  employed  whenever  the  case  j^resents  a  perfect  clin- 
ical picture  of  diphtheria,  or  when  there  are  severe  symptoms  and  diphtheria  bacilli 
are  present  in  numbers,  although  the  case  may  not  resemble  diphtheria  clinically. 

The  bacteriologic  examination  would  be  of  much  greater  clinical  value  if  dry 
cultures  could  be  made  from  the  pharynx  directly  in  every  case.  The  chief  error 
in  the  modern  culture  method  is  that  mere  chance  in  inoculation  may  alter  the 
numeric  relation  of  the  bacteria,  and  some  species  may  be  entirely  suppressed.  In 
one  case  the  diphtheria  bacilli  may  be  concealed  by  other  bacteria  and  be  totally 
overlooked,  and  in  another  a  few  diphtheria  bacteria  may  overgrow  everything 
else,  although  in  the  actual  illness  they  may  be  of  little  or  no  etiologic  significance. 
In  a  dry  preparation  the  conditions  are  represented  as  they  actually  exist.  In  the 
bacteriologic  diagnosis  of  the  upper  air  passages,  just  as  in  the  bacteriologic  diag- 
nosis of  peritonitis  or  cystitis,  culture  results  may  be  misleading.  It  seems  prob- 
able to  the  writer  that  when  dry  preparations  are  granted  their  proper  place  in  the 
diagnosis  of  angina,  the  noticeable  contradictions  between  clinical  conditions  and 
bacteriologic  examinations  will  disappear.  But  the  seat  from  which  a  dry  prepa- 
ration is  made  must  be  selected  far  more  intelligently  than  in  the  present  culture 
examination  method-^that  is,  when  the  diseased  region  is  easily  accessible,  a  slide 
must  be  prepared  from  it,  and  when  diphtheria  is  in  the  larynx  alone,  more  than  the 
saliva  must  be  examined.  Especial  attention  should  be  paid  to  the  tonsils  and  to 
the  soft  palate.  Sometimes  it  may  be  necessary  to  make  several  preparations,  just 
as  it  is  in  the  examination  of  sputum  for  tubercle  bacilli.  In  making  cultures,  the 
importance  of  selecting  the  proper  regions  is  often  forgotten.  In  addition  to 
the  factors  already  mentioned,  this  neglect  may  explain  the  unsatisfactory  lack 
of  harmony  between  the  clinical  diagnosis  and  the  bacteriologic  examination. 
Dry  preparations  made  from  material  sent  for  examination  do  not  always  fulfil 
the  above  demands,  because  the  material  may  not  be  suited  for  microscopic 
examination. 

The  occurrence  of  diphtheria  bacilli  in  the  throats  of  healthy  people  or  of 
those  without  clinical  diphtheria  or  without  croup  has  caused  a  great  deal  of  confu- 
sion. The  term  ' '  pseudodiphtheria  bacilli ' '  has  been  applied  to  such  organisms, 
but  their  characteristics  really  do  not  differ  from  those  of  the  true  diphtheria 
bacilli.  Virulence  can  be  tested  upon  animals  only  after  the  bacteria  have  been 
altered  biologically  by  making  cultures.  Hence  it  is  clear  a  priori  that  animal 
experiments  do  not  prove  anything  regarding  the  bacterial  virulence  in  man. 
Besides,  it  has  even  been  demonstrated  that  diphtheria  bacilli  taken  from  the 
buccal  cavity  of  healthy  people,  although  usually  considered  pseudodiphtheria 
bacilli,  may  sometimes  be  just  as  virulent  for  animals  as  true  diphtheria  bacilli 
taken  from  patients  suffering  from  diphtheria.  The  different  influences  of  diph- 
theria serum  upon  animals  inoculated  with  true  and  false  diphtheria  cannot  be 


686  EXAMINATION  OF  THE  MOUTH  AND  PHARYNX. 

used  as  a  differential  point,  because  such  a  differentiation  begs  the  question,  taking- 
it  for  granted  that  the  cultures  which  act  differently  to  the  serum  must  of  neces- 
sity belong  to  different  species.  The  numei-ous  efforts  to  separate  the  pseudo- 
diphtheria  bacilli  from  the  true  bacilli  have  been  absolutely  fruitless.  It  seems 
to  the  author  better  to  assume  that  the  variability  of  the  attacks  of  diphtheria  in 
man  is  due  to  individual  differences  in  species  and  to  the  continual  reinoc- 
ulation.  The  general  endeavor,  however,  is  to  continue  the  search  for  new 
points  of  differentiation.  It  seems  doubtful  if  this  effort  will  meet  with  any 
success. 

One  of  the  most  recent  points  of  distinction  is  the  double  stain  recommended 
by  Neisser.^  He  found  that  if  dry  specimens  are  prepared  from  a  Loffler's  serum 
culture  ten  to  twenty  hours  old  at  35°  C,  stained  for  one  to  three  seconds  with 
acetic  acid  methylene-blue,  v/ashed  in  water,  and  then  stained  with  aqueous 
vesuvin  ^  three  to  five  seconds,  certain  portions  of  the  organisms,  the  so-called 
isolated  polar  bodies,  stain  blue.  He  claims  that  true  diphtheria  bacilli  exhibited 
this  peculiarity,  but  not  the  pseudo-bacilli. 

This  is  in  itself  very  interesting  ;  but  it  is  quite  incomprehensible  to  the 
writer  that  these  authors  fail  to  recognize  that  they  argue  in  a  circle  in  all  these 
endeavors  to  discover  points  of  differentiation  between  true  and  false  diphtheria 
bacilli.  Because  the  older  differential  characteristics  have  proved  unreliable, 
they  unconsciously  fall  back  upon  the  clinical  diagnosis  by  assuming  that  the  true 
diphtheria  bacilli  must  come  from  a  case  that  is  clinically  diphtheria.  Neisser's 
results,  we  believe,  prove  nothing  more  than  that  the  polar  stain  is  present 
in  serum  cultures  made  from  clinical  diphtheria,  but  is  absent  in  cases  which 
cannot  be  considered  diphtheria  from  a  clinical  standpoint  (liealthy  people, 
follicular  tonsillitis,  and  doubtful  clinical  cases).  According  to  the  author's 
opinion,  this  peculiarity  does  not  prove  anything  about  the  differentiation  be- 
tween true  and  false  diphtheria  bacilli,  nor  does  it  indicate  the  diagnosis  in  any 
given  case.  In  typical  cases  there  is  no  need  of  this  criterion.  The  test  does  not 
decide  whether  these  diphtheria  bacilli  called  false  by  Neisser  are  anything  more 
than  varieties  of  so-called  true  diphtheric  bacilli.  Biologic  variations  responsible 
for  the  lack  of  a  clinical  picture  of  diphtheria  may,  of  course,  be  equally  respon- 
sible for  the  absence  of  his  reaction.  Neisser  considers  his  stain  is  available  only 
for  very  young  cultures  upon  Loffler's  serum,  which,  of  course,  means  that  this 
criterion  is  not  adapted  to  differentiate  variations  of  species.  The  emphasis 
placed  upon  the  age  of  a  culture  and  the  statement  that  false  diphtheria  bacilli 
when  old  may  react  in  the  same  way  show  how  little  valuable  the  method  really 
is.  The  writer's  critical  objections  to  the  bacteriologic  methods  of  making  diag- 
noses in  diphtheria  should  by  no  means  influence  the  reader's  opinion  regarding 
the  etiologic  significance  of  diphtheria  bacilli  in  relation  to  serum  treatment. 

Virulent  diphtheria  bacilli  may  be  found  in  the  fluids  of  the  mouth  months 
after  diphtheria  has  disappeared.  Theoretically,  this  fact  is  veiy  important  for 
prophylaxis,  although  it  makes  it  very  difficult  or  even  impossible  to  keep  up  a 
proper  quarantine.  It  is  hardly  possible  to  isolate  the  majority  of  convalescent 
diphtheria  cases.  The  scheme  at  the  end  of  this  book  shows  how  diphtheria  cases 
are  examined  at  Bern. 

The  presence  of  streptococci  and  staphylococci  is  of  interest  in  the  etiologic 
study  of  the  different  types  of  sore  throat.  They  may  often  be  present  at  the 
same  time  with  diphtheria  bacilli  (compare  Figs.  218  and  219).  Frankel's  pneu- 
mococcus  (Fig.  214),  the  Micrococcus  tetragenus  (Fig.  217),  the  Micrococcus 
conglomeratus,  and  several  others  may  also  occur.  All  these  bacteria  frequently 
inhabit  a  normal  mouth,  so  that  little  importance  can  be  attached  to  their  demon- 
stration by  culture  methods  as  compared  with  the  demonstration  of  their  presence 
in  large  numbers  in  freshly  prepared  dry  slides.  (Regarding  the  method  of  prep- 
aration, see  p.  596.) 

1  Zeils.  f.  Hyg.,  1897,  vol.  xxiv. 

^  One  gram  of  methylene-blue  (Griibler)  dissolved  in  20  c.c.  of  96  per  cent,  alcoho], 
and  then  950  c.c.  of  distilled  water  and  50  c.c.  of  acetic  acid  added. 


PLATE  9. 


Fig.  1. 


Fig.  2. 


Fig.  3. 


Fig.  4. 


The  pathognomonic  sign  of  measles  (Koplik's  spots). 

Fig.  1. — The  discrete  measles-spots  on  the  buccal  or  labial  mucous  membrane,  showing  the 
isolated  rose-red  spot,  with  the  minute  bluish-white  center,  on  the  normally  colored  mucous 
membrane. 

Fig.  2. — The  partially  diffuse  eruption  on  the  mucous  membrane  of  the  cheeks  and  lips ;  patches 
of  pale  pink  interspersed  among  rose-red  patches,  the  latter  showing  numerous  pale  bluish-white 
spots. 

Fig.  3. — The  appearance  of  the  buccal  or  labial  mucous  membrane  when  the  measles-spots 
completely  coalesce  and  give  a  diffuse  redness,  with  the  myriads  of  bluish-white  specks.  The 
exanthem  is  at  this  time  generally  fully  developed. 

Fig.  4. — Aphthous  stomatitis,  likely  to  be  mistaken  for  measles-spots.    Mucous  membrane  nor- 
mal in  hue.    Minute  yellow  points  are  surrounded  by  a  red  area.    Always  discrete. 
(The  Medical  News,  June  3,  1899.) 


EXAMINATION  OF  THE  ESOPHAGUS.  687 

Retropharyngeal  abscesses  present  a  visible  and  palpable 
swelling  in  the  posterior  pharyngeal  wall.  They  may  cause  dyspnea. 
Hypertropkiexl  tonsils  are  evident  to  inspection.  Adenoids  can  be  felt  in 
the  nasopharyngeal  space.  The  mobility  of  the  soft  palate  should  often 
be  noted.  For  a  jxiralysis  of  the  palate  or  for  absence  of  the  palate 
reflex  (hysteria),  see  section  upon  Rhinoscopy  and  Laryngoscopy. 

Direct  Rhinopharyngoscopy. — W.  Lindt/  of  Bern,  has  recently  announced 
a  method  for  direct  insjiection  of  the  nasopharyngeal  space.  This  is  accomplished 
by  pulling  the  soft  palate  forward  and  upward  by  means  of  the  retractor  depicted 
in  Fig.  249.  With  the  illumination  from  an  ordi- 
nary head  mirror,  the  posterior,  lateral,  and  upper 
walls  of  the  nasopharynx  can  thus  be  examined, 
and  most  easily  if  the  head  is  bent  slightly  back- 
ward. The  anterior  and  posterior  walls  of  the  soft 
palate  must  be  cocainized  (2  to  4  per  cent,  solu- 
tion) in  sensitive  individuals  (compare  p.  696). 
This  method  of  examination  is  valuable  espe- 
cially for  the  purpose  of  detecting  adenoids. 

Hard  Palate. — We  should  look  espe- 
cially for  syphilitic  perforation  of  the  palate, 
and  in  children  for  the  so-called  Bednar's    ^''^-  ^'^^■di^i?t^rhin^o^sc^opy^''°''  ^°'" 
aphthae.^ 

Buccal  Mucous  Membrane. — Besides  the  conditions  of  the 
mucous  membrane  described  in  connection  with  other  portions  of  the 
mouth,  we  may  look  for  cancrum  oris,  stomatitis,  etc.  A  rare  gangren- 
ous condition  of  the  mucous  membrane  of  the  cheek,  called  noma,  is 
sometimes  found  in  children.  Koplik's  spots,  an  early  sign  in  measles, 
should  also  be  remembered  (see  Plate  9). 

Secretion  of  Saliva. — Increased  salivation  accompanies  all  types 
of  stomatitis  and  chronic  mercury-poisoning.  (In  one  of  the  writer's 
cases  this  persisted  for  one-half  year  after  a  single  dose  of  calomel.) 
The  secretion  of  saliva  is  diminished  \n  fever,  diabetes  mellitus,  cholera^ 
atropin-poisoning ,  and  in  facial  and  bulbar  paralysis. 


EXAMINATION    OF    THE    ESOPHAGUS. 

In  the  diagnosis  of  diseases  of  the  esophagus,  we  should  be  on  the 
watch  for  disturbances  in  function,  for  pain  upon  swallowing,  signs  of 
stenoses,  or  regurgitation,  in  addition  to  the  direct  method  of  examina- 
tion about  to  be  described.  We  must  differentiate  between  regurgitated 
material  from  the  esophagus  and  vomitus  (p.  361).     The  surgical  rules 

^  "  Die  directe  Besichtigung  und  Behandlung  der  Gegend  der  Tonsilla  pharyngea 
und  der  Plica  salpingopharyngea  in  ihrem  obersten  T\iei[e,^'Arch.f.Laryngologie,\o\. 
vi.,  p.  1. 

^  [Mucous  and  mycotic  patches  are  also  sometimes  seen.  A  high-arched  palate  sug- 
gests a  defoimed  nasal  septum  and  the  former  presence  of  adenoids. — W.  S.  B.] 


EXAMINATION  OF  THE  ESOPHAGUS. 

for  palpation  apply  to  the  external  examination  of  the  esophagus. 
Attention  should  be  paid  to  tumors  which  compress  the  esophagus,  to 
swollen  glands,  to  thyroid  enlargements,  to  sensitiveness  along  the  course 
of  the  esophagus,  etc.  Diverticula  of  the  esophagus  are  characterized 
by  their  variations  in  volume  and  by  the  fact  that  they  can  be  emptied. 

Esophageal  Sounds  or  Tubes. — The  well-known  whalebone 
sounds,  to  the  tip  of  which  an  ivory  olive  of  varying  caliber  may  be 
screwed,  or  the  hollow  elastic  English  tubes  of  varying  caliber  are  em- 
ployed. Before  introducing  one  of  these  instruments  we  should  be  sure 
that  they  are  in  perfect  condition,  as  a  faulty  instrument  may  sometimes 
injure  the  patient. 

The  esophageal  bougie  is  held  in  the  right  hand,  close  to  the  end, 
very  much  like  a  pen  ;  the  tip  is  smeared  with  a  little  oil  or  glycerin, 
and  the  patient,  in  the  sitting  posture,  is  told  to  open  his  mouth  wide  and 
bend  the  head  back  as  far  as  possible.  The  tip  of  the  bougie  is  intro- 
duced into  the  pharynx,  covered  by  two  fingers  of  the  left  hand,  and 
pressed  slightly  forward.  It  is  kept  as  much  as  possible  in  the  median 
line.  After  passing  the  slight  physiologic  resistance  at  the  level  of  the 
cricoid  cartilage,  the  bougie  will  pass  into  the  stomach  with  ease,  pro- 
vided there  is  no  pathologic  obstruction.  Efforts  to  swallow  should,  if 
possible,  be  avoided,  as  they  are  unnecessary  and  only  produce  a  gag- 
ging, on  account  of  the  contact  of  the  soft  palate  with  the  bougie.  It 
is  important  for  the  patient  to  breathe  regularly.  (Compare  Stomach 
Examinations,  p.  364.)  If  the  examiner  is  awkward,  or  if  there  is  a 
paralysis  or  lack  of  sensation  in  the  pharyngeal  region,  a  hard  bougie 
will  enter  the  larynx  more  readily  than  a  soft  one.  But  this  fault  can 
easily  be  avoided  if  the  point  of  the  bougie,  while  being  introduced,  is 
allowed  to  pass  along  the  posterior  wall  of  the  pharynx.  When  hard 
hollow^  bougies  are  employed  a  peculiar  whistling  respiratory  noise  comes 
from  the  end  of  the  bougie  upon  introduction  (p.  365).  An  inexperienced 
operator  may  be  alarmed  by  this,  believing  that  the  tube  has  entered  the 
larynx.  The  noise  is  in  reality  produced  by  the  respiratory  variations 
of  pressure  in  the  interior  of  the  thorax,  which  are  transmitted  in  suffi- 
cient strength  to  the  esophagus  tO  produce  an  in-and-out  current  of  air 
through  the  bougie,  unless  its  opening  is  occluded  by  the  esophageal  wall 
(esophageal  breathing).  This  can  be  easily  demonstrated  by  placing  a 
burning  candle  before  the  end  of  a  stomach  tube  in  position.  The  flame 
will  flicker  regularly  with  respiration.  The  greater  size  of  the  hard 
tubes  and  their  resonance  probably  explain  why  this  sound  is  much 
more  intense  when  these  are  employed  than  when  soft  ones  are  intro- 
duced. The  moment  the  opening  of  the  bougie  enters  the  stomach  this 
noise  ceases.  If  the  bougie  enters  the  larynx  dyspnea  follows  immedi- 
ately, and,  in  case  the  larynx  is  not  anesthetized,  violent  attacks  of 
coughing  and  severe  pain. 

Esophageal  bougies  w^ill  demonstrate  the  presence  of  stenoses  by 
transmitting  a  sensation  of  resistance  to  their  advance.  The  most  fre- 
quent cause  of  stenoses  of  the  esophagus  is  carcinoma ;  then  come 
diverticula,  foreign  bodies  (bits  of  bone,  false  teeth,  coins,  etc.),  syphil- 


ESOPHAGEAL  SOUNDS  OR   TUBES.  689 

itic  strictures,  strictures  from  burns,  compression  of  the  esophagus  from 
without  by  thyroid  tumors,  neoplasms,  or  aneurisms  of  the  aorta,  etc. 

With  signs  of  stenosis  of  the  esophagus,  it  is  a  good  plan  to  attempt 
a  preliminary  diagnosis  regarding  the  nature  of  the  disturbance  before 
passing  the  bougie,  taking  the  history  and  the  general  condition  into 
consideration.  If  aneurism  of  the  aorta  is  suspected  the  bougie  should 
not  be  passed. 

The  bougie,  particularly  by  indicating  the  location  of  the  obstruction, 
may  throw  some  light  on  the  nature  of  the  stenosis.  The  following 
data  should  be  remembered  :  Distance  from  the  incisor  teeth  to  the 
entrance  of  the  esophagus  equals  15  cm.  (6  in.);  distance  from  the 
incisor  teeth  to  the  bifurcation  of  the  trachea,  about  25  cm.  (10  in.) ; 
distance  from  the  incisor  teeth  to  the  cardia,  about  40  cm.  (16  in.). 

The  consistence  of  an  obstruction  is  also  of  considerable  importance 
— e.  g.,  it  may  be  shown  by  the  noise  produced  by  contact  of  the  bougie 
against  a  hard  substance,  such  as  pieces  of  bone,  coins,  etc. 

It  is  also  important  to  determine  the  degree  of  stenosis.  This  is 
accomplished  by  trying  a  series  of  sounds  of  decreasing  caliber  until 
one  is  found  sufficiently  small  to  slip  through  the  obstruction.  In  the 
patient's  interest  we  should  not  employ  any  force  while  making  this 
attempt. 

It  is  also  necessary  to  estimate  the  length  of  the  obstruction.  This 
is  very  difficult  to  determine  with  the  ordinary  stomach  tubes,  but  quite 
simple  if  we  employ  the  whalebone  sound.  For  this  purpose  the  latter 
is  furnished  with  an  "  olive  "  (of  ivory  or  bone)  which  can  be  screwed 
or  fastened  over  one  end  of  the  sound.  Varying  sizes  of  "  olives  "  are 
necessary,  so  that  one  can  be  selected  which  will  pass  through  the 
obstruction.  After  slipping  by  the  obstruction  the  sound  is  withdrawn 
until  the  lower  edge  of  the  obstruction  can  be  plainly  felt ;  then  by 
comparing  the  position  of  the  upper  and  the  lower  edge  of  the  obstruc- 
tion we  can  readily  determine  its  vertical  extent.  In  the  same  way 
multiple  obstructions  can  be  located  and  measured. 

Repeated  examinations  of  an  esophageal  stenosis  sometimes  reveal 
this  peculiarity — at  one  attempt  the  obstruction  can  be  overcome  very 
readily,  while  at  another  it  is  very  difficult  or  quite  impossible.  Per- 
haps this  depends  upon  the  fact  that  the  esophagus  may  alter  its  condi- 
tion quickly,  due  to  the  atrophy  of  ulcerations  or  to  the  persistence  of 
food  residue.  Frequently,  however,  it  depends  upon  some  dilatation 
of  the  esophagus  above  the  stenosis,  so  that  the  sound  slips  into  a  sort 
of  pocket,  and  ])erhaps  does  not  always  meet  the  obstruction  in  exactly 
the  same  way.  It  may  also  be  due  to  spastic  conditions  of  the  esophagus, 
which  may  be  added  to  the  anatomic  obstruction  by  the  irritation  in 
sounding.  It  is  also  possible  that  a  saccular  "  pressure  diverticulum  " 
crowds  against  the  esophagus,  and  Avhen  filled  compresses  its  lumen, 
and  so  stops  the  sound,  although  when  the  diverticulum  is  empty 
the  sound  readily  slips  by.  However,  before  assuming  the  exist- 
ence of  such  a  diverticulum,  we  should  always  bear  in  mind  that  the 
saccular  "  pressure  diverticula  "  are  found  only  in  the  neck  at  the  upper- 

44 


690  EXAMINATION  OF  THE  ESOPHAGUS. 

most  part  of  the  esophagus,  and  if  filled  are  usually  palpable  externally. 
"  Traction  diverticula  "  occur  in  the  lower  part  of  the  esophagus.  They 
cause  no  stenosis. 

In  sounding  the  esophagus  the  exhibition  of  a  circumscribed  pain  at 
the  moment  when  the  tip  of  the  sound  passes  over  a  definite  place  is  of 
considerable  diagnostic  importance.  Such  a  painful  condition  is  observed 
in  carcinoma  of  the  esophagus  and  of  the  cardiac  orifice  of  the  stomachy 
sometimes,  when  there  is  no  stenosis,  in  the  rare  affection  esophagitis, 
and  in  the  quite  as  rare  ulceixttion  of  the  esophagus  and  of  the  cardiac 
orifice. 

With  every  attempt  to  sound  the  esophagus  we  should  always  care- 
fully examine  the  sound  as  soon  as  it  is  withdrawn,  and  especially  the 
window  at  the  tip  of  the  stomach  tube  if  the  latter  is  employed,  in  order 
to  determine  whether  any  fragments  have  been  scraped  off.  Small  bits 
of  tissue  are  not  infrequently  found  adhering  to  the  window  of  the 
stomach  tube  in  cases  of  carcinoma  of  the  esophagus,  and  are  often  large 
enough  to  be  sectioned  after  hardening  in  formalin,  or  with  the  aid  of 
the  freezing  microtome  (see  p.  427,  note).  In  this  way  the  diagnosis  of 
carcinoma  may  sometimes  be  confirmed.  In  "thrush"  involving  the 
esophagus,  the  fungous  elements  may  be  demonstrated  microscopically 
in  particles  adhering  to  the  withdrawn  sound  (compare  p.  603,  Fig. 
223).  The  window  of  the  sound  frequently  contains  bloody  mucous 
in  carcinomatous  and  non-carcinomatous  ulcerations  of  the  esophagus. 

Other  methods  of  examining  the  esophagus  are  subordinate  to  the  methods  of 
palpation  and  of  sounding.  Auscultation  of  the  esophagus  has  thus  far  furnished 
rather  barren  results.  Hamburger  and  Zenker  auscultate  the  swallowing  murmur 
in  the  neck  upon  the  left  side  of  the  trachea,  and  in  the  chest  to  the  left  of  the 
spinal  column,  at  the  level  of  the  eighth  dorsal  vertebra.  Here,  during  the  act 
of  swallowing,  we  can  hear  a  characteristic  clucking  and  rattling  murmur.  With 
pronounced  esophageal  stenoses  the  swallowing  murmur  may  either  disappear 
entirely  or  may  be  delayed  from  the  level  of  the  stenosis  downward.  Meltzer  ^ 
studied  more  minutely  the  murmur  which  arises  upon  the  entrance  of  nourish- 
ment into  the  stomach,  and  which  we  hear  best  by  auscultating  with  the  stetho- 
scope in  the  neighborhood  of  the  xiphoid  process.  He  arrived  at  the  following 
conclusions :  In  normal  individuals,  six  to  seven  seconds  after  the  beginning  of  a 
separate  act  of  swallowing  fluid  or  gruel,  we  hear  at  that  point  a  more  or  less 
distinct  prolonged  murmur,  as  if  air  or  fluid  was  being  squeezed  through  a 
sphincter-like  opening  (squeezing  murmur).  According  to  Kronecker  and  Melt- 
zer's  examinations,  fluids  are  squirted  into  the  lowest  part  of  the  esophagus  at  the 
very  commencement  of  the  act  of  swallowing.  Hence  we  are  entitled  to  conclude 
from  the  delay  of  the  murmur  at  the  cardiac  orifice  that,  normally,  what  is  swal- 
lowed in  each  separate  act  of  swallowing  remains  six  to  seven  seconds  just  above 
the  cardiac  orifice  before  it  reaches  the  stomach.  With  a  relaxed  (insufiicient)  or 
paralyzed  cardiac  orifice,  a  distinct  murmur  can  be  heard  immediately  after  the  begin- 
ning of  the  act  of  swallowing  (squirting  murmur).  If  this  ' '  squirting  murmur  "  is 
plainly  to  be  heard,  the  later  "squeezing  murmur  "  is  lacking.  The  former  sliows 
that  the  action  of  the  mylohyoid  muscle  and  the  base  of  the  tongue  squirts  the  swal- 
lowed material  directly  into  the  stomach  without  any  obstruction.  In  some  cases 
both  murmurs  can  be  heard  one  after  the  other.  Either  one  or  the  other  murmur 
can  be  heard  in  all  but  very  few  cases.  Swallowing  warm  fluids  seems  to  make  the 
"  squeezing  murmur  "  more  distinct.    It  occurs  earlier  in  weak  individuals,  perhaps 

^  Centralbl.  f.  d.  med.   Wiiisejisehaften,  1883,  No.  1. 


ESOPHAGEAL  SOUNDS  OR   TUBES.  691 

three  to  four  seconds  after  the  act  of  swallowing.  If  several  swallows  succeed  each 
other  rapidly,  the  result  is  not  uniform.  Either  the  "squirting  murmur"  becomes 
more  distinct  with  the  rapid  swallowing,  even  where  it  was  not  heard  with  a 
single  swallow,  or  we  hear  only  a  "squeezing  murmur"  six  to  seven  seconds  after 
the  last  swallow,  or,  finally,  we  may  hear  nothing  at  all.  Meltzer  considers  the 
occurrence  of  a  distinct  ' '  squirting  murmur "  as  a  trustworthy  symptom  of  in- 
sufficiency of  the  cardiac  orifice.  He  found  it  in  individuals  who  complained  of 
regurgitating  their  food  with  coughing,  and  exceptionally  in  patients  with 
advanced  recurring  syphilis.  Meltzer' s  swallowing  murmur  has  thus  far  proved 
of  limited  clinical  value.  Quincke  ^  pointed  to  a  decided  objection  in  that  the 
swallowing  murmur  is  differently  affected  by  the  way  in  which  the  fluid  is  mixed 
with  air  during  the  swallowing  and  by  the  condition  of  fulness  of  the  stomach. 

Percussion  of  the  esophagus  may  in  rare  instances  aid  in  the  diagnosis  of  large 
"pressure  diverticula"  of  the  esophagus.  If  the  diverticulum  is  filled  with  air, 
a  tympanitic  note  can  be  elicited  in  the  cervical  region  or  at  the  superior  thoracic 
aperture.  If  the  diverticulum  contains  food  or  liquid,  the  note  will  be  dulled  or 
flat.  The  variations  depending  upon  the  ingestion  of  nourishment  are  especially 
characteristic  and  important  for  the  diagnosis. 

Esophagoscopy  is  the  inspection  of  the  esophagus  with  the  aid  of  a  specially 
constructed  instrument,  a  so-called  esophagoscope,  furnished  with  electric  illumi- 
nation. Further  experience  with  this  instrument  may  demonstrate  its  practical 
utility,  but  thus  far  its  application  is  too  troublesome  and  too  heroic  for  most 
patients. 

Mikulicz^  has  recently  fiirnished  interesting  and  important  information  in 
reference  to  the  measurement  of  the  intra-esophageal  pressure,  which  indicates 
both  the  motor  power  of  the  esophageal  musculature  and  the  tonus  of  the  cardia. 
It  is  necessary  to  have  a  mercury  manometer  with  an  index  of  100  mm. ;  the 
pocket  mercury  manometer  described  upon  p.  136  may  be  employed.  A  thin, 
soft  esophageal  tube  with  an  open  end,  and  made  of  patent  rubber  (see  p.  364)  of 
sufficient  resistance  to  overcome  lateral  compression,  is  introduced  into  the  esoph- 
agus so  that  its  open  end  is  at  the  level  of  the  manubrium.  Before  the  intro- 
duction of  the  tube  its  outer  end  is  clamped,  and  the  clamp  is  not  removed  until 
the  tube  has  been  connected  with  the  manometer.  When  the  clamp  is  removed 
the  mercury  usually  falls,  indicating  that  the  end  of  the  tube  is  within  the  air- 
containing  thoracic  portion  of  the  esophagus.  When  the  patient  swallows  the 
mercury  rises,  and  this  elevation,  according  to  Mikulicz,  should  amount  to  about 
10  mm.  A  diminution  of  this  pressure  may  be  due  either  to  atony  of  the  esoph- 
ageal musculature  or  to  a  diminished  tonus  of  the  cardia,  which  prevents  the 
production  of  a  greater  pressure.  The  tonus  of  the  cardia  is  now  estimated  by 
determining  the  pressure  at  which  fluids  flow  into  the  stomach.  For  this  pur- 
pose a  T-tube  is  inserted  between  the  esophageal  tube  and  the  manometer,  and  its 
vertical  limb  connected  with  a  funnel  by  rubber  tubing.  Fluid  at  body  temper- 
ature is  then  poured  into  the  funnel,  and  the  pressure  is  read  from  the  manometer 
at  the  moment  the  fluid  commences  to  run  into  the  stomach.  In  carrying  out 
the  latter  manipulation,  the  lower  end  of  the  esophageal  tube  must  be  pushed 
down  to  just  above  the  cardia,  otherwise  the  hydrostatic  pressure  of  the  column 
of  fluid  collecting  between  the  opening  in  the  end  of  the  tube  and  the  cardia 
would  be  lost.  Since  the  tube  and  its  connections  with  the  manometer  are  filled 
with  fluid,  care  must  also  be  taken  to  bring  the  zero  point  of  the  manometer  to 
the  level  of  the  cardia,  since  it  is  at  this  point  that  we  wish  to  determine  the 
pressure.  According  to  Mikulicz,  the  initial  pressure  at  which  lukewarm,  indif- 
ferent fluids  flow  into  the  stomach  varies  between  2  and  17  mm.  of  mercury. 
The  resistance  of  the  cardia  is  shown  by  the  values  obtained  by  this  method. 
Abnormally  low  or  high  pressures  are  indicative  of  corresponding  variations  in 
the  tonus  of  the  cardia.  With  due  regard  to  the  results  obtained  by  this  method, 
we  may  determine  whether  a  low  or  a  high  pressure  during  deglutition  is  due 

^  Arch.  f.   erper.  Path.,  vol.  xxii.,  p.  395. 
^Deutsch.  med.  WocL,  1904,  Nos.  1  and  2. 


692 


EXAMINATION  OF  THE  ESOPHAGUS. 


simply  to  a  diminished  or  an  increased  resistance  of  the  cardia  or  to  abnormal 
conditions  of  the  esophageal  musculature.  After  the  introduction  of  the  fluid,  it 
is  well  for  the  patient  to  repeat  the  act  of  deglutition,  when  the  pressure  should 
be  measured  again. 

This  procedure  may  also  be  employed  for  the  estimation  of  the  capacity  of 
the  esophagus,  which  is  of  importance  for  the  diagnosis  of  diffuse  esophageal  dila- 
tation, a  subject  about  which  so  much  has  recently  been  written.  The  greater 
the  amount  of  fluid  which  can  be  poured  into  the  esophagus  before  any  of  it 
escapes  into  the  stomach,  the  greater  is  the  esophageal  capacity.  If  such  a  diffuse 
esophageal  dilatation  be  due  to  cardiospasm,  as  is  usually  the  case,  it  will  be 
found  not  only  that  a  large  quantity  of  fluid  may  be  introduced 
into  the  esophagus  before  any  of  it  flows  into  the  stomach,  as 
indicated  by  a  sudden  fall  of  the  mercury,  but  that  the  fluid 
does  not  enter  the  stomach  until  it  is  acted  upon  by  an  abnor- 
mally high  pressure. 

Several  other  methods  of  esophageal  investigation  have 
recently  been  tried  in  order  to  gain  information  in  reference  to 
diffuse  dilatation  and  deep-seated  diverticula.  One  of  these, 
for  example,  consists  of  the  introduction  into  the  esophagus 
of  a  rubber  balloon,  and  its  subsequent  inflation.  If  this  bal- 
loon can  be  markedly  dilated  by  slight  pressure,  without  an- 
noyance to  the  patient,  and  at  all  points  of  the  esophagus,  a 
diagnosis  of  diffuse  dilatation  is  indicated.  The  size  of  the 
rubber  bag  or  the  caliber  of  the  esophagus  may  even  be  made 
visible  by  means  of  a  skiagraph,  a  procedure  which  is  facili- 
tated by  filling  the  balloon  with  a  bismuth  subnitrate  suspen- 
sion instead  of  with  air.  The  esophagus  itself  may  be  filled 
with  a  mixture  of  potato  soup  and  bismuth  subnitrate,  when 
a  skiagraph  will  reveal  the  presence  of  diffuse  dilatation  or  of 
esophageal  diverticula. 

Mention  must  also  be  made  of  Rumpel' s  experiment  for  dif- 
ferentiating spindle-shaped  dilatations  of  the  esophagus  from 
deep-seated  diverticula.  Rumpel  introduces  a  rather  soft  tube 
which,  in  addition  to  the  end  opening,  has  a  number  of  lateral 
perforations  in  its  lower  half  When  it  is  certain  that  the  tip 
of  this  tube  is  in  the  stomach,  a  second  tube  is  introduced  into 
the  esophagus  alongside  of  the  first  one.  Water  is  then  poured 
into  the  esophagus  through  the  second  tube.  If  a  spindle- 
shaped  dilatation  be  present,  the  water  immediately  flows  into 
the  stomach  through  the  lateral  perforations  in  the  tube  first 
introduced,  so  that  none  of  it  may  be  recovered  by  means  of 
the  second  tube.  If  there  be  a  diverticulum,  however,  at  least 
a  portion  of  the  water  introduced  may  sometimes  be  siphoned 
out  by  means  of  the  second  tube.  A  number  of  difficulties  are 
encountered  in  carrying  out  this  experiment  in  practice.  In 
the  first  place,  it  is  not  always  easy  to  determine  that  the  first 
tube  extends  into  the  stomach,  since  it  may  become  bent 
ujaon  itself  either  in  a  spindle-shaped  dilatation  or  in  a  diver- 
ticulum. If  a  diverticulum  be  present,  moreover,  it  is  not  such  a  simple  matter 
to  introduce  the  second  tube  into  it.  The  first  difficulty  may  be  overcome  by 
performing  the  experiment  u^jon  a  full  stomach,  and  introducing  the  first  tube 
so  far  that  all  of  the  perforations  are  presumably  in  the  stomach  ;  the  gastric 
contents  are  then  siphoned  out,  indicating  that  the  tube  has  really  passed  the 
cardia.  The  tube  is  now  withdrawn  until  only  the  open  end  remains  in  the 
stomach,  and  the  experiment  is  then  carried  out  in  the  usual  manner.  To  diag- 
nose a  diverticulum,  it  is  necessary  not  only  to  introduce  a  tube  into  it,  but  also 
to  recover  through  this  tube  a  part  or  all  of  the  fluid  introduced. 

In  view  of  these  difficulties  and  the  further  one  of  introducing  a  second  tube 
alongside  of  one  already  in  the  esophagus,  the  author  will  also  give  a  procedure 


Fig.  250.— Lary 
mirror. 


EXAMINATION   WITH  THE  AW   OF  A  MIRROR.  693 

suggested  by  Eicliartz '  for  the  differentiation  of  spindle-shaped  dilatations  of  the 
esophagus  from  deep-placed  esophageal  diverticula.  The  esophagus  is  first 
dilated  and  well  irrigated,  so  that  all  particles  of  food  are  removed.  A  tube 
similar  to  that  used  by  Rumpel,  with  an  end  opening  and  numerous  lateral  per- 
forations, is  then  introduced  almost  to  the  cardia.  This  tube  is  connected  with  a 
funnel.  The  esophagus  is  then  thoroughly  irrigated  with  a  solution  of  methyl- 
ene-blue,  the  fluid  being  introduced  and  withdrawn  a  number  of  times,  so  as  to 
be  sure  that  a  diverticulum,  if  present,  is  filled  with  the  methylene-blue  solu- 
tion. If  the  patient  strain  slightly,  some  of  the  solution  will  be  forced  back 
into  the  funnel,  proving  that  the  tip  of  the  tube  is  within  the  esophagus.  The 
tube  is  now  slowly  pushed  down  into  the  cardia,  allowed  to  remain  there  a  short 
time,  and  then  drawn  back  to  its  former  position.  In  pushing  the  tube  down- 
ward, the  fluid  in  the  esophagus  runs  into  the  stomach.  Clear  water  is  then 
introduced  into  the  esophagus  through  the  funnel  and  recovered  by  siphonage, 
and  this  procedure  is  repeated  several  times.  If  a  fusiform  dilatation  be  present, 
the  water  returns  colorless  ;  whereas  if  there  be  a  diverticulum,  the  returning 
water  will  be  stained  from  the  retained  methylene-blue  solution. 

Under  certain  circumstances,  Rumpel's  experiment  may  be  simplified  by 
introducing  the  perforated  tube  just  to  the  cardia,  filling  the  esophagus  with 
water,  and  then  pushing  the  tube  downward  into  the  stomach,  when  the  water 
will  flow  into  the  stomach,  provided  that  it  has  not  been  caught  by  a  diverticu- 
lum. The  tube  is  then  withdrawn  until  the  end  is  just  above  the  cardia.  If 
the  patient,  by  straining  slightly,  is  now  able  to  empty  a  portion  of  the  fluid 
introduced,  it  necessarily  follows  that  a  diverticulum  must  be  present. 

These  and  similar  experiments  may  be  carried  out  with  variations  dependent 
upon  the  individual  case. 


LARYNGOSCOPY  AND   TRACHEOSCOPY;    AUTOS- 
COPY   OF  THE   LARYNX  AND  TRACHEA. 

EXAMINATION   WITH    THE    AID    OF   A    MIRROR. 

Since  the  invention  of  the  laryngeal  mirror  by  Garcia,  Tiirk,  and 
Czermak,  mirror  examination  has  played  the  most  important  part  in  the 
diagnosis  of  diseases  of  the  larynx  and  trachea. 

The  principle  of  this  method  of  examination  is  as  follows :  A 
reflector  (a  perforated,  slightly  concave  mirror),  which  is  ordinarily 
fastened  to  the  examiner's  head  so  that  the  central  opening  is  opposite 
one  of  his  eyes,  collects  the  rays  of  light  from  the  source  of  illumination 
(Argand  burner,  Welsbach  light,  electric  light,  or  student  lamp)  and 
throws  them  upon  a  small  mirror,  attached  at  an  angle  of  about  45 
degrees  to  a  fairly  firm  handle,  which  the  examiner  holds  at  the  back  of 
the  patient's  throat  (Fig.  250).  The  reflector  and  the  laryngeal  mirror 
are  so  arranged  as  to  throw  an  intense  illumination  into  the  larynx,  and 
at  the  same  time  reflect  an  actual  mirror  picture  of  the  illuminated  parts 
to  the  examiner's  eye. 

In  the  ordinary  position  the  base  of  the  tongue  hides  the  opening  of 
the  larynx,  so  that  it  is  necessary  for  the  patient  to  protrude  his  tongue 
as  far  as  possible,  while  the  examiner  at  the  same  time  holds  it  firmly  in 

'  Deutsch.  med.  Woch.,  1904,  No.  21. 


694 


LARYNGOSCOPY  AND   TRACHEOSCOPY. 


position  with  the  aid  of  a  napkin  or  towel  wrapped  about  it.  Fig.  251 
and  the  following  pages  explain  the  methods  of  application  of  the  laryn- 
goscope. Fig.  252  shows  the  path  of  the  rays  of  light  in  laryngoscopy 
and  tracheoscopy.  The  latter  figure  clearly  illustrates  the  fact  that  to 
see  the  larynx  plainly  the  laryngeal  mirror  must  be  held  more  vertically 
and  introduced  farther  backward  ;  whereas,  to  observe  the  trachea,  it 
must  be  held  more  horizontally  and  farther  forward.  The  lower  the 
handle  is  depressed,  the  more  the  parts  which  lie  still  farther  backward 
come  into  the  field  of  vision.  The  following  sequence  in  the  appear- 
ance of  the  parts  in  the  field  of  vision  is  accomplished  by  gradually 
depressing  the  handle  of  the  mirror  :  epiglottis  and  base  of  the  tongue, 


Fig.  251.— Technic  of  laryngoscopy. 


anterior  commissure  of  the  vocal  cords  and  anterior  laryngeal  wall, 
anterior  tracheal  wall,  bifurcation,  posterior  tracheal  wall,  posterior 
laryngeal  wall  and  arytenoid  cartilage.  Fig.  253,  copied  from  Heitz- 
mann,  represents  a  normal  laryngeal  picture. 

A  few  details  for  the  practical  employment  of  laryngoscopy  :  The 
source  of  light  and  the  heads  of  the  examiner  and  patient  should  be 
practically  upon  the  same  horizontal  plane.  The  laryngeal  mirror  should 
be  heated  over  the  lamp  immediately  before  each  introduction,  to  prevent 
its  being  dimmed  by  condensed  steam.'  In  warming  the  mirror  the 
glass  side  should  be  held  at  some  little  distance  above  the  flame,  and  the 
degree  of  warmth  tested  by  touching  the  back  of  the  mirror  to  the  exam- 

^  The  same  purpose  can  be  accomplished  by  coating  the  surface  of  the  mirror  witli 
a  very  thin  invisible  layer  of  soap. 


EXAMINATION  WITH  THE  AID   OF  A    MIRROR. 


696 


iner's  hand.  Not  only  is  it  necessary  for  the  examiner  to  hold  the  tongue 
firmly  as  well  as  carefully,  but  it  should  be  actively  protruded  by  the 
patient,  as  otherwise  a  little  pain  and  a  reflex  bulging  of  the  posterior  part 
may  be  produced  and  render  the  examination  difficult.  In  order  to  pre- 
vent gagging  and  choking  movements,  the  pharyngeal  parts  should  not, 
if  possible,  be  touched  with  the  mirror.  The  posterior  pharyngeal  wall 
and  the  base  of  the  tongue  are  especially  to  be  avoided.     Touching  the 


■Lower  1CUC 


Fig.  252.— Diagrammatic  representation  of  direction  of  rays  of  light  in  laryngoscopy  and 
tracheoscopy  (sagittal  section  of  head  and  neck) :  a,  Position  of  mirror  for  laryngoscopy ;  o,  posi- 
tion of  mirror  for  tracheoscopy. 

uvula  ordinarily  causes  less  trouble,  and,  as  it  so  often  drops  down  in 
front  of  the  mirror,  one  can  sometimes  simplify  the  examination  by 
supporting  and  pressing  it  upward  and  backward  with  the  back  of  the 
mirror.  The  examination  is  almost  always  facilitated  by  convinciug 
the  patient  that  it  is  not  in  any  way  painful,  and  that,  even  though  at 
the  beginning  the  procedure  may  produce  gagging  movements,  quiet  and 
patience  will  always  accomplish  the  result.  The  patient  should  always 
breathe  in  quietly  and  regularly,  and  should  intone  with  expiration  either 


696 


LARYNGOSCOPY  AND   TRACHEOSCOPY, 


a  prolonged  "ah"  or  "a"  (as  in  bake).  This  device  elevates  the  epi- 
glottis, and  so  permits  the  examination  of  the  interior  of  the  larynx.  If 
the  epiglottis  is  depressed  enough  to  obstruct  the  view,  intoning  "  ee  " 
will  usually  elevate  it  sufficiently.  It  is  rarely  necessary  to  employ  an 
instrument  which  has  been  constructed  for  the  purpose  of  elevating  the 
epiglottis,  nor  to  cocainize  the  pharynx,  provided  one  takes  the  time 


Fig.  253.— Normal  laryngeal  picture  (after  Heitzmann). 

and  patience  to  get  the  patient  somewhat  accustomed  to  the  examination. 
If  cocain  is  to  be  employed,  the  pharyngeal  parts  should  be  quickly 
painted  with  a  brush  dipped  in  5  per  cent,  solution  of  cocain  hydro- 
chlorid,  and  the  patient  should  be  instructed  to  spit  out  the  solution 
immediately  after  its  application,  in  order  to  prevent  intoxication.     In 


Fig.  254.— Paralysis  of  both  thyro-ary- 
tsenoidei  int.  (tensors),  due  to  acute  laryn- 
gitis. Position  of  cords  during  phonation 
(after  v.  Ziemssen). 


Fig.  255.— Pcslicua  paralysis.  Bilateral 
complete  paralysis  of  crico-arytaenoidei  pos- 
tici  (dilators)  at  moment  of  inspiration  (after 
V.  Ziemssen). 


Fig  256 —Arytcenoideus  paralysis  Paraly- 
sis of  interarytaenoidei  transversi  and  obliqui 
(respiratory  closers  of  glottis)  m  laryngitis. 
Position  of  cords  in  phonation  with  open  glot- 
tis respiratoria  (after  v.  Ziemssen). 


Fig.  2.57.— Recurrence  paralysis.  Cadaver 
position  of  left  cord  (midway  between  adduc- 
tion and  abduction,  with  complete  paralysis  of 
laryngeus  recurrens  Bin).  Inspiratory  position 
of  right  cord  (after  v.  Ziemssen). 


EXAMINATION  WITH  THE  AID  OF  A  MIRROR. 


697 


Fig.  258.— Carcinoma  of  right  false  and 
true  cords.  Ant.  commissure  of  cords  pushed 
to  left  (after  v.  Ziemssen). 


Fig.  259.— Pedunculated  fibrous  polyp  arising 
from  lower  surface  of  left  cord.  Inspiratory  posi- 
tion (after  v.  Ziemssen). 


Fig.  260.' 


-First  stage  of  tuberculosis  of  larynx.    Ulceration  of  right  cord  and  swelling  of  inter- 
^  arytenoid  region  with  formation,  of  folds.    May  be  early  ulceration  here. 


Fig.  261.— Tracheoscopic  picture  of  anterior 
tracheal  wall  and  of  bifurcation :  at.  Anterior 
tracheal  wall ;  rvc  and  Ivc,  right  and  left  cords ; 
rh  and  lb,  right  and  left  main  bronchi ;  bs,  seat 
of  bifurcation  (after  Mackenzie). 


Fig.  262.— Tracheoscopic  picture  of  pos- 
terior tracheal  wall  and  bifurcation :  p,  Pos- 
terior tracheal  wall;  sg,  regio  subglottica; 
bs,  seat  of  bifurcations  (after  Mackenzie). 


examining  the  larynx  we  should  pay  especial  attention  to  the  mobility 
of  the  parts,  especially  the  vocal  cords,  to  their  color,  to  accidental 
alterations  in  the  surface  (swelling,  utcerations,  coating  with  mucus, 
etc.).  It  is  impossible  to  go  into  a  detailed  description  of  the  results 
of  examination,  and  so  the  author  will  limit  himself  to  appending  the 
accompanying  seven  illustrations,  which  represent  a  few  of  the  com- 
monest and  most  important  findings. 

The  same  principles  and  rules  apply  to  tracheoscopy.  The 
patient  should,  however,  sit  considerably  higher  than  the  physician,  so 
that  the  mirror  can  be  held  more  horizontally  and  looked  up  into  from 
below.  Further,  the  patient  should  hold  his  trunk  and  neck  quite 
straight,  and  at  the  same  time  bend  his  head  forward  at  the  atlanto- 
occipital  joint  (chin  against  the  neck).  This  position  brings  the  axis 
of  the  pharynx  into  a  more  favorable  position  for  tracheoscopy.  The 
trachea  cannot  be  observed  well  in  all  individuals,  but  in  many  we  can 


698  LARYNGOSCOPY  AND  TRACHEOSCOPY. 

get  a  look  as  far  as  the  bifurcation  without  any  special  difficulty.  In 
such  cases  all  sorts  of  tracheal  stenoses  can  be  examined  and  recognized. 
Fig.  261  represents  the  normal  tracheoscopic  picture  with  the  anterior 
tracheal  wall.  Fig.  262  represents  the  same  wdth  the  posterior  tracheal 
wall  (a  different  position  of  the  mirror).  Both  represent  the  bifurcation 
of  the  trachea. 

Inferior  tracheoscopy  or  laryngoscopy  means  the  examination  of  the 
trachea  or  larynx  from  a  tracheotomy  wound.  For  this  purpose  we 
employ  a  so-called  "  subglottic  mirror,"  which  is  constructed  in  quite 
the  same  fashion  as  the  laryngeal  mirror,  except  that  it  is  much  smaller 
(diameter  of  7  to  10  mm,).  This  is  introduced  through  the  tracheal 
wound,  and  the  illumination  is  thrown  in  from  the  reflector  in  the  same 
way  as  described  above.  Its  principal  use  is  to  determine  the  causes 
which  prevent  the  withdrawal  of  the  cannula  in  croup  operations. 

DIRECT   EXAMINATION   OF   THE  LARYNX,   TRACHEA, 

AND  BRONCHL 

(Autoscopy;  Orthoscopy;   Direct  Laryngoscopy  and  Tracheoscopy; 

Bronchoscopy. ) 

A.  Kirstein '  lias  described  a  new  method  of  examining  the  larynx  and  trachea 
without  employing  a  mirror.  The  base  of  the  tongue  is  drawn  forward  with  the 
aid  of  a  spatula- shaped  instrument,  and  the  larynx  and  trachea  are  then  examined 
directly.  Kirstein  described  this  method  under  a  rather  unfortunate  term — "  autos- 
copy ' '  of  the  larynx  and  trachea.  It  would  seem  to  the  author  more  correct  to 
name  the  procedure  ' '  orthoscopy  of  the  larynx  and  trachea, "  or  "  direct  laryngos- 
copy and  direct  tracheoscopy ' '  (as  opposed  to  indirect  or  mirror  laryngoscopy  and 
tracheoscopy).  Kirstein  employs  for  direct  laryngoscopy  the  instrument  pictured 
in  Fig.  263,  the  so-called  "autoscope";  but  for  most  cases  he  has  more  recently 
substituted  a  simpler  instrument,  which  is  nothing  but  a  tongue  depressor  of  a 
particular  shape  (Fig.  265).  The  original  "autoscope"  is  now  recommended  by 
Kirstein  only  for  performing  autoscopic  operations  for  demonstration  and  for  exam- 
ining children. 

The  "autoscope"  (Fig.  263,  1)  consists  of  a  grooved  metallic  spatula  {S) 
about  12  cm.  long  and  about  3  cm.  wide.  The  groove  varies  from  1  to  2.5  cm. 
in  depth.  It  is  attached  at  a  right  angle  to  the  handle  {G),  and  well  rounded  off 
to  prevent  injury.  The  anterior  end  {d)  of  the  normal  spatula  is  quite  sharply 
bent  downward.  Attached  to  the  end  of  the  spatula,  next  to  the  handle,  is  an 
electric  lighting  apparatus  (not  shown  in  the  figure),  so  arranged  that  a  cone  of 
rays  is  transmitted,  by  means  of  a  prism,  along  the  groove  exactly  in  its  long 
diameter.  A  contact  contrivance  for  the  electric  light  is  shown  in  the  figure. 
The  part  r,  which  is  movable,  forms  a  kind  of  a  roof  or  sheath  to  the  grooved 
spatula,  and  so  prevents  the  upper  lip  or  the  moustache  from  obstructing  the  view. 
The  application  of  the  instrument  can  be  readily  understood  by  studying  Fig.  264. 

The  instrument  is  grasped  by  the  handle  and  inserted  so  that  the  tip  of  the 
grooved  spatula  lies  between  the  base  of  the  tongue  and  the  epiglottis.  The  base 
of  the  tongue  is  then  hooked  downward  and  forward  by  raising  the  handle  of  the 
instrument  a  little,  and  at  the  same  time  the  epiglottis  is  slightly  raised  by 
pulling  upon  the  median  glosso-epiglottic  ligament.  Pressure  upon  the  teeth 
must  be  avoided.  If  the  epiglottis  obscures  the  view  into  the  larynx,  cocain  may 
be  applied  and  the  instrument  introduced  directly  behind  the  epiglottis.  For  this 
purpose  a  differently  shaped  spatula  (Fig.  263,  2)  is  employed. 

1  Thera'p.  Monatshefte,  1895,  vol.  ix.,  p.  361;  Ibid.,  1896,  p.  370;  Encyklop.  Jahr- 
biicher,  1896,  vol.  vi.,  p.  30. 


DIRECT  EXAMINATION  OF  LARYNX,  TRACHEA,  BRONCHI.     699 

After  the  instrument  is  properly  introduced,  the  examiner  looks  down  between 
the  upper  teeth  and  the  grooved  spatula  while  illuminating  the  depths  interior  with 


Fig.  263.— Kirstein's  autoscope :  1,  Ordinary  spatula ;  2,  intralarj  ngeal  spatula. 

the  electric  light.     Fig.  264  illustrates  the  position  of  the  patient,  with  the  trunk 
bent  slightly  forward  and  the  head  thrown  back  a  little.     This  position  brings  the 


Fig.  264.— Technic  of  autoscopy  (Kirstein). 

axis  of  the  larynx  and  trachea  in  as  direct  a  line  as  possible  with  the  axis  of  the 
mouth.     More  recent  experience  has  led  Kirstein  to  recommend  the  instrument 


700 


LARYNGOSCOPY  AND   TRACHEOSCOPY. 


pictured  in  Fig.  265  (a  simple  tongue  spatula  with  a  special  groove)  for  most 
cases  where  direct  laryngoscopy  is  advisable.  The  illumination  is  furnished  by 
the  ordinary  head  mirror.  The  advantage  of  Kirstein's  method  is  that  the 
parts  are  seen  more  naturally  than  by  a  mirror,  with  richer  and  more  vivid  shades 
of  color.  Nevertheless  the  author  is  convinced  that  direct  laryngoscopy  will 
never  usurp  the  j^lace  of  mirror  laryngoscopy.  The  application  of  the  instru- 
ment is  much  more  disagreeable  to  most  individuals  than  indirect  larj^ngoscopy, 
and  almost  always  necessitates  the  employment  of  cocain.  Besides,  we  can  rarely 
view  the  entire  larynx,  and  still  less  the  trachea.  In  many  cases  the  anatomic 
position  of  the  parts  is  such  that  we  do  not  see  any  farther  than  to  the  ej^iglottis. 
The  method  furnishes  very  incomj^lete  conclusions  about  the  motility  of  the 
larjmx,  because  the  mobility  of  the  parts  is  disturbed  by  the  examination.  Advan- 
tages of  the  method,  however,  are  the  directness  of  the  picture  and  the  ease  with 
which  the  posterior  parts  of  the  larynx  can  be  examined.  These  are  very  difficult 
to  see  in  the  ordinary  laryngeal  mirror,  and,  if  seen,  are  sharply  shortened;  they  are 


Fig.  265.— Kirstein's  tongue  spatula  for  autoscopy :  a,  Lateral  view  ;  b,  end  of  spatula,  seen 

from  above. 

very  important  in  the  diagnosis  of  initial  tuberculosis  aflFecting  the  arytenoid  folds. 
Still  other  advantages  are  that  direct  laryngoscopy  can  be  usually  accomplished 
quite  easily  in  small  children  ;  that  in  difficult  cases  the  examination  can  be  effected 
under  chloroform  anesthesia ;  that  it  decidedly  simplifies  intralaryngeal  operations, 
and  that  it  allows  of  such  operations  to  be  carried  on  under  narcosis. 

Kirstein  has  even  succeeded  in  introducing  a  small  so-called  subglottic  mirror 
into  the  larynx  of  patients  who  have  been  cocainized.  He  attached  this  with  a 
long  rod  to  the  autoscope,  and  was  able  to  examine  the  inferior  surface  of  the 
vocal  cords. 

It  must  be  acknowledged  that  considerable  practice  is  necessary  for  orthoscopy 
as  well  as  for  the  mirror  examinations.  To  anyone  who  is  accustomed  to  the  indi- 
rect or  mirror  laryngoscopy,  the  direct  picture  is  so  unusual  that  it  is  quite  difficult 
to  orient  properly  the  api^arently  transposed  parts,  and  still  more  difficult  to  correct 
certain  habits  of  movement  in  the  application  of  instruments,  etc. 


BRONCHOSCOPY. 

The  procedure  of  bronchoscopy  has  recently  been  so  perfected  that  it  is  pos- 
sible to  inspect  the  interior  of  the  bronchi  by  means  of  an  endoscopic  appliance 
which  may  be  introduced  either  through  the  intact  laiynx  or  through  a  trach- 
eotomy wound.  Although  this  procedure  has  already  been  proved  to  be  of 
considerable  value,  particularly  for  the  extraction  of  foreign  bodies,  it  will  not 
be  described,  since  it  is  difficult  of  application  by  the  general  practitioner. 


COMBINED  LARYNGOSCOPY.  701 

COMBINED   LARYNGOSCOPY. 

Kirstein  and,  later,  Leo  have  recommended  a  combination  of  direct 
and  indirect  laryngoscopy,  under  the  name  of  "  combined  laryngos- 
copy," for  cases  which  are  very  difficult  to  see.  The  base  of  the 
tongue  is  depressed  with  the  spatula  of  the  orthoscope,  and  then 
the  laryngoscopic  mirror  is  introduced  much  farther  down  into  the 
depths  of  the  throat  opposite  the  epiglottis. 


RHINOSCOPY. 


The  nasal  cavities  can  be  examined  from  in  front  and  from  behind 
from  within  the  pharynx.  In  the  former  case  we  speak  of  anterior 
rhinoscopy  ;  in  the  latter  case,  of  posterior  rhinoscopy. 

For  anterior  rhinoscopy  we  employ  a  nasal  speculum  to  dilate 
the  nasal  openings  a  little,  and  then  supply  an  illumination  reflected 
from  the  head  mirror  into  the  nasal  cavities  directly  from  in  front.  In 
this  way  we  can  observe  the  nasal  septum,  the  inferior  and  a  part  of 
the  middle  turbinate  bone.  Quite  exceptionally  we  also  can  see  a 
small  part  of  the  superior  turbinate  bone.  A  very  desirable  nasal 
speculum  is  pictured  in  Fig.  266.     Catarrhal  conditions  of  the  nasal 


Fig.  266. — Frankel's  nasal  speculum  (one-half  natural  size). 

mucous  membranes  are  readily  recognized  by  antei'ior  7-hinosGopy ; 
also  the  atrophied  dilatation  of  the  nasal  cavities  due  to  ozena,  nasal 
polypi,  and  the  peculiar  vasomotor  engorgement  of  the  erectal  tissues  in 
nervous  nasal  alFections  and  in  hay  fever.  The  latter  is  specially 
pronounced  in  the  inferior  turbinate  bone. 

Posterior  rhinoscopy  depends  uj)on  the  same  principle  as  laryn- 
goscopy. A  cone  of  rays  is  thrown  from  the  reflector  upon  a  small 
laryngeal  mirror  which  is  introduced  behind  the  uvula,  with  its  reflect- 
ing surface  turned  upward  and  forward.  This  mirror  reflects  the  illumi- 
nation to  the  posterior  nares  and  transmits  the  reflected  image  of  these 
parts  to  the  observer's  eyes.  The  path  of  the  rays  of  light  and  the 
position  of  the  mirror  are  shown  in  Fig.  267.  In  regard  to  the  prac- 
tical application  of  posterior  rhinoscopy,  the  following  difi^erences  between 
it  and  laryngoscopy  should  be  noted  :  In  the  first  place  the  tongue  should 
not  be  protruded ;  we  use  a  very  much  smaller  laryngeal  mirror,  per- 
haps the  smallest  size ;  and  we  must  be  very  careful  not  to  touch  any 
part  of  the  pharynx-wall.  The  patient  simply  breathes  naturally  with 
a  relaxed  palate  and  does  not  intone.     If  the  root  of  the  tongue  bulges 


702 


RHINOSCOPY. 


upward,  it  may  be  depressed  by  means  of  a  tongue  depressor,  held  by 
the  examiner's  left  hand,  or  sometimes  by  the  shaft  of  the  mirror. 


^jaw. 


Fig.  267.— Course  of  light  rays  in  posterior  rhinoscopy.    Sagittal  section  of  head. 

By  accustoming  the  patient  to  this  method,  it  will  succeed  just  as  well  as 
in  laryngoscopy,  even  in  very  difficult  cases.  If  success  is  impossible 
otherwise,  cocain  may  be  employed. 


Fig.  268.— Normal  picture  in  posterior  rhinoscopy.  Diagrammatic  in  that  to  obtain  complete 
picture  the  position  of  mirror  must  be  repeatedly  changed :  S.n.,  Septum;  Ch.,  choana;  P.m., 
soft  palate;  [/.,  uvula;  C.i.,  lower  turbinate  bone ;  Cm.,  middle  turbinate  bone;  C.s.,  upper 
turbinate  bone;  beneath  each  turbinated  the  corresponding  fossa;  0.  if.,  roof  of  pharynx ;  T., 
opening  of  Eustachian  tube;   TF.,  promontory  of  tube;  iJ,  Rosenmiiller's  fossa  (after  Schnitzler). 

Fig.  268  represents  a  normal  picture  in  'posterior  rMnoscopy.  The 
main  object  of  posterior  rhinoscopy  is  to  observe  :  adenoid  vegetations 


OPHTHALMOSCOPY.  703 

and  tumors  of  the  nasal  pharynx,  nasal  polypi,  inflammatory  affections 
of  the  nasal  cavities,  alterations  in  the  openings  of  the  Eustachian  tubes 
in  middle-ear  disease,  etc.  (Compare  p.  687  in  regard  to  completing 
posterior  rhinoscopy  by  direct  rhinopharyngoscopy.) 


OPHTHALMOSCOPY. 

Without  going  into  the  technic  of  ophthalmoscopy,  a  description 
of  the  more  important  changes  in  the  eyegrounds  will  be  given  : 

In  Plates  10  and  11  several  of  these  conditions  are  pictured.  The  drawings 
have  been  generally  made  in  the  upright  image,  though  they  have  been  reduced 
to  the  size  of  the  inverted  image. 

Plate  10,  Figs.  1,  2,  and  3. — Various  forms  or  stages  of  optic  neuritis  and 
choked  disk. 

Fig.  1.  Beginning  Optic  Neuritis. — The  disk  is  congested,  the  temporal  mar- 
gin is  slightly  veiled  and  swollen,  the  veins  are  moderately  dilated  and  tortuous, 
the  arteries  are  somewhat  contracted. 

Fig.  2.  Pronounced  Optic  Neuritis. — The  disk  is  distinctly  enlarged,  with  ill- 
defined  margins.  It  presents  radial  striations,  and  is  opaque  from  exudates  and 
hemorrhages  ;  it  is  very  congested  and  swollen.  The  veins  are  greatly  dilated; 
the  arteries  very  much  constricted. 

Fig.  3.  Optic  Neuritis  of  tke  Highest  Qrade,  So-called  Choked  Disk. — The  disk 
is  ill-defined.  It  is  prominent  like  a  mushroom,  and  projects  2  to  3  mm. 
There  is  a  diflference  in  refraction  of  at  least  two  dioptrics  between  the  apex  of 
the  swelling  and  the  surrounding  retina.  The  vessels  make  a  sharp  bend  at  the 
papillary  margin.  The  disk  at  its  margin  is  gray.  In  the  center  it  is  covered  by 
a  white  exudate  which  hides  the  congestion.  The  veins  are  very  much  dilated 
and  tortuous  ;  the  arteries  are  narrow.  Both  are  covered  by  exudates  in  the 
center  of  the  disk,  and  make  their  appearance  at  the  margin.  The  central  ends 
of  the  blood-vessels  appear  to  taper.  There  are  striated  hemorrhages  arranged 
radially  on  the  disk  and  in  the  grayish  surrounding  retina. 

Between  Figs.  1,  2,  and  3  there  are  only  differences  in  grade.  All  three  varieties 
may  occur  from  local  inflammations,  as  well  as  from  an  increase  of  intracranial 
pressure.  Forms  such  as  Fig.  1  are  occasionally  observed  in  hypermetropia 
and  after  overuse  of  the  eyes  following  functional  hyperemia.  Pronounced  forms 
like  Fig.  3  are  most  frequently  met  with  in  conjunction  with  brain  tumors  and 
tuberculous  meningitis  following  protracted  and  marked  increase  of  intracranial 
pressure.  Occasionally  in  these  diseases  forms  like  Figs.  1  and  2  are  observed. 
The  clinical  conditions,  therefore,  speak  against  a  sharp  separation  of  the  condi- 
tion known  as  optic  neuritis  (Figs.  1  and  2)  from  that  known  as  choked  disk 
(Fig.  3). 

Optic  neuritis  occurs  in  intracranial  tumors  (in  70  to  85  per  cent,  of  the  cases), 
in  syphilis  of  the  central  nervous  system  (in  14  per  cent,  of  the  cases,  presumably 
where  an  intracranial  tumor  or  a  basal  gummatous  meningitis  is  present),  in 
tuberculous  menjngitis  rarely,  in  purulent  meningitis  often,  in  primary  internal 
hydrocephalus  in  case  it  leads  to  increased  intracranial  pressure,  rarely  in  brain 
abscesses  and  internal  hemorrhagic  pachymeningitis,  rarely  in  traumatic  intra- 
cranial hemorrhages  ;  furthermore,  in  certain  affections  of  the  orbit,  es];)ecially 
tumors  (in  the  latter  case  combined  with  exophthalmos,  and,  in  distinction  from 
the  other  cases,  occurring  on  one  side  only),  in  polyneuritis,  in  chronic  nephritis, 
especially  contracted  kidney ;  in  diabetes  mellitus,  in  scrofula,  in  disturbances  of 
menstruation  during  pregnancy,  and  in  labor ;  in  chlorosis,  in  severe  chronic  and 
acute  anemia,  especially  after  gastric  hemorrhages,  and  in  acute  infectious  dis- 


704  OPHTHALMOSCOPY. 

eases.  In  the  last-mentioned  diseases,  not  depending  upon  intracranial  lesions, 
the  picture  of  ordinary  neuritis  or  papillitis  without  pronounced  swelling  of  the 
disk  is  common  (Figs.  1  and  2). 

For  purposes  of  diagnosis  it  must  be  remembered  that  an  optic  neuritis,  even 
in  its  most  intense  form,  may  be  combined  with  unaffected  vision.  Hence  the 
rule  that  in  all  cerebral  affections  the  ophthalmoscope  should  be  employed,  even 
when  no  disturbance  of  vision  is  present.  Furthermore,  it  must  be  mentioned 
that  in  brain  tumors  the  size  and  the  site  of  the  tumor  are  not  of  exclusive  im- 
portance for  the  development  of  a  choked  disk,  but  that  the  rapidity  of  growth 
and  other  unknown  factors  play  as  important  roles. 

Fig.  4.  Changes  of  the  Eyeground  in  a  Case  of  Severe  Purpura  Hcemorrhagica.  — 
Extensive  hemorrhages  with  inflammatory  changes  of  the  disk.  The  disk  is  not 
distinctly  swollen.  Its  margins  are  completely  lost  from  the  exudation,  and  suf- 
fused with  blood.  There  are  numerous  striated  hemorrhages  situated  in  the 
retina  and  arranged  in  a.  radiating  fashion.  The  color  of  the  hemorrhages  varies 
from  a  pale  red  to  a  dark  or  even  black  red.  Within  the  zone  filled  with  hemor- 
rhages, as  well  as  in  the  region  of  the  disk,  the  blood-vessels  are  scarcely  visible. 
In  the  periphery  of  the  eyeground  the  veins  are  thickened  and  tortuous,  the 
arteries  constricted  (not  visible  in  the  figure).  The  picture  resembles  that  of 
a  thrombosis  of  the  central  vein.  In  this  case  the  comparative  improvement  of 
vision  spoke  against  this  diagnosis.  A  moderate  degree  of  neuritic  atrophy 
remained. 

Fig.  5.  Albumitiuric  Neuroretinitis. — This  occurs  in  the  various  forms  of 
chronic,  more  rarely  acute,  nephritis,  generally  in  contracted  kidney.  The  disk 
presents  the  signs  of  a  neuritis.  It  is  blurred,  not  especially  swollen,  hyperemic, 
ill-defined.  The  veins  are  dilated,  the  arteries  contracted.  There  are  radiating 
hemorrhages  in  the  disk  and  in  the  surrounding  retina,  with  numerous  white 
patches  (fatty  degeneration),  especially  in  the  neighborhood  of  the  disk  and  in 
the  peculiar  characteristic  star-shaped  figure  about  the  macula  lutea.  The 
changes  in  the  region  of  the  macula  lutea  furnish  the  anatomic  explanation  for 
the  usually  very  pronounced  loss  of  sight.  It  should  also  be  mentioned  that  in 
nephritis  these  changes  of  the  retina  may  occur  without  changes  in  the  disk  (pure 
albuminuric  retinitis),  as  well  as  neuritic  changes  of  the  disk  without  changes  of 
the  retina  (albuminuric  neuritis).  The  changes  of  the  retina  and  of  the  optic 
nerve  in  diabetes  mellitus  are  often  like  those  found  in  nephritis. 

Fig.  6.  The  Eyeground  in  Pernicious  Anemia. — The  fundus  appears  unusually 
pale,  and  is  covered  with  numerous  irregular  retinal  hemorrhages  and  a  few  white 
patches.  In  one  place,  as  occurs  frequently,  a  white  spot  occupies  the  center  of 
a  hemorrhage.  The  hemorrhages  and  the  blood-vessels  have  turned  out  some- 
what too  dark  in  the  drawing.  The  former  appear  so  pale  in  the  pronounced 
anemia  that  they  are  recognized  with  difficulty  and  are  frequently  overlooked. _  This 
condition  occurs  in  a  variety  of  severe  forms  of  anemia,  most  pronounced  in  the 
so-called  pernicious  anemia  (compare  p.  660),  but  is  also  found  in  bothrioceph- 
alus  and  ankylostomum  anemia  and  in  leukemia.  The  changes  are  not  so  intense 
and  usually  not  so  pronounced  in  the  severe  anemias  of  certain  cancers  of  the 
stomach,  and  are  practically  absent  in  simple  chlorosis. 

Fig.  7.  The  Eyeground  in  Hereditary  Syphilis. — Perivasculitis  of  the  retinal 
vessels  and  choroiditis.  Perivasculitis  is  especially  characteristic  for  syphilis. 
The  vessels,  especially  the  arteries,  appear  to  be  outlined  in  white,  owing  to 
thickening  of  their  walls.  In  one  place  the  changes  are  so  pronounced  that  a 
vessel  is  converted  into  a  white  strand,  through  which  the  blood-current  can  no 
longer  be  observed.  The  picture  presents  the  characteristic  spots  of  choroidal- 
atrophy,  and  pigment  deposits  in  the  choroid.  The  macula  lutea  is  especially 
plainly  visible. 

Fig.  8.  Choroidal  Tubercle  in  Acute  Miliary  Tuberculosis. — The  choroidal 
tubercles  are  characterized  as  ill-defined  white  spots  which  become  more  intensely 
white,  usually  of  an  absolutely  round  form,  measuring  one-quarter  to  one-half  a 
papilla  in  diameter.  In  the  later  stages  they  are  larger,  and  their  site  is  independ- 
ent of  the  course  of  the  blood-vessels.     If  they  are  situated  in  the  region  of  a 


PLATE   10. 


1,  Early  stage  of  optic  neuritis;  2,  optic  neuritis  ;  S,  cholced  disk  ;  4,  neuroretinitis  haemor- 
rhagica  iii  purpura  ;  u  albuminuria  neuroretinitis ;  6,  hemorrhagic  retinitis  in  pernicious 
anemia  ;  7,  syphilitic  chorioretinitis  ;  S,  miliary  tubercle  of  the  choroid  ;  9,  medullated  nerve- 
noers. 


OPHTHALMOSCOPY.  705 

blood-vessel,  they  are  covered  by  the  latter.  The  drawing  shows  recent  and  old 
tubercles.  Especially  characteristic  in  cases  where  the  nature  of  these  struc- 
tures is  not  clear  is  their  sudden  appearance  and  increase  within  a  few  days. 
They  can  be  distinguished  from  retinal  spots  by  their  usually  circular  form  and 
the  ill-defined  margins  of  the  choroidal  tubercle.  In  the  case  depicted  in  the 
figure,  in  addition  to  the  miliary  tubercles,  there  was  a  complicating  tuberculous 
meningitis,  which  explains  the  hyperemic  and  blurred  appearance  of  the  disk 
(beginning  neuritis).  Contrary  to  a  well-spread  belief,  the  jjresence  of  choroidal 
tubercles  is  a  rarity  in  uncomplicated  tuberculous  meningitis.  Choroidal  tuber- 
cles in  almost  all  cases  point  to  the  presence  of  a  general  miliary  tuberculosis. 
The  characteristic  condition  of  a  tuberculous  meningitis  is,  on  the  other  hand, 
optic  neuritis. 

Fig.  9.  MeduUated  nerve  fibers  of  the  retina,  presenting  a  white,  glistening 
figure,  beginning  at  the  disk  and  striated  radially.  In  the  upper  part  of  the 
picture  a  retinal  blood-vessel  is  partly  covered  by  this  white  structure;  otherwise, 
the  eyeground  is  normal.  This  condition  is  without  functional  importance.  It 
must,  however,  be  recognized  in  order  to  distinguish  it  from  pathologic  changes. 
Plate  11  gives  a  summary  of  the  ophthalmoscopic  pictures  occurring  in  the 
various  forms  of  optic  atrophy,  which  it  is  of  great  diagnostic  interest  to  distinguish. 

Fig.  1.  Simple  Atrophy  of  the  Optic  Disk. — The  disk  is  white  and  shining, 
the  margins  are  unusually  sharp,  the  light  scleral  ring  is  visible  especially  on  the 
temporal  side,  the  lamina  cribrosa  appear  as  a  glistening  network,  including 
angular,  grayish  areas  representing  bundles  of  atrophic  nerve  fibers.  The  exca- 
vation of  the  atrophic  disk  is  shallow,  like  that  of  a  plate,  and  therefore  recog- 
nized with  difliculty.  The  color  of  the  disk  is  usually  most  pale  about  the 
entrance  of  the  blood-vessels  and  in  the  temporal  half  of  the  disk.  The  caliber 
of  the  blood-vessels  usually  remains  normal.  The  very  small  blood-vessels 
which  furnish  nutrition  to  the  disk  are  usually  very  few  and  thin.  The  large 
vessels,  especially  the  arteries,  usually  diminish  in  size  only  after  the  atrophy  has 
existed  for  a  long  time.  The  atrophic  excavation  of  the  disk  develops  generally 
only  in  the  later  stages,  beginning  at  the  margin  of  the  disk  and  gradually  pro- 
ceeding to  the  center. 

To  distinguish  this  simple  atrophy  from  inflammatory  atrophy,  it  is  of 
importance  to  note  the  normal  condition  of  the  blood-vessels,  the  visibility  of  the 
lamina  cribrosa,  the  well-defined  margins  of  the  disk  with  distinct  scleral  ring. 

Simple  atrophy  occurs  most  frequently  in  tabes  dorsalis  and  in  progressive 
paralysis;  furthermore,  in  the  so-called  gray  degeneration  of  the  optic  nerve  with- 
out spinal  or  cerebral  symptoms.  In  some  cases  of  multiple  sclerosis  simple  optic 
atrophy  has  occurred;  in  others  neuritic  atrophy.  It  should  further  be  men- 
tioned that  simple  atrophy  of  the  optic  nerve  may  occur  as  an  interruption  in 
the  course  of  the  optic  nerve  or  of  the  oj^tic  tract,  as  in  chronic  hydrocephalus, 
where  the  distended  inftindibulum  presses  upon  the  chiasm. 

Fig.  2.  Atrophy  of  the  Optic  Nerve  after  Embolism  of  the  Central  Artery ,  Fol- 
lowing Ligature  of  the  Common  Carotid  in  a  Case  of  Pulsating  Exophthalmus. — 
Complete  blindness.  The  disk  is  grayish  white.  The  margins  have  a  distinct 
scleral  ring;  the  lamina  cribrosa  is  visible.  In  the  center  the  central  canal 
appears  as  a  grayish  dot.     The  vessels  are  contracted  to  mere  threads. 

Fig.  3.  Atrophy  (^Primary  Atrophy)  of  the  Opjtic  Nerve  in  Glaucoma  Simplex. 
— Complete  blindness.  The  disk  is  grayish  white;  the  lamina  appear  in  the 
center.  The  entire  disk  is  deeply  excavated.  The  vessels  make  a  sharp  bend  at 
the  margin  and  disappear  in  the  depth.  A  few  again  appear  at  the  bottom  of  the 
excavation;  some  are  broader  and  lighter  in  color.  The  veins  are  somewhat 
dilated,  the  arteries  slightly  contracted.  There  is  a  yellow  area  with  several  pig- 
ment spots  about  the  excavated  disk  (halo  glaucomatosus). 

Fig.  4-.  Neuritic  Atroi^hy  of  the  OjMc  Disk. — Incomplete  blindness.  The 
disk  appears  dull  white  ;  the  nasal  half  is  still  slightly  red  in  color.  The  mar- 
gins of  the  disk  ai-e  soft,  ill-defined,  without  distinct  scleral  ring.  The  lamina 
cribrosa  are  not  visible.  The  vessels  are  moderately  contracted,  especially  the 
arteries.  Some  are  surrounded  by  narrow  white  lines  characteristic  for  sclerosis 
45 


706  OPHTHALMOSCOPY. 

of  the  vessel-wall.  Occasionally  pigment  is  present  in  the  form  of  small  spots 
at  the  margin  of  the  disk.  These  features  (ill-defined  margins  of  the  disk,  con- 
traction of  the  blood-vessels,  lamina  cribrosa  and  scleral  ring  not  visible)  differ- 
entiate this  form  from  that  of  simple  atrophy. 

Any  inflammation  in  the  course  of  the  optic  nerve  may  lead  to  neuritic 
atrophy.  In  some  of  the  cases  of  multiple  sclerosis,  as  has  been  above  stated, 
the  atrophies  observed  have  been  of  an  inflammatory  type.  The  illustration  is 
of  one  of  these  cases. 

Fig.  5.  Papillitic  Atrophy. — Blindness.  The  disk  is  dull  white  and  uni- 
formly discolored.  The  margins  are  even  less  sharp  than  in  Fig.  4,  passing  over 
into  the  choroidal  changes  which  surround  the  disk  (the  pigment  is  often  lack- 
ing; in  other  cases  it  is  deposited  irregularly).  The  lamina  cribrosa  are  invis- 
ible. The  vessels  are  distinctly  contracted.  These  changes  represent  simply  a 
higher  grade  of  neuritic  atrophy  (Fig.  4),  which  is  spoken  of  as  papillitic 
atrophy,  because  in  its  occurrence  the  disk  is  included  in  the  neuritic  process. 
Consequently  papillitic  atrophy  is  a  frequent  sequence  to  true  optic  neuritis, 
especially  in  brain  tumors.  As  the  choked  disk  proceeds  to  atrophy,  the  disk 
remains  swollen  for  a  length  of  time,  the  vessels  show  a  distinct  bend,  as  in  Fig. 
3,  Plate  III. ,  while  it  gradually  assumes  more  and  more  the  character  of  papil- 
litic atrophy  (whitish  discoloration,  constriction  of  the  blood-vessels).  In  this 
condition  the  color  of  the  disk  is  often  a  dirty  grayish  yellow. 

Fig.  6.  Papillitic  Atr^phij  after  Tfirombosis  of  the  Central  Retinal  Vein,  Fol- 
lowing Chronic  Meningitis. — The  disk  is  discolored,  grayish  white.  Its  margin  on 
one  side  is  distorted.  It  is  surrounded  by  extensive  changes  in  the  choroid  and 
pigment  accumulations.  In  the  center  the  central  canal  appears  as  a  grayish  dot.^ 
The  vessels  are  converted  into  thin  white  strands  (progressive  organized  throm- 
bosis).    In  this  form  the  condition  of  the  blood-vessels  is  characteristic. 

Fig.  7.  Retinal  Atrophy  in  Old  Chorioretinitis. — The  latter  affection  in  this 
case  was  the  result  of  unusually  prolonged  lactation,  presumably  developing 
upon  a  syphilitic  basis.  In  any  case,  it  resembled  certain  late  stages  of  syphilitic 
chorioretinitis.  Incomplete  blindness.  The  disk  is  of  a  dirty-yellowish-gray- 
color.  The  margins  in  this  case  are  sharply  defined;  sometimes,  however,  they 
are  blurred.  The  lamina  markings  are  not  visible.  The  vessels  are  unusually 
narrow.  The  retina  and  the  choroid  are  very  much  changed,  the  choroidal  ves- 
sels presenting  evidences  of  sclerosis.  The  intravascular  spaces  are  dark.  There- 
is  moderate  pigment  accumulation  in  the  retina. 

Similar  changes  of  the  disk  to  those  which  have  just  been  described  may  occur 
in  retinitis  pigmentosa  and  in  other  chronic  inflammatory  processes  of  the  retina, 
as  well  as  in  detachment  of  the  retina.  The  retinal  and  choroidal  changes  are 
characteristic  in  differential  diagnosis. 

Fig.  8.  Atrophic  Discoloration  of  the  Temporal  Half  of  the  Disk  in  Alcohol 
Amblyopia  {Central  Scotoma  for  Green  and  Red;  Vision  Very  Much  Reduced). — The 
temporal  half  of  the  disk  is  grayish  white,  the  margins  are  sharp,  the  scleral 
ring  is  distinct,  the  lamina  are  not  visible,  and  the  vessels  are  of  normal  caliber. 

This  is  a  case  of  atrophy  of  the  papillomacular  bundle  of  the  optic  fibers. 
As  it  occurs  through  toxic  influences  (especially  alcohol,  rarely  tobacco,  stra- 
monium, carbon  disulphid  and  chloral),  16.5  per  cent,  of  alcoholic  subjects  and 
65  per  cent,  of  patients  with  alcoholic  amblyopia  show  these  changes.  Similar 
changes  have  been  observed  after  diabetes  mellitus  and  after  taking  cold.  It  is 
important  to  remember  that  in  1  per  cent,  of  persons  with  normal  sight  a  some- 
what similar  pallor  of  the  temporal  half  of  the  disk  can  be  observed. 

While  in  this  illustration  toxic  atrophy  of  the  temporal  half  of  the  disk  pre- 
sents the  characteristics  of  a  simple  atrophy,  it  may  in  other  cases  show  the 
peculiarities  of  an  inflammatory  atrophy  (indistinct  margins,  slight  sclerosis  of 
the  vessels,  as  in  Fig.  4).  Both  forms  are  frequently  spoken  of  as  retrobulbar 
neuritis,  from  the  supposition  that  the  cause  of  the  changes  is  a  retrobulbar  optic 
neuritis.  This,  however,  is  not  quite  correct,  as  an  inflammation  of  the  optic 
nerve  behind  the  eyeball  should  lead  to  changes  in  the  entire  disk,  in  the  form 
of  a  simple  atrophy  (descending  atrophy)  or  of  a  neuritic  atrophy. 


PLATE  n. 


1,  Simple  atrophy  of  the  optic  disk  in  tabes  dorsalis;  2,  simple  atrophv  in  embolism  of  the 
central  arttry  ;  3  pressure  atrophy  in  glaucoma  simplex  ;  4,  neuritic  atrophv";  5,  parullitic  atroi>hv 
rinAo*^  ^^*^^  di.sk  m  gumma  of  the  brain:  f,,  papillitic  atrophy  after  thrombosis  of  the  central 
retinaMein:/  retinal  atrophy  from  chorioretinitis  following  prolonged  lactation  with  a  prob- 
able syphilitic  basis ;  S,  atrophy  of  temporal  portion  following  retrobulbar  neuritis  from  alco- 


EXPLORATORY  PUNCTURES.  IQl 

EXPLORATORY   PUNCTURES  AND   HARPOONING. 

EXPLORATORY  PUNCTURES. 

By  an  exploratory  puncture  we  mean  the  introduction  of  a  fine  hol- 
low needle,  attached  to  a  test  puncture  or  aspirating  syringe,  into  a 
diseased  area,  and  a  subsequent  aspiration  in  order  to  examine  the 
character  of  the  material  withdrawn,  and  especially  to  determine  the 
presence  or  absence  of  collections  of  fluid. 

SYRINGES  FOR  EXPLORATORY  PUNCTURES. 

The  appropriate  syringe  is  a  little  larger  than  the  ordinary  hypo- 
dermic syringe,  and  is  furnished  with  a  longer  and  rather  coarser  needle. 
The  hypodermic  syringe  may  also  be  used  if  such  a  large  needle  be 
fitted  to  it  tightly.  A  syringe  which  will  contain  5  to  10  c.c.  of  fluid 
is  large  enough.  It  should  furnish  adequate  aspiration  force  to  with- 
draw even  quite  solid  fragments  of  tissue  and  suflicient  fluid  for  a  sat- 
isfactory chemical  or  bacteriologic  examination.  The  essentials  for  a 
serviceable  exploratory  puncture  (or  aspiration)  syringe  are  the  follow- 
ing :  The  glass  cylinder  should  have  a  uniform  caliber,  so  that  the  pis- 
ton fits  accurately  throughout  its  path.  The  packing  must  be  absolutely 
tight,  so  that  if  the  end  is  closed  and  the  piston  withdrawn  the  latter 
will  slip  back  quickly  into  its  former  position  by  the  force  of  suction. 
The  needle  must  be  fitted  on  absolutely  tight,  so  that  the  same  test  can 
be  successfully  applied  after  the  needle  is  screwed  to  the  syringe.  If 
the  material  withdrawn  is  to  be  examined  bacteriologically,  the  syringe 
must  be  carefully  sterilized.  This  can  most  easily  be  done  with  the 
glass  syringes  furnished  with  a  metal  mounting,  asbestos  packing,  and 
asbestos  valves,  as  they  can  be  boiled.  The  most  perfect  are  furnished 
with  a  contrivance  for  compressing  the  asbestos-packing  valves  against 
the  cylinder,  so  that  it  can  be  made  as  tight  or  as  loose  as  is  desired. 
The  cannulas  or  needles  should  be  of  an  appropriate  size.  This  is  not 
always  the  case  with  all  the  varieties  on  sale.  They  should  be  6  to  7 
cm.  (2|-2|  in.)  long  (not  including  the  connecting  portion)  and  about 
1  mm.  (yL  in.)  external  diameter,  so  that  the  puncture  shall  be  suffi- 
ciently large.  Such  fine  needles  practically  obviate  the  possibility  of 
any  danger. 

METHOD  OF  MAKING  EXPLORATORY  PUNCTURES,  AND  THE 
GENERAL  RESULTS  OBTAINED. 

Before  each  attempt  the  needle  must  be  carefully  disinfected  accord- 
ing to  the  strictest  surgical  rules.  This  means  that  after  being  used  it 
should  be  carefully  washed  in  water,  and  then  either  boiled,  or  left  in 
5  per  cent,  carbolic  solution  for  at  least  three  hours  (being  careful  that 
the  solution  fills  the  bore  of  the  needle).  Just  before  using  the  needle, 
a  few  moments'  immersion  in  strong  carbolic  solution  will  be  sufficient. 
The  needle  should  be  freed  from  carbolic  solution   by  squirting  sterile 


:708  EXPLORATORY  PUNCTURES  AND  HARPOONING. 

water  through  it,  otherwise  the  carbolic  might  produce  a  cloudiness  in 
the  fluid  withdrawn,  which  might  lead  to  error.  For  a  bacteriologic 
examination  the  syringe  must  also  be  disinfected  quite  as  carefully.  For 
this  purpose  the  syringes  with  asbestos  valves,  as  already  mentioned, 
are  the  most  convenient.  They  can  be  boiled  readily.  The  asbestos 
valves  must  then  be  loosened  a  little  by  means  of  the  contrivance  de- 
scribed above,  as  otherwise  they  are  apt  to  swell  a  little  too  much.  Ten 
minutes'  boiling  in  water,  or,  better,  in  a  1  per  cent,  soda  solution,  is 
sufficient.  Air  bubbles  should,  of  course,  be  expelled  both  from  the 
syringe  and  the  needle. 

Immediately  before  the  puncture  is  attempted,  the  spot  selected  must 
be  very  carefully  disinfected  (soap,  alcohol,  1  per  cent,  sublimate  solu- 
tion). After  the  puncture  the  spot  should  be  covered  with  a  piece  of 
adhesive  plaster  moistened  in  sublimate. 

The  skin  should  first  be  stretched  tightly  and  the  needle  inserted 
perpendicular  to  the  surface,  and  not  too  quickly,  so  as  to  avoid  any 
bony  parts  by  slightly  altering  the  direction.  During  the  introduction 
of  the  needle  we  should  pay  special  attention  to  the  resistances  met  with 
at  the  different  levels.  AVe  are  then  able  to  select  the  appropriate  moment 
for  aspiration  ;  this  should  be  when  we  feel  that  the  needle  has  passed  all 
obstructions,  entered  a  cavity,  and  is  freely  movable.  Such  f>alpation 
with  the  needle  should  never  be  neglected.  Sometimes,  however,  a 
slight  amount  of  fluid  is  obtained  while  the  needle  seems  to  be  sticking 
into  perfectly  solid  tissue.  We  should  not  desist  if  we  obtain  no  fluid 
by  aspiration,  provided  we  have  good  reason  to  believe  that  fluid  is 
there.  Frequently  we  have  penetrated  too  far  or  not  far  enough,  and 
a  slight  push  or  withdrawal  of  the  needle  will  be  sufficient  to  obtain 
fluid.  In  other  cases  we  withdraw  the  needle  partially  and  then  point 
it  in  another  slightly  difl^erent  direction.  At  the  same  time  we  must  be 
careful  to  notice  any  chance  movements  which  may  be  imparted  to  the 
point  of  needle  by  parts  which  have  been  punctured  or  touched,  such 
as  the  lungs,  diaphragm,  liver,  spleen,  heart.  Such  movements  are  of 
the  greatest  importance  for  diagnosis.  If  the  first  puncture  is  unsuc- 
cessful and  the  examiner  is  still  convinced  of  the  presence  of  fluid 
in  the  vicinity,  the  procedure  should  be  repeated  at  an  adjoining 
spot  after  he  has  again  more  carefully  examined  the  locality. 
In  everv  case  Avhere  we  find  fluid,  it  is  advisable  to  aspirate  a  suf- 
ficient quantity  to  perform  all  the  necessary  examinations.  If  the 
needle  enters  solid  tissue,  and  we  wish  to  examine  this  tissue  histologi- 
cally, we  can  generally  obtain  a  specimen  by  pulling  the  needle  back 
and  forth  a  few  millimeters,  twisting  it  at  the  same  time  so  that  it  acts 
a  good  deal  like  a  cork  borer.  Then  with  sufficiently  strong  aspiration 
we  can  suck  out  a  fragment  of  the  tissue  large  enough  for  microscopic 
examination.  In  this  attempt  the  needle  must  be  very  carefully  with- 
drawn after  the  aspiration.  Its  contents,  which  often  consist  of  quite 
small  tissue  fragments,  can  usually  be  forced  out  upon  a  glass  slide  by 
a  vigorous  push  of  the  ]nston.  The  fragments  may  then  be  teased 
apart  and  examined   microscopically.     Whenever  in  any  exploratory 


EXPLORATORY  PUNCTURES.  709 

puncture  aspiration  brings  no  fluid,  we  should  never  neglect  to  examine 
the  contents  of  the  needle  carefully  in  the  way  described.  Aspiration 
frequently  obtains  only  tiny  flakes  of  pus  from  purulent  infiltrated 
tissue  or  from  thick  collections  of  pus.  Such  flakes  microscopically 
demonstrated  are  oftentimes  quite  sufficient  for  diagnostic  purposes. 

Where  we  obtain  a  large  amount  of  fluid  from  an  exploratory  punc- 
ture, the  first  essential  always  is  to  examine  this  fluid  macroscopically ; 
thereby  we  determine  definitely  whether  it  is  serous  or  purulent,^  clear 
or  turbid,  colorless  or  colored,  odorless  or  foul-smelling,  and  whether  a 
purulent  fluid  contains  the  characteristic  kernels  of  the  actinomycosis 
(see  p.  603).  In  turbid  serous  fluids  the  naked-eye  appearances  are 
often  sufficient  to  decide  between  a  purulent  and  a  fibrinous  turbidity, 
since  the  latter  is  characterized  by  the  presence  of  flocculi. 

In  many  cases  a  microscopic  examination  must  be  made.  This 
will  also  furnish  information  in  reference  to  the  so-called  chylous 
character  of  a  fluid — i.  e.,  a  turbidity  caused  by  the  presence  of 
minute  particles  of  fat.  Chylous  fluid  in  a  cavity  may  be  due  to  a 
number  of  different  causes.  As  a  result  of  a  stasis  of  lymph  in  the 
thoracic  duct,  the  fluid  may  become  admixed  with  chyle  by  diapedesis 
without  there  being  any  solution  of  continuity  of  the  tissues.  In  tuber- 
culosis or  malignant  tumors  of  the  pleura  or  of  the  peritoneum,  the 
thoracic  duct  or  some  of  the  smaller  lymphatic  vessels  may  be  opened 
up  by  the  destructive  process  and  the  chyle  poured  out  into  the  affected 
cavity.  In  all  these  cases,  as  in  chyluria,  the  admixture  ivith  chyle  may 
be  recognized  by  the  microscopic  examination  of  the  fluid.  The  fat  is 
not  present  in  large  drops,  but  in  the  finest  of  granules,  which  in  size 
somewhat  resemble  micrococci,  and  usually  exhibit  the  so-called  Brown- 
ian  movement.  In  addition  to  the  fact  that  they  do  not  stain  well  in 
dry  preparations  (see  p.  596),  they  may  be  differentiated  from  micro- 
organisms by  their  great  quantity,  since  such  a  large  number  of  micro- 
organisms could  scarcely  be  present  in  a  non-purulent  fluid.  They 
also  show  an  additional  peculiarity  in  that  they  tend  to  collect  in  a  layer 
upon  the  upper  surface  of  the  fluid  when  it  is  allowed  to  stand.  Chemi- 
cal tests  may  also  be  applied  after  removing  the  fat  from  the  fluid  by 
agitation  with  ether.  From  a  chemical  standpoint  it  should  also  be 
noted  that  amounts  of  sugar  greater  than  those  found  in  the  blood  are 
not  to  be  expected  in  chylous  fluids,  since  sugar  leaves  the  intestine 
through  the  veins  and  not  through  the  lymphatics.  True  chylous  fluids 
have  also  been  found  in  cavities  under  circumstances  which  have  not 
yet  been  explained,  there  being  neither  a  lymph  stasis  nor  a  rupture  of 
a  chyliferous  vessel.  In  these  cases  the  affected  serosa  is  possibly 
abnormally  permeable  to  fat-particles,  which,  as  is  well  known,  are 
present  in  large  numbers  in  normal  blood  after  the  ingestion  of  food. 

'  Although  it  seems  veiy  simple  to  differentiate  a  serous  from  a  purulent  exudate  by 
means  of  exploratory  puncture,  errors  may  easily  be  made,  since  thin,  purulent  exudates 
exhibit  a  marked  inclination  to  sedimentation,  so  that  if  the  puncture  be  made  high  up, 
nothing  but  a  clear  serum  may  be  obtained,  the  pus  corpuscles  having  settled  to 
the  lowermost  part  of  the  cavity.  In  doubtful  cases  it  is  consequently  advisable  to  make 
a  second  puncture  at  a  lower  level  than  that  of  the  first. 


710  EXPLORATORY  PUNCTURES  AND  HARPOONING. 

These  true  chylous  exudates  and  transudates  are  not  to  be  confounded 
with  fluids  in  which  the  turbidity  depends  upon  the  presence  of  larger 
fat-globules.  In  the  latter  instance  the  finding  of  cells  containing  fat- 
droplets  demonstrates  that  the  admixture  is  dependent  upon  fatty 
degeneration  of  endothelial  cells  or  of  tumor  cells. 

Microscopic  examination  will  also  give  information  in  reference  to 
the  presence  of  leukocytes  and  admixtures  with  blood  which  would  escape 
macroscopic  inspection  (see  also  p.  714  et  seq.),  and  to  the  presence  of 
cholesterin  crystals  in  old  serous  exudates  (Fig.  211,  6) ;  it  will  also 
reveal  the  presence  of  hematoidin  crystals  (Fig.  211,  d)  in  purulent 
collections  (pleural  empyemata,  subphrenic  abscesses,  pulmonary  ab- 
scesses, and  biliary  collections),  and  particularly  the  presence  of  bacteria 
in  exudates.  In  the  latter  case  cover-glass  preparations  should  be  made 
according  to  the  rules  previously  given  for  the  examination  of  sputum 
(see  p.  696)  ;  it  is  best  to  select  fibrinous  flocculi  obtained  by  ceutrifu- 
gation,  since  the  bacteria  are  caught  in  the  meshes  of  the  fibrin  network. 
When  a  serous  exudate  contains  but  few  bacteria,  their  discovery  may 
be  facilitated  by  centrifngation  in  accordance  to  the  method  suggested 
by  Ilkewitsch  for  the  examination  of  sputum  for  tubercle  bacilli.  The 
nucleoproteid  is  precipitated  by  the  addition  of  acetic  acid,  and  the 
bacteria  settle  with  the  proteid.  In  addition  to  the  foul  odor,  the  micro- 
scopic demonstration  of  food  particles  and  innumerable  bacteria  in  the 
fluid  obtained  from  the  peritoneal  cavity  by  exploratory  puncture  is  of 
great  importance  for  the  demonstration  of  a  perforation  of  the  stomach 
or  intestine.  The  microscopic  demonstration  of  particles  of  tumors  in 
fluids  obtained  by  puncture  is  also  of  importance.  They  may  be  found 
as  isolated  cells  differing  from  the  normal  endothelium  or  as  peculiar 
cell  conglomerations,  the  latter  being  evidence  of  a  much  more  positive 
character. 

When  a  serous  fluid  is  obtained,  it  is  sometimes  of  importance  to 
determine  by  the  examination  of  this  fluid  whether  it  be  an  exudate 
or  a  transudate  (in  cases  where  the  determination  is  impossible  by 
other  means).  This  may  be  done  by  estimating  the  quantity  of  con- 
tained proteid,  determining  the  specific  gravity  and  the  number  of 
leukocytes,  and  demonstrating  the  presence  of  a  proteid  which  is  pre- 
cipitated by  acetic  acid. 

The  proteid  contained  in  the  fluid  withdrawn  is  most  accurately  esti- 
mated by  weighing  the  precipitated  proteid  according  to  the  method 
mentioned  upon  p.  505  for  the  urine.  Esbach's  method,  although  rea- 
sonably accurate  for  urinary  examination  (p.  505  et  seq.)  is  not  applicable 
for  serous  fluid.  A  very  large  number  of  statements  are  to  be  found  in 
literature '  upon  the  proteid  content  of  exudates  and  transudates.  The 
various  authors  practically  agree  that  hydropic  transudates  contain  much 
less  proteid  than  inflammatory  exudates.  Nevertheless  most  observers 
contend  that  the  distinction  is  not  sufficiently  sharp,  and  that  the  rules 
are  not  sufficiently  general  in  their  application  to  permit  of  a  differential 

'  Compare  for  example  Vierordt,  Daten  und  Tahellen,  1888 ;  Bernheim,  Virchow's 
Archiv,  vol.  cxxxvii.,  and  othere. 


EXPLORATORY  PUNCTURES.  711 

diagnosis  between  exudates  and  transudates.  Runeberg/  however,  con- 
tends very  emphatically  that  the  proteid  content  in  serous  fluid  is  of 
distinct  diagnostic  significance.  He  believes  that  the  difficulties  which 
have  'thus  far  militated  against  the  diagnostic  importance  of  the  proteid 
content  mainly  depend  upon  the  fact  that  various  observers  have  con- 
trasted merely  inflammatory  with  hydropic  affections^  whereas  in  reality 
the  distinction  must  also  be  made  between  (a)  congestion  transudates 
and  (6)  hydremic  transudates.  Besides,  these  authors  have  not  heeded 
the  possibility  of  a  combined  origin  for  these  exudates,  and  have  not 
taken  the  trouble  to  diagnose  such  causes.  Runeberg  considers  that  his 
experience  shows  that  the  estimation  of  the  proteid  content  of  the  fluid 
is  very  essential  in  the  diagnosis  of  such  combined  forms.  He  deter- 
mined the  proteid  content  as  from  4  to  6  per  cent,  in  inflammatory 
exudates  (including  tuberculosis  and  carcinoma  of  the  serous  mem- 
branes) ;  whereas  the  proteid  content  in  pure  congestion  transudates 
varied  between  1  and  3  per  cent.,  and  in  pure  hydremic  transudates  from 
0.1  to  0.3  per  cent.,  scarcely  ever  exceeding  0.5  per  cent.  These  figures 
may  be  employed  in  the  diagnosis  of  fresh  effiisions,  without  any  further 
■criticisms  ;  but  in  order  to  prevent  incorrect  conclusions  it  should  be 
remembered  that  the  proteid  content  falls  after  a  time  in  old  congestion 
transudates  where  they  are  under  high  pressure,  where  they  are  under- 
going absorption,  or  where  changes  in  the  serous  membranes,  nearly 
related  to  inflammatory  changes,  are  developed  under  the  influence  of 
chronic  congestions  (connective-tissue  sclerosis,  endothelial  disintegra- 
tion). In  such  cases  we  are  in  reality  dealing  with  combined  forms, 
and  their  occurrence  will  explain  most  of  the  apparent  contradictions  to 
the  above-mentioned  rules. 

These  combined  forms  are  naturally  much  more  difficult  to  classify ; 
but  as  a  matter  of  fact  the  proteid  content  of  the  fluid  really  enables  us 
at  least  frequently  to  analyze  clinically  such  a  disease  picture,  and  is 
especially  valuable  in  the  determination  of  the  proper  therapy.  Alter- 
ations of  the  proteid  content  during  the  same  clinical  observation  may 
furnish  valuable  conclusions.  For  example,  they  may  suggest  the 
appearance  of  a  carcinomatous  peritonitis  as  a  complication  of  a  portal 
stasis  produced  by  carcinotna,  or,  again,  the  addition  of  congestion  to 
a  pure  renal  hydrops.  The  great  difficulty  in  practically  employing 
these  important  facts  is  the  complexity  of  an  exact  quantitative  pro- 
teid estimation ;  it  is  too  difficult  for  bedside  work.  To  overcome 
this  difficulty  Runeberg  has  adopted  a  method  which,  although  it  does 
not  estimate  the  proteid  content  exactly,  at  the  same  time  is  suffi- 
ciently accurate  for  the  purpose  in  view.  He  adds  a  few  drops  of 
nitric  acid  to  the  withdrawn  fluid  in  a  reagent  glass,  and  then  judges  by 
the  shape  and  consistence  of  the  precipitate.  In  exudates  which  depend 
upon  a  local  afi^ection  of  the  serous  membrane  (inflammation,  tubercu- 
losis, carcinoma),  the  precipitate  forms  thick,  heavy  plaques  which 
quickly  sink   to   the  bottom  of  the  glass  ;    in   congestion  transudates, 

^  "  Von  der  diagnostischen  Bedeutung  des  Eiweissgehaltes  in  pathologischen  Trans- 
und  Exsadaten,"  Berlin,  klin.  Woch.,  1897,  No.  33. 


712  EXPLORATORY  PUNCTURES  AND  HARPOONING. 

abundant  large  flocculi,  which  ordinarily  sink  to  the  bottom  also, 
but  which  are  more  loosely  and  more  lightly  precipitated ;  in  pure 
hydremic  transudates,  merely  a  decided  opalescence  or  small,  loose 
flakes  which  float  for  a  long  time  in  the  fluid.  Evidently  a  certain  per- 
sonal experience,  acquired  from  sharply  defined  cases,  is  essential  for 
correctly  differentiating  the  mixed  forms.  Runeberg  also  emphasizes  in 
the  differentiation,  in  addition  to  the  proteid  content,  the  reaction  with 
acetic  acid  (see  below). 

The  specific  gravity  of  serous  fluids  is  approximately  proportional  to 
the  proteid  content,  and  may  therefore  be  utilized  for  the  approximate 
percentage  of  the  latter.  According  to  Ruess,^  the  following  figures 
represent  the  relation  between  the  specific  gravity  and  proteid  content : 

Specific  gravity.  Proteid  content. 

1018 higher  than  4.0  per  cent. 

1015 lower  than  2.5 

1012 "         "  1.5  to  2.0       " 

1010 "        "  1.0  to  1.5       " 

1U08.8 "         "  0.5  to  1.0        " 

An  ordinary  urinometer  (p.  451)  is  sufficiently  accurate  and  the  most 
convenient  instrument  to  employ  for  estimating  the  specific  gravity.  A 
sufficient  quantity  of  fluid  is  obtained,  before  the  needle  is  withdrawn, 
by  repeated  suction  and  emptying  of  the  syringe.  If  necessary  the 
specific  gravity  may  also  be  estimated  from  a  smaller  quantity  of  fluid 
by  the  pyknometric  method  described  for  the  blood  at  p.  612,  or  by 
Hammerschlag's  method,  although  the  latter  procedure  is  more  difficult. 

It  is  probable  that  on  the  number  of  leukocytes  or  the  quantity  of 
their  products  of  decomposition  in  a  fluid  obtained  by  aspiration 
depends  the  amount  of  contained  proteid  which  is  precipitated  by 
acetic  acid.  The  demonstration  of  this  proteid  was  first  shown  by 
Primavera  and  Rivalta  ^  to  possess  a  certain  importance  for  the  differen- 
tiation between  exudates  and  transudates.  An  abundance  of  this 
proteid  is  evidence  in  favor  of  an  inflammatory  exudate  and  against  a 
transudate.  Rivalta's  test  is  performed  in  the  following  manner  :  An 
exceedingly  dilute  aqueous  solution  of  acetic  acid  (2  drops  of  glacial 
acetic  acid  to  200  c.c.  of  water)  is  prepared,  and  a  drop  of  the  fluid  to 
be  examined  is  allowed  to  fall  into  this  solution  from  a  glass  rod.  If 
the  fluid  contain  a  considerable  quantity  of  the  substance  in  question, 
the  drop  immediately  sinks  to  the  bottom  of  the  acid  solution,  producing 
a  turbidity  resembling  a  cloud  of  cigar  smoke.  If  the  questionable 
substance  be  absent  no  turbidity  appears  ;  if  present  in  slight  amount 
the  cloudiness  is  very  slight  and  of  gradual  develojmient.  Following 
the  suggestion  of  Paijkull,  Runeberg  demonstrates  the  presence  of  this 
substance  simply  by  the  addition  of  a  few  drops  of  acetic  acid  to  the 
fluid.  In  inflammatory  exudates  a  more  or  less  marked  turbidity 
appears,  while  in  transudates  this  is  very  slight  or  entirely  absent.  The 
nature  of  this  substance  is  still  under  discussion.  Rivalta  formerly 
believed  it  to  he  nucleo-albumin,  but  now  ^  regards  it  as  a  mixture  of 

^  Of.  Vierordt,  Daten  und  Tubellen,  1888.  ^  Riforma  med.,  April,  1895. 

3  Policlinico,  1904. 


EXPLORATORY  PUNCTURES.  713 

euglobulin  (paraglobulin)  and  pseudoglobulin.  Umber  ^  thinks  it  is  a 
mucin,  and  designates  it  as  serosamucin,  while  Staheliu  ^  arrives  at  the 
conclusion  that  it  is  related  more  closely  to  the  globulins  than  to  the 
mucins.  It  would  seem  that  the  different  authors  are  not  working  with 
the  same  substance,  since  Rivalta,  for  example,  expressly  states  that  it 
is  soluble  in  a  slight  excess  of  acetic  acid,  while  Umber  declares  the 
opposite  to  be  the  case. 

Another  important  criterion  for  the  inflammatory  origin  of  a  serous 
fluid  is  its  content  of  fibrin  ferment,  which  is  manifested  by  the  sponta- 
neous formation  of  fibrin  either  before  or  after  the  withdrawal  of  the  fluid. 

The  presence  of  biliary  pigment  in  the  fluid  may  also  be  important, 
particularly  so  when  the  biliary  passages  perforate  into  the  peritoneal 
or  pleural  cavities.  In  addition  to  the  characteristic  yellowish-brown 
or  greenish  discoloration,  the  reactions  for  the  biliary  pigments  may  be 
demonstrated  by  the  same  methods  as  those  employed  for  the  urine. 

For  a  hacteriologio  examination  of  aspirated  fluid  the  culture  method 
is  to  be  recommended,  because  with  serous  fluids  an  ordinary  micro- 
scopic examination  rarely  furnishes  a  positive  result.  With  a  purulent 
exudate,  except  with  purulent  tuberculosis,  the  ordinary  stick  or  streak 
inoculation  frequently  furnishes  positive  results ;  but  with  serous  exu- 
dates, w^hich  contain  very  few  micro-organisms,  a  much  larger  amount  of 
fluid  must  be  employed  for  inoculation,  just  as  in  the  bacteriologic  exam- 
ination of  the  blood  (see  p.  652).  A  number  of  drops,  from  5  to  10,  may 
be  squirted  from  the  syringe  directly  into  culture  tubes  with  agar-agar 
gelatin  bouillon.  Plate  cultures  may  be  employed,  as  is  mentioned  in 
the  examination  of  the  blood.  In  regard  to  the  technic  of  culture- 
making,  text-books  on  bacteriology  should  be  consulted. 

Gas  as  well  as  fluid  is  sometimes  withdrawn  in  punctures ;  for  ex- 
ample, in  abdominal  punctures  when  the  point  of  the  needle  penetrates 
the  stomach  or  the  intestines,  in  pyopneumothoraces,  and  in  abscesses 
which  contain  gas.  This  finding  may  have  some  diagnostic  signifi- 
cance, but  only  when  we  are  sure  that  the  gas  was  aspirated  through 
the  needle  and  that  it  was  not  admitted  through  an  imperfect  fitting  of 
the  syringe. 

In  addition  to  the  determination  of  the  presence  of  fluid  collections, 
as  well  as  their  peculiarities  and  characteristics,  exploratory  punctures 
are  especially  important  in  order  to  decide  upon  the  spot  for  attempting 
therapeutic  punctures.  Immediately  before  any  therapeutic  puncture  we 
should  demonstrate  the  presence  of  fluid  by  an  exploratory  puncture 
exactly  at  the  spot  to  be  selected,  and  should  demonstrate  the  free 
mobility  of  the  puncture  needle  in  a  cavity.  Otherwise  we  run  a 
danger  of  causing  some  injury  in  a  therapeutic  puncture  with  the  coarse 
and  much  more  injurious  instruments  should  we  penetrate,  for  example, 
local  adhesions  of  the  lungs  or  heart,  or  in  abdominal  punctures  an  over- 
lying full  intestinal  coil. 

'  Zeifs.f.  klin.  Med.,  vol.  xlviii.,  parts  v.  and  vi.,  yt.  364. 
2  3Iunch.  med.  Wock,  1902,  p.  34. 


714  EXPLORATORY  PUNCTURES  AND  HARPOONING. 

CYTODIAGNOSIS. 

A  method  of  investigation  rejoicing  in  the  promising  title  of  cytodiagnosis 
has  recently  been  introduced  by  French  writers,  particularly  by  Widal  and  his 
pupils.  It  consists  of  the  study  of  the  character  and  number  of  the  cellular 
constituents  of  exudates  and  transudates,  and  of  subsequent  deductions  from 
these  studies  as  to  the  nature  of  the  fluids. 

The  sediment  obtained  by  gravity  or  centrifugation  is  either  subjected  to 
direct  microscopic  observation,  or  when  greater  accuracy  is  required,  is  utilized 
for  the  preparation  of  cover-glass  specimens.  In  such  dry  preparations  the  rela- 
tive numbers  of  the  different  varieties  of  cells  may  be  observed,  particularly  of 
the  leukocytes.  For  this  purpose  the  movable  stage  or  Ehrlich's  ocular  dia- 
phragm (p.  644)  may  be  employed. 

If  the  exudate  coagulate  rapidly  soon  after  its  withdrawal,  Widal  advises  that 
the  coagula  be  broken  up  by  agitation  Avith  glass  beads  before  centrifugation. 
It  is  doubtful  whether  accurate  results  are  obtained  by  this  procedure,  since  a 
great  many  of  the  cellular  elements  will  always  remain  embedded  in  the  coagula. 
Instead  of  utilizing  this  procedure,  the  writer  has  several  times  prevented  the 
coagulation  of  the  fluid  by  aspirating  it  into  a  syringe  half-fllled  with  ammo- 
nium oxalate  solution  or  leech  infusion.  The  ammonium  oxalate  solution  con- 
sisted of  2  parts  of  ammonium  oxalate  to  1000  parts  of  normal  saline  solution. 
The  leech  infusion  was  prepared  by  cutting  the  head  of  a  leech  into  small  pieces 
and  rubbing  them  up  in  a  mortar.  This  mixture  was  then  diluted  with  cold 
normal  saline  infusion,  allowed  to  stand  for  an  hour,  during  which  time  it  was 
frequently  stirred,  and  finally  filtered.  Instead  of  this  infusion,  physiologic 
saline  solution  to  which  a  small  amount  of  hirudin  (1  mg.  to  a  few  cubic  centi- 
meters) has  been  added  may  also  be  employed.  The  employment  of  these  agents 
preventing  coagulation  is  to  be  particularly  recommended  when  the  sediment  is 
obtained  by  gravity  rather  than  by  centrifugation,  since  in  the  necessary  interval 
some  of  the  leukocytes  may  become  disintegrated  and  be  caught  in  the  fibrin 
network. 

The  morphologic  elements  demanding  our  attention  in  cytodiagnosis  are: 
erythrocytes,  the  various  kinds  of  leukocytes,  endothelial  or  epithelial  cells,  and 
the  cells  of  tumors. 

The  microscopic  study  of  the  erythrocytes  furnishes  but  little  additional 
information  to  that  obtained  by  a  macroscopic  inspection  of  the  fluid.  The 
presence  of  blood  may  be  demonstrated  also  by  chemical  means  (for  methods 
employed  see  section  upon  Urinary  Examination),  but  the  microscopic  demon- 
stration is  a  more  refined  diagnostic  procedure.  Large  quantities  of  blood  are 
found  in  carcinomatous,  tubercular,  and  nephritic  exudates,  in  the  transudates 
of  marked  venous  congestion,  and  in  all  of  the  hemorrhagic  diatheses. 

The  literature  of  cytodiagnosis  is  already  quite  extensive,  and  the  greatest 
discussion  has  been  in  reference  to  the  leukocytes  contained  in  the  fluid.  It  is 
to  be  supposed  a  priori  that  a  large  number  of  leukocytes  speaks  for  an  inflam- 
matory origin  of  the  particular  fluid,  and  that  the  number  of  leukocytes  is  pro- 
portional to  the  intensity  of  the  inflammation,  as  may  be  easily  verified  by 
studying  the  occurrence  of  suppuration  in  any  serous  exudate.  Cytodiagnosis, 
however,  has  gone  much  farther,  and  just  as  certain  blood-pictures  have  been 
accepted  as  characteristic  of  certain  diseases  of  the  blood  and  hematopoietic 
organs,  definite  cytodiagnostic  formulas,  based  upon  the  nature  and  relative 
numbers  of  the  leukocytes  contained  in  the  fluid  in  a  cavity,  have  been  sug- 
gested for  the  diagnosis  of  the  underlying  disease  process.  This  is  particularly 
noticeable  in  the  attempts  that  have  been  made  to  differentiate  tubercular  exu- 
dates, non-tubercular  exudates,  and  the  exudates  of  malignant  tumors,  from  the 
relative  numbers  of  the  polynuclear  and  mononuclear  elements. 

It  would  seem  that  these  efforts  have  gone  too  far,  and  that  the  empiric  or 
statistic  findings  have  not  been  tested  by  our  knowledge  of  general  pathology. 
Although  we  know  that  the  emigration  of  polynuclear  leukocytes  is  one  of  the 
essential  characteristics  of  inflammation,   it  has  not  yet  been  decided  whether 


EXPLORATORY  PUNCTURES.  715 

mononuclear  cells  or  leukocytes  ever  pass  out  of  the  blood-vessels.  It  is  gen- 
erally supposed  that  by  far  the  greater  number  of  the  mononuclear  cells  are  the 
result  of  regenerative  processes  which  are  associated  with  aud  consecutive  to  the 
inflammation,  and  that  they  originate  in  the  lymphoid  tissue  which  is  found  dis- 
seminated throughout  almost  all  of  the  viscera. 

If  we  abandon  the  crude  empiric  or  statistic  standpoint  from  which  the  question 
of  cytodiagnosis  is  usually  considered,  and  which  leads  to  erroneous  conclusions 
because  it  does  not  lay  sufficient  stress  upon  the  difierent  stages  and  degrees  of  the 
inflammatory  process,  it  would  seem  that  a  large  number  of  polynuclear  cells  is 
indicative  of  marked  and  recent  inflammations,  while  a  considerable  quantity  of 
mononuclear  elements  signifies  either  a  milder  degree  and  later  stage  of  an  inflam- 
mation or  the  presence  of  a  non-inflammatory  process. 

Accepting  this  general  view,  we  shall  readily  understand  that  a  preponderance 
of  mononuclear  cells  has  generally  been  found  in  tubercular  exudates.  This  is 
explained  by  the  fact  that  these  tubercular  exudates  are  usually  of  insidious  develop- 
ment and  accompanied  by  a  slightly  marked  inflammatory  process.  Many  of  them 
may  be  transudates  resulting  from  local  disturbances  of  the  circulation,  in  which 
there  is  an  admixture  of  the  mononuclear  cells  of  the  tubercular  proliferation.  In 
this  connection  it  should  not  be  forgotten  that  the  tubercle  is  not  an  inflammation, 
although  it  may  excite  a  more  or  less  marked  inflammation  in  its  vicinity.  It  has 
also  been  established  that  acute  tubercular  inflammations  of  the  j^leura  and  of  the 
peritoneum  may  furnish  exudates  in  which  there  is  a  preponderance  of  polynuclear 
cells.  Upon  the  other  hand,  in  the  later  stages  of  non-tubercular  inflammations 
of  the  serous  membranes,  it  is  undoubtedly  true  that  the  mononuclear  cells  are  in 
the  majority. 

It  consequently  seems  to  the  author  that  the  predominance  of  either  variety 
of  cell  in  an  exudate  is  less  indicative  of  the  etiology  of  the  inflammation  than  it 
is  of  its  stage  and  severity.  It  is  a  fact  that  mononuclear  cells  predominate  in 
the  majority  of  pleuritic  inflammations  of  unknown  origin;  but  if  we  assume 
from  this  that  tubercular  pleurisy  is  much  more  frequent  than  was  formerly  sup- 
posed, we  base  our  assumption  upon  something  which  remains  to  be  proved,  and 
which,  in  fact,  cannot  be  proved — namely,  that  a  preponderance  of  mononuclear 
cells  is  pathognomonic  of  tubercular  exudates.  What  is  true  of  pleural  and 
peritoneal  exudates  is  also  true  of  exudates  in  other  cavities,  and  particularly  so 
of  the  cerebrospinal  fluid. 

A  great  obstacle  to  the  utilization  of  cytodiagnostic  findings  is  that  the  fluid 
obtained  by  aspiration  by  no  means  accurately  represents  the  characteristics  of 
the  same  fluid  within  the  body  and  at  the  moment  of  its  origin.  It  is  well  known 
that  the  cellular  elements  of  a  fluid  may  be  so  influenced  by  sedimentation 
within  the  body  that  a  serous  fluid  may  be  obtained  by  exploratory  puncture, 
although  a  complete  evacuation  of  the  accumulation  might  demonstrate  its  puru- 
lent character  (see  footnote,  p.  709).  Since  the  various  kinds  of  leukocytes 
sediment  with  different  degrees  of  rapidity  dependent  upon  their  variations  in 
size,  it  also  follows  that  we  cannot  always  depend  upon  their  relative  numbers 
as  determined  by  a  study  of  the  evacuated  fluid.  The  excessive  formation  of 
fibrin  may  also  modify  the  findings,  as  a  variable  number  of  leukocytes  are 
required  to  produce  coagulation  and  still  others  are  caught  in  the  fibrinous 
masses,  and  it  is  by  no  means  necessary  that  all  varieties  of  the  leukocytes  should 
be  implicated  in  the  same  proportions. 

All  these  reasons  lead  the  author  to  regard  the  conclusions  obtained  by  cyto- 
diagnosis as  very  deceptive,  and  to  state  that  they  should  never  be  employed  as 
the  sole  foundation  of  a  diagnosis.  In  his  opinion  the  establishment  of  rigid 
cytodiagnostic  formulas  is  as  much  opposed  to  our  knowledge  of  general  path- 
ology as  it  is  to  the  first  commandment  of  clinical  diagnosis — that  we  should 
diagnose  from  all  of  the  symptoms  and  never  from  a  single  one.  Cytodiagnosis, 
like  many  other  modern  methods  of  investigation,  rejoices  in  a  loud-sounding 
title,  which  causes  us  to  forget  that  it  has  to  do  only  with  the  establishment  of  a 
single  symptom,  and  it  has  consequently  awakened  false  hopes  which  will  never 
be  realized.     These  conclusions  have  been  forced  upon  the  author  both  by  his 


716  EXPLORATORY  PUNCTURES  AND  HARPOONiyO. 

own  experience  and  also  by  the  contradictory  results  obtained  by  means  of  cyto- 
diagnosis  as  they  have  been  published.^ 

We  must  be  equally  cautious  in  basing  conclusions  upon  the  presence  of 
endothelial  or  epithelial  cells  in  the  fluids  obtained  by  aspiration.  Their  presence 
is  indicative  only  of  the  desquamation  of  these  elements,  and  such  desquamation 
may  be  due  to  the  most  varied  influences.  They  are  found  unassociated  with 
leukocytes  chiefly  in  transudates,  although  they  may  also  occur  in  inflammations, 
particularly  when  the  process  is  not  sufficiently  acute  to  produce  large  amounts 
of  fibrin,  which  would  destroy  or  entangle  them  in  its  meshes.  We  must  also 
remember  that  the  differentiation  of  certain  forms  of  mononuclear  leukocytes 
from  isolated  endothelial  cells  is  by  no  means  certain  with  the  methods  of  inves- 
tigation now  at  our  command,  particularly  since  the  cells  in  an  exudate  are  sub- 
ject to  manifold  changes  produced  by  osmosis  and  other  causes. 

The  demonstration  of  specific  tumor  cells  is  very  important  for  the  diagnosis 
of  exudates  dependent  upon  the  presence  of  malignant  gro\\1:hs.  They  may 
sometimes  be  recognized  when  they  are  present  in  large  numbers  and  when  their 
mutual  relations  are  undisturbed,  but  we  must  not  forget  that  they  are  some- 
times isolated  ;  and  that,  upon  the  other  hand,  normal  endothelial  cells  may  be 
held  together  by  fibrin,  causing  them  to  simulate  particles  of  tumors.  Isolated 
tumor  cells  may  occasionally  be  recognized  by  their  abnormal  size  and  manifold 
outlines,  but  their  differentiation  from  normal  endothelial  cells  is  nevertheless 
most  uncertain. 

OSMOTIC  PRESSURE  OF  FLUIDS  OBTAINED  BY  PUNCTURE. 

The  osmotic  pressure  of  these  fluids  is  obtained  in  a  manner  similar  to  that 
employed  for  the  blood  (see  pp.  546  et  seq.  and  667).  This  method  of  study  has 
not  been  crowned  by  practical  results.  Ketly  and  Torday^  state  that  exudates 
and  transudates  cannot  be  diflferentiated  by  variations  in  their  osmotic  pressure. 
It  may  be  said,  however,  that  the  lower  the  osmotic  jjressure  of  an  exudate  or 
transudate  as  compared  with  that  of  the  blood,  the  greater  is  the  likelihood  of 
the  speedy  absorption  of  the  fluid.  In  reference  to  the  freezing-points  of  these 
pathologic  fluids,  it  may  be  stated  that  they  are  exceedingly  variable,  and  may  be 
far  above  or  below  that  of  the  blood.  This  is  due  not  only  to  the  initial  differ- 
ences in  the  qualities  of  the  particular  fluids,  but  also  to  the  different  stages  of 
osmotic  interchange  at  which  they  are  obtained. 

Despite  Prof.  Sahli's  logical  objections  to  the  clinical  value  of  cytodiagnosis, 
the  editors  insert  in  the  following  a  note  which  was  prepared  by  Dr.  Musgrave 
for  the  translation  of  the  last  edition. 

DIAGNOSTIC  VALUE  OF  PLEURAL  FLUIDS. 

In  the  last  three  years  many  investigators  in  Europe  have  done  a  large  amount 
of  work  with  reference  to  determining  the  cause  of  pleural  effusions,  and  two 
new  and  valuable  methods  of  investigation  have  been  published. 

In  1900  Widal  and  Ravaut  published  the  results  of  their  researches  based 
upon  the  differential  enumeration  of  the  white  blood-corpuscles  and  endothelial 
cells  found  in  the  sediments  of  serous  fluids,  and  as  a  result  have  formulated  the 
following  laws,  or  so-called  cytologic  formulas  : 

1.  A  predominance  of  lymphocytes  means  a  tubercular  effiision. 

2.  A  predominance  of  polynuclear  leukocytes  means  an  effiision  of  an  acute 
infectious  origin. 

3.  A  large  number  of  endothelial  cells,  occurring  especially  in  sheets  or 
plaques,  means  a  mechanical  eff'usion  or  transudate. 

They  also  divide  tuberculous  pleurisy  into  two  classes  :  the  primary  form, 
in  which  there  are  no  discoverable  lesions  of  the  lungs,  and  the  secondary  form, 
resulting  from  an  underlying  tuberculous  lung  focus. 

'  See  the  comprehensive  presentation  of  Brion,  Centmlhl.  f.  allg.  Path.,  vol.  siv., 
p.  609,  1908.  -  ArcJi.f.  klin.  Med.,  vol.  Ixxix. 


KXPL  OR  A  TOR  Y  P  UNCTURES. 


717 


In  the  secondary  variety  the  lymphocytic  formula,  as  seen  in  the  primary 
form,  does  not  usually  hold  good,  but  instead  the  sediment  is  almost  entirely  com- 
posed of  necrotic  cells  and  detritus.     Of  the  distinguishable  cells,  a  large  proper- 


% 

1 

, 

• 

• 

• 

• 
• 

• 
• 

• 

•  , 

• 

m 

• 

• 

• 
• 

Fig.  269.— Lymphocytosis  :  Case  of  primary  tuberculous  pleurisy  (Percy  Musgrave ;  photographed 

by  L.  S.  Brown). 

tion  may  be  polynuelear.  This  difference  is  probably  due  to  a  mixed  infection. 
Of  the  acute  infectious  varieties,  they  note  those  due  to  the  pneumococcus, 
streptococcus,  and  staphylococcus.  In  the  pneumococcus  variety  they  described 
the  occurrence  of  considerable  numbers  of  large  cells  having  phagocytic  prop- 


FiG.  270.— Acute  Infectious  pleurisy,  showing  polynuelear  leukocytes  and  large  phagocytic 
endothelial  cells  (Percy  Musgrave;  jjhotographed  by  L.  S.  Brown). 


erties.     In   the  streptococcus  variety  these  cells  are  comparatively  few  in  num- 
ber, and  the  percentage  of  polynuelear  leukocytes  is  greater. 

These  formulas  have  been  extensively  investigated  by  numerous  observers, 
especially  in  France,  and  to  a  lesser  extent  in  Germany,  and  have  in  the  main 


718 


EXPLORATORY  PUNCTURES  AND  HARPOONING. 


been  found  correct.  Certain  modifications,  however,  must  be  taken  in  consider- 
ation. The  chief  of  these  modifications,  which  has  been  pointed  out  especially 
by  Naunyn,  is  that  lymphocytes  may  also  predominate  in  transudates  of  long- 
standing or  near  the  end  of  an  acute  infectious  case  where  the  process  is  subsid- 
ing or  where  the  infection  is  a  very  mild  one.  The  specific  gravity  and  the 
amount  of  albumin  aid  us  in  eliminating  the  first  mentioned  of  these  conditions, 
and  the  clinical  evidence  usually  gives  a  clue  to  the  nature  of  the  process  in  the 
second.      Both  of  these  conditions  are  rarely  met. 

In  the  first  week  or  ten  days  of  a  tuberculous  effusion  polynuclear  elements 
may  predominate,  but  these  rapidly  disappear  and  give  place  to  a  purely  lympho- 
cytic formula. 

The  phagocytic  cells  mentioned  above  as  occurring  especially  in  the  cases  of 
pneumococcus  origin  are  of  very  large  diameter  as  compared  with  the  other  ele- 
ments occurring  in  the  sediment,  and  the  writer  has  frequently  found  that  they 
measure  as  much  as  20  ^.  These  cells  frequently  contain  partly  digested  poly- 
nuclear and  other  cellular  elements,  which  can  easily  be  seen  included  in  their 
protoplasm.  Their  occurrence  in  large  or  increasing  numbers  is  usually  a  good 
prognostic  sign  ;  and  their  absence,  together  with  the  presence  of  bacteria,  is 
usually  a  warning  of  approaching  empyema.'    From  the  observations  which  the 


Fig.  271. 


-Endothelial  cells  from  a  pleural  transudate  due  to  cardiac  disease  (Percy  Musgrave; 

photographed  by  L.  S.  Brown). 


writer  has  been  able  to  make,  the  presence  of  polynuclears  in  a  proportion  of  over 
90  per  cent. ,  and  the  presence  of  bacteria  in  most  cases,  precedes  an  empyema  by 
only  a  few  days. 

Little  need  be  said  of  the  formula  for  the  transudates  except  that  the  diag- 
nosis is  occasionally  complicated  by  the  presence  of  a  considerable  amount  of 
blood,  which  raises  the  specific  gravity  and  the  amount  of  albumin.  This  blood 
is  usually  accidental. 

In  addition  to  these  three  classes  of  fluids  we  have  the  cancerous  cases. 
These  are  difiicult  to  diagnose,  since  the  majority  of  pathologists  agree,  the 
writer  thinks,  in  saying  that  it  is  difiicult  to  differentiate  the  so-called  cancer 
cells  from  endothelium,  unless  actual  pieces  of  the  cancerous  tissue  can  be 
isolated.  The  iodin  reaction  (showing  glycogenic  degeneration)  was  thought  at 
one  time  to  be  suggestive  of  the  cancer  cells,  but  this  reaction  is  very  commonly 
seen  in  the  endothelial  cells  of  simple  transudates  and  in  other  conditions  where 
endothelium  is  found. 

The  few  cases  of  cancer  that  the  writer  has  been  able  to  study  have  shown  a 
high  specific  gravity,  1018  or  over,  and  an  albumin  content  of  over  1.5  per  cent. 
The  sediment  has  shown  many  more  endothelial  cells  than  are  found  in  the 
tuberculous  cases,  and  these  cells  are  often  found  in  plaques,  which  is  very  rare 


EXPLORATORY  PUNCTURES.  719 

in  tuberculosis.  Tliere  is  usually  a  much  larger  number  of  lymphocytes  pro- 
portionally than  in  the  simple  transudates. 

In  addition  to  the  above  method  of  investigating  pleural  fluids,  to  which  the 
writers  have  given  the  name  Cytodiagnosis,  Jousset  has  published  a  new  pro- 
cedure for  the  detection  of  tubercle  bacilli  in  these  fluids,  to  which  he  has  given 
the  name  of  Inoscopy,  and  which  is  of  value  in  some  cases. 

The  technie  of  cytodiagnosis  is  as  follows :  The  fluid  should  be  drawn 
with  the  usual  aseptic  precautions  into  sterilized  flasks  or  tubes.  If  it  is  already 
clotted  when  received  for  examination,  it  should  be  shaken  and  stirred  with  a 
glass  rod  until  the  clot  is  thoroughly  contracted,  and  the  clot,  or  all  clots  of 
large  size,  should  be  removed.  This  is  necessary  because  some  of  the  cellular 
elements  are  entangled  in  the  fibrinous  meshes,  and  by  contraction  of  the  clot 
are  set  free.  Widal  and  Ravaut  accomplished  the  process  of  defibrination  by 
placing  sterilized  glass  pearls  in  the  flask  and  shaking  the  fluid  thoroughly. 
This  the  writer  does  not  believe  is  essential  for  an  accurate  differential  estimate 
of  the  cellular  elements.  The  fluid  is  then  placed  in  centrifuge  tubes  and  centri- 
fugalized  for  five  minutes,  at  least.  The  supernatant  fluid  is  decanted  gently  at 
first,  and  when  only  a  small  amount  remains  the  tube  is  inverted  for  a  few 
seconds.  A  few  drops  will  adhere  to  the  side.  The  sediment  is  stirred  thor- 
oughly with  a  small  platinum  loop,  the  sides  of  the  glass  being  rubbed  to  remove 
adherent  portions.  When  the  sediment  is  thoroughly  mixed  with  the  few  drops 
of  fluid  remaining  after  decantation,  a  drop  of  the  mixture  is  removed  with  the 
platinum  loop,  and  a  cover-slip  smear  made.  This  is  allowed  to  dry  sponta- 
neously or  by  gently  heating  the  preparation.  (Heating  at  the  boiling-point 
will  spoil  the  preparation.) 

Many  methods  of  fixing  and  staining  these  preparations  have  been  used  by 
the  various  investigators.  Alcohol,  ether,  chloroform  vapor,  and  osmic  acid  have 
been  used  as  fixative  agents.  Ehrlich's  triple  stain,  hemotoxylin  and  eosin, 
methylene-blue  and  eosin,  Loffier's  blue,  and  a  great  variety  of  other  stains  have 
been  employed.  Some  writers  have  maintained  that  careful  differential  staining 
is  not  essential,  but  from  the  writer's  observations  he  cannot  agree  with  them, 
for  the  reason  that  careful  differential  staining  of  the  protoplasm  and  granules  of 
the  polynuclear  elements  is  essential,  since  the  nuclei  of  these  elements  are  often 
globular  when  the  cell  is  degenerated,  and  they  may  be  mistaken  for  lymphocytes. 

The  method  of  staining  which  has  given  the  best  results  in  the  hands  of  the 
writer  is  practised  as  follows  : 

Cover  the  preparation  with  a  staining  fluid  composed  of : 

Wright's  blood-stain 3  parts; 

Pure  methylalcohol 1  part. 

Allow  this  mixture  to  remain  on  the  preparation  twenty  to  forty-five  seconds, 
then  dilute  it  with  8  or  10  drops  of  water,  and  allow  it  to  stand  one  to  two 
minutes.  Wash  very  gently,  preferably  by  flooding  the  slide  with  a  dropper. 
Do  this  four  or  five  times,  allowing  the  water  to  remain  on  the  slide  a  few  seconds 
each  time.  Vigorous  or  forcible  washing  will  destroy  the  film  and  sijoil  the 
preparation.  Dry  the  preparation  by  holding  it  between  the  thumb  and  fore- 
finger and  waving  it  through  the  Bunsen  or  alcohol  flame.  Do  not  attempt  to 
blot  the  preparation  or  heat  it  above  the  temperature  which  the  fingers  will  bear. 
Mount  in  xylolbalsam  and  examine  with  an  oil-immersion  lens. 

Inoscopy  is  practised  as  follows  : 

1.  The  fluid  should  be  drawn  with  aseptic  precautions  into  sterilized  flasks 
(Erlenmeyer  flasks  preferably).  At  least  100  c.c.  should  be  taken,  although 
results  may  sometimes  be  obtained  with  much  smaller  amounts.  Allow  the  fluid 
thus  taken  to  clot. 

2.  Shake  the  fluid  gently  to  contract  the  clot  as  much  as  possible  and  then 
wash  it,  on  a  piece  of  sterile  linen  or  fine  gauze  wrapped  over  the  end  of  a  fiinnel, 
until  all  the  serum  is  washed  away. 


720  EXPLORATORY  PUNCTURES  AND  HARPOONING. 

3.  Remove  tlie  clot  or  clots  with  a  sterile  spatula,  and  place  them  in  a  small 
flask  with  suflicient  of  the  following  fluid  to  digest  them : 

Pepsin 2  gm. ; 

Pure  glycerin, 

Strong  HCl da    10  c.c. ; 

Sodium  fluorid 3  gm. ; 

Distilled  water 2000  c.c. 

The  necessary  amount  of  this  fluid  will  vary,  of  course,  with  the  size  of  the 
clot  to  be  digested,  but  in  most  cases  20  or  30  c.c.  are  suflicient.  A  freshly 
prepared  pepsin  (HCl  solution)  apparently  serves  as  well  as  the  above  fluid,  but 
will  not  keep  on  standing  as  the  above  fluid  does. 

4.  Place  the  above  preparation  in  the  incubator  or  oven  until  the  clot  is 
digested.  A  temperature  of  37°  C.  for  two  or  three  hours  will  sufiice,  but  the 
time  is  shortened  if  it  is  kept  at  a  temperature  of  50°  C. 

5.  When  the  clot  has  disappeared,  pour  the  mixture  into  centrifuge  tubes 
and  centrifugalize  for  five  to  ten  minutes.  Decant  the  supernatant  fluid  as 
described  under  Cytodiagnosis. 

6.  Make  a  cover-slip  preparation  and  stain  it  for  tubercle  bacilli.  Care, 
however,  should  be  taken  not  to  decolorize  too  long — one-half  to  three-quarters 
of  a  minute  with  Gabbet's  solution  is  sufficient.      Dry  and  mount. 

The  majority"  of  the  bacilli  found  by  this  method  are  shorter  and  broader,  as 
a  rule,  than  the  tubercle  bacilli  usually  seen  in  sputum,  and  some  are  paler  red, 
but  all  forms  occur.  These  bacilli  may  occur  singly  or  in  groups.  The  largest 
part  of  the  sediment  consists  of  undigested  nuclei  and  a  small  amount  of  detritus. 

Observations  ^  made  by  the  writer  at  the  Laboratory  of  the  Massachusetts 
General  Hospital  on  72  cases  examined  with  reference  to  physical  properties, 
albumin,  animal  inoculation,  inoscopy,  and  cytodiagnosis  resulted  as  follows  : 
Fifty-one  cases  were  classed  as  tuberculous;  46  of  these  were  classified  as  primary 
and  5  as  secondary  (bacilli  in  the  sputum).  Of  the  46  secondary  cases,  50  per 
cent.  (23  cases)  were  proved  tuberculous  by  one  or  more  tests — viz.,  guinea-iDig 
inoculation,  inoscopy,  or  operation.  Animal  inoculation  was  positive  in  15  cases 
(82  per  cent.),  and  inoscopy  in  10  out  of  22  cases  examined  by  this  method.  One 
case  was  proved  at  oj^eration.  In  5  of  the  23  unproved  cases  the  examination  of 
the  fluid  probably  led  to  faulty  conclusions.  There  were  12  acute  infectious  cases, 
all  showing  a  predominance  of  polyuuclear  leukocytes.  Six  followed  pneumonia, 
1  infection  of  the  limg,  3  started  from  unknown  sources,  1  from  traiuna,  and  1 
from  abscess  of  the  liver.  There  were  5  cases  of  simjile  transudate  ;  4  due  to 
cardiac  disease  and  1  to  nephritis.  There  were  3  cancerous  cases  ;  2  positive  and 
1  doubtful,  all  following  cancer  of  the  breast. 

As  a  result  of  the  study  of  this  subject  the  writer  thinks  that  we  are  justifled 
in  coming  to  the  conclusion  that  routine  and  systematic  examination  of  pleural 
fluids  will  aid  us  greatly  in  diagnosis  and  in  determining  the  etiology  of  pleurisy. 
Of  the  methods  of  which  he  has  spoken,  cytodiagnosis  is  the  only  one  which 
can  easily  be  employed  clinically,  for  the  reason  that  animal  inoculation,  inoscopy, 
and  culture  methods  can  be  emjjloyed  only  in  the  laboratoiy.  Cytodiagnosis  is  not 
accurate  in  every  case  any  more  than  any  other  clinical  method,  but  the  writer 
thinks  that  he  is  justified  in  saying  that  it  is  sufficiently  accurate,  especially  when 
taken  in  conjunction  with  the  history  and  bedside  examination,  to  justilH'  its  use 
as  a  routine  procedure.  In  some  cases  it  has  not  only  been  of  more  than  probable 
diagnostic  value,  but  has  given  us  positive  and  signal  results.  Routine  examina- 
tion of  pleural  fluids  will  not  only  enable  us  to  study  the  question  of  pleurisy  with 
effusion  with  reference  to  etiology  and  diagnosis,  but  will  establish  a  basis  upon 
which  accurate  prognostic  statistics  can  subsequently  be  based. — Percy  Musgrave.] 

I  Trans.  Mass.  Med.  Soc,  1904. 


EXPLORATORY  PUNCTURES  IN  DISEASED  CONDITIONS.     721 

DETAILS  OF  EXPLORATORY  PUNCTURES  IN  DIFFERENT 
DISEASED  CONDITIONS. 

PLEURAL   EXPLORATORY  PUNCTURES. 

The  most  important  rules  for  aspirating  the  j^leural  cavity  in  order  to  deter- 
mine the  existence  of  exudates  or  transudates  are  similar  to  those  for  therapeutic 
puncture.  We  should  not  introduce  the  needle  too  near  the  upper  or  too 
near  the  lower  border  of  the  pleura.  If  we  puncture  too  low,  the  needle  fre- 
quently only  goes  through  the  pleural  complementary  sides  stuck  together  with 
fibrin.  If  we  puncture  too  high,  we  are  apt  to  penetrate  the  compressed  lung, 
for  the  latter  often  causes  a  dulness  above  the  level  of  the  fluid.  IS^aturally 
there  are  no  generally  applicable  rules  for  the  place  of  exploratory  puncture,  but 
we  must  follow  the  results  of  physical  examination  and  puncture  at  a  point 
where  we  find  decided  dulness,  diminished  or  bronchial  breathing,  and  dimin- 
ished fi-emitus.  Generally  speaking,  however,  in  typical  pleural  exudations  we 
select  the  fifth  and  sixth  intercostal  sj^aces  in  the  anterior  axillary  line,  and  the 
area  just  below  the  angle  of  the  scapula  behind.  In  a  test  puncture  of  the 
pleura  it  is  especially  important  to  palpate  carefully  by  means  of  moving  the 
needle  up  and  down,  and  so  determine  by  its  mobility  whether  it  has  penetrated 
a  large  cavity,  in  order  that  we  may  be  enabled  to  select  the  best  spot  for  a  thera- 
peutic puncture  or  for  the  drainage  of  a  jjleural  empyema,  and  prevent  penetrat- 
ing the  lung  and  the  diaphragm.  (Compare  the  following  in  regard  to  the  dis- 
tinction between  pleural  empyemata  and  intrapulmonary  cavities.) 

EXPLORATORY  PUNCTURES  TO  DEMONSTRATE  PULMONARY 

CAVITIES. 

It  is  sometimes  very  desirable,  especially  for  determining  upon  an  operative 
procedure,  to  employ  physical  diagnosis,  and  more  jjarticularly  exploratory 
punctures,  in  order  to  demonstrate  pulmonary  cavities  (tuberculous  cavities, 
bronchiectasies,  and  abscess  cavities)  and  to  determine  their  exact  position  and 
size.  This  naturally  succeeds  only  when  the  cavities  are  filled  with  purulent 
secretion.  It  is  therefore  advisable  to  undertake  the  puncture  at  a  time  when 
the  patient  has  not  expectorated  for  a  long  period.  If  we  succeed  in  aspi- 
rating purulent  material,  but  only  in  small  quantity,  it  may  be  obtained  from  a 
bronchus  affected  with  a  catarrh.  It  is  important,  therefore,  to  empty  as  large 
amounts  of  pus  as  possible,  and  to  determine  with  slight  movements  of  the  needle 
whether  the  latter  has  penetrated  a  large  cavity,  an  attempt  that  will  succeed 
only  when  the  cavities  are  situated  superficially.  The  contents  of  j^ulmonary 
cavities  are  usually  offensive  in  odor;  for  this  reason  the  determination  of  the 
odor  of  the  material  withdrawn  by  the  puncture,  and  its  identification  with  the 
odor  of  the  sputum,  are  sometimes  of  considerable  significance. 

Quite  as  important  a  question,  in  cases  where  we  have  determined  the  exist- 
ence of  a  cavity,  is  whether  the  cavity  is  really  situated  within  the  lung  or  is 
part  of  a  pleural  empyema,  the  indications  for  operative  interference  often 
depending  upon  such  a  distinction.  The  depth  from  which  the  pus  is  with- 
drawn will  often  be  an  important  consideration  in  settling  this  question.  We 
determine  this  depth  by  successive  aspirations,  pushing  the  needle  little  by  little 
back  and  forth. .  The  characteristics  of  the  pus  may  also  sometimes  be  employed 
for  determining  the  position  of  the  accumulation  ;  if  it  is  rather  slimy,  it  is 
probably  partly  derived  from  an  intrapulmonary  cavity,  at  least  one  lined 
with  mucous  membrane  (bronchiectasis).  It  may  also  be  noted  that  the  pus  of 
abscess  cavities  and  tubercular  cavities  is  not  slimy.  A  mixture  of  air  and  pus 
argues  in  favor  of  an  intrapulmonary  cavity  and  against  a  pleural  empyema ; 
provided,  of  course,  that  the  physical  signs  of  a  pneumothorax  are  absent  and 
that  we  are  sure  that  the  needle  is  not  stojiped  up  and  the  air  derived  from  a 
leak  in  the  syringe.  The  air  must  also  be  withdrawn  at  the  same  time  and  from 
46 


722  EXPLORATORY  PUNCTURES  AND  HARPOONING. 

tlie  same  depths  as  tlie  pus,  and  the  amount  of  the  withdrawn  pus  must  prove 
the  existence  of  a  pathologic  cavity.  If  this  is  not  the  case,  we  must  always 
consider  the  possibility  that  the  air  simply  comes  from  a  bronchus.  The  micro- 
scopic examination  of  the  purulent  fluid  furnishes  certain  conclusions  about  the 
nature  of  the  cavity.  Such  an  examination  is  performed  like  a  sputum  examina- 
tion (elastic  fibers,  tubercle  bacilli  and  other  bacteria,  crystals,  etc.)  (see  p.  587 
et  seq.).  The  presence  of  elastic  fibers  argues  especially  against  empyema  and  in 
favor  of  a  destructive  pulmonary  lesion — i.  e.,  cavit}^  formation. 

EXPLORATORY  PUNCTURE  OF  THE  PERICARDIUM. 

In  exploratoiy  puncture  of  the  pericardium,  injury  to  the  heart  is  best 
avoided  by  introducing  the  cannula  almost  in  the  sagittal  plane  and  directed  but 
slightly  toward  the  median  line.  The  puncture  should  be  made  at  the  left  border 
of  the  cardiac  dulness  and  to  the  outer  side  of  the  apex  beat,  in  case  the  latter 
be  present.  According  to  Dobert,^  however,  there  are  cases  in  which  a  puncture 
in  this  location  gives  a  negative  result,  and  in  which  the  fluid  may  be  more  easily 
reached  through  the  fourth  intercostal  space  to  the  right  of  the  sternum.  The 
only  cases  in  which  this  procedure  is  applicable  are  those  in  which  there  is  a 
very  pronounced  and  undoubted  pericardial  broadening  of  the  cardiac  dulness- 
toward  the  right.  In  this  situation  the  right  ventricle  and  auricle  are  uncom- 
fortably close,  and  their  thin  walls  might  easily  be  injured  by  the  cannula.  The 
cannula  must  be  cautiously  introduced,  and  the  introduction  must  be  suspended 
at  the  moment  when  resistance  is  no  longer  encountered  or  the  heart  is  felt 
striking  against  the  instrument.  Since  the  danger  of  injuring  a  coronary  artery 
or  the  heart  itself  (tearing  of  the  thin-walled  portions  of  the  heart  upon  the 
cannula,  Kronecker's  "co-ordination  center")  is  not  to  be  despised  and  cannot 
certainly  be  avoided,  the  author  does  not  advocate  exploratory  puncture  of 
the  pericardium  for  purely  diagnostic  purposes.  He  believes  it  should  be 
employed  chiefly  in  those  cases  of  large  pericardial  exudate  in  which  there  is  an 
urgent  indication  for  the  removal  of  the  fluid,  and  where  a  point  must  be 
selected  at  which  the  cannula  may  readily  enter  the  pericardial  cavity. 

EXPLORATORY  PUNCTURES  OF  INTRATHORACIC  AND 
ABDOMINAL  CYSTS. 

Both  in  solid  tumors  and  in  those  with  fluid  contents  exploratory  puncture 
will  afford  useful  conclusions,  in  the  one  case  by  the  demonstration  of  character- 
istic morphologic  tumor  elements,  and  in  the  other  case  by  the  demonstration  of 
fluid  and  the  possibility  of  exactly  examining  it. 

So  far  as  the  technical  details  are  concerned,  it  is  almost  always  a  good  rule 
to  puncture  tumors  only  in  those  places  where  the  tumor  lies  superficially 
according  to  palpation  and  percussion.  It  is  not  wise  to  puncture  through  the 
intestine,  although  experience  has  shown  that  such  a  puncture  with  a  verj'  fine 
needle  will  probably  not  cause  any  damage. 

To  illustrate  the  diagnostic  value  of  exploratoiy  punctures  in  intrathoracic 
tumors,  the  author  wishes  to  mention  the  results  of  aspirating  a  lung  tumor  at  the 
Bern  Clinic.  Abundant  myelin  bodies  were  found  in  the  fluid  extracted.  They 
showed  in  this  case  even  mo-re  bizarre  shapes  than  are  found  in  the  sputum  (see 
Fig.  272).  Dr.  Zollikoffer  proved  that  these  myelin  bodies,  like  those  of  the 
sputum,  consisted  essentially  of  protagon  (Fig.  209,  g.).  The  microscopic  exam- 
ination of  the  tumor  showed  that  these  bodies  were  situated  exclusively  in  the 
remaining  bronchi  and  alveoli.  Their  large  amount  should  perhaps  be  attributed 
to  the  stagnation  of  the  secretion  associated  with  the  tumor  formation.  Zollikoffer 
obtained  similar  results  in  studying  anatomic  preparations  of  pneumonia  and  tuber- 
culosis. The  appearance  is  therefore  not  specific  of  pulmonary  tumors,  although 
in  none  of  the  last  mentioned  cases  was  there  such  an  abundance  of  the  myelin 
bodies  as  in  the  pulmonary  tumors.     The  author  considers  that  their  presence  in 

1  Berlin,  klin.  Woch.,  190-4,  Xo.  18. 


EXPLORATORY  PUNCTURES  IN  DISEASED  CONDITIONS.     723 

the  fluid  withdrawn  by  puncture  shows  surely  that  the  aspirated  part  belongs  to 
the  lung,  which  is  significant  in  the  local  diagnosis  of  intrathoracic  tumors,  and 
in  distinguishing  pleural  thickenings  from  pulmonary  infiltrations  and  pulmonary 
tumors. 

Only  very  fine  needles  should  be  employed  to  puncture  abdominal  cystic 
tumors,  because,  if  no  adhesions  are  formed,  the  fluid  may  trickle  into  the  abdo- 
minal cavity  and,  if  infectious,  produce  serious  consequences. 

To  prove  that  a  cystic  tumor  belongs  to  the  gall-bladder,  it  is  necessary  to 
determine  constituents  of  the  bile  in  the  fluid  withdrawn  (the  bile-tinge  to  the 
color,  the  chemical  determination  of  biliary  coloring  matter  (p.  472  et  seq.),  the 
microscopic  demonstration  of  cholestrin  crystals  (Fig.  211,  b). ).  But  it  must  be 
emphasized  that  closed-off"  gall-bladders  frequently  contain  no  more  biliary  con- 
stituents, cholestrin  persisting  the  longest  of  any  of  them.  If  the  aspirating 
needle  strikes  against  a  hard  mass,  this  would  be  of  considerable  diagnostic 
importance. 

The  microscopic  demonstration  in  the  aspirated  fluid  from  echinococcus  cysts 
of  echinococcus  scolices,  brood  capsules,  and  the  laminated  remains  of  the  mem- 
branes (see  Fig.  204)  is  of  diagnostic  importance.  (See  also  the  plates  in  Kiich- 
enmeister  and  Ziirn's  Die  Parasiten  des  Menschen,  2d  ed.,  Plate  III.)     With  good 


Fig.  272. — Myelin  kernels  (protagon)  obtained  by  exploratory  puncture  from  tumor  of  the  lung. 


fortune  we  can  sometimes  obtain  from  the  fluid  in  multilocular  cysts  both  scolices 
and  hooks,  although,  on  account  of  the  small  size  of  the  bladders,  the  fluid  can  be 
obtained  only  in  traces.  However,  in  this  case  we  should  not  necessarily  expect 
a  positive  result,  because  the  majority  of  the  bladders  in  multilocular  echinococci 
are  sterile.  Provided  the  cortex  or  investing  membrane  is  not  inflamed,  the  echino- 
coccus fluid  is  chemically  characterized  by  the  absence  of  jjroteid  content  and  the 
presence  of  succinic  acid.  (For  demonstration  see  below.)  The  thickness  of 
the  fluid — i.  e.,  the  viscidity  of  the  contents — is  characteristic  of  ovarian  cysts  as 
contrasted  with  parovarian  cysts.  Oftentimes  this  cannot  be  determined  by  the 
fluid  withdrawn  from  a  very  fine  needle;  in  such  cases  the  chemical  demonstration 
of  paralbumin -proteid  is  in  itself  sufliciently  characteristic. 

The  demonstration  of  pancreatic  ferment  in  the  fluid  withdrawn  is  of  import- 
ance in  the  diagnosis  of  pancreatic  cysts.  (For  demonstration  see  below.)  H. 
Zeehuisen  1  obtained  the  following  results  in  this  connection:  The  positive  occur- 
rence of  ti'ypsin  in  the  fluid  supports  the  diagnosis  of  a  pancreatic  cyst  very 
decidedly,  as  does  the  demonstration  of  a  fat-splitting  ferment.  The  negative 
results  to  both  tests  do  not,  however,  argue  with  certainty  against  pancreatic  cysts. 
Diastatic  action  is  useless  for  the  diagnosis,  as  all  sorts  of  fluids  withdrawn  possess 

1  Centralbl.  f.  innere  Med.,  1896,  vol.  xl.,  p.  1017. 


724  EXPLORATORY  PUNCTURES  AND  HARPOONING. 

tMs  peculiarity.  The  occurrence  of  tyrosin  and  leucin  crystals  in  pancreatic 
cysts  is  of  diagnostic  interest  (Fig.  211,  c).  Hydronephroses  and  other  cysts 
which  are  connected  with  the  urinary  tracts  are  oftentimes  characterized  by  a  con- 
siderable urea  content.^  (For  demonstration  see  below.)  However,  if  the  cyst 
has  been  shut  oflF  for  any  length  of  time,  urea  may  be  absent. 

Demonstration  of  Succinic  Acid  in  Echinococciis  Fluid. — Hoppe-Seyler  ^ 
describes  a  method  of  demonstrating  succinic  acid  in  the  blood,  employing  this 
method  also  with  echinococcus  fluid.  The  method  is  as  follows:  After  the  fluid 
has  been  carefully  acidified  with  hydrochloric  acid,  it  is  freed  from  albumin  by 
boiling.  This  is  necessary  only  when  the  fluid  comes  from  inflamed  echinococcus 
sacs,  because  normally  echinococcus  fluid  is  free  from  albumin.  The  clear  fluid 
is  neutralized  as  carefully  as  possible  with  caustic  potash,  concentrated  over  a 
water  bath  till  it  is  somewhat  thickened,  and  completely  precipitated  with  alcohol 
(alkahne  salts  of  succinic  acid  are  insoluble  in  alcohol).  The  ijrecii^itate  dissolved 
in  water,  filtered,  and  compressed  may  show  crystals  of  succinic  acid  alkaline 
salts.  Succinic  acid  may  be  produced  by  adding  to  the  aqueous  solution  a 
mixture  of  equal  parts  of  alcohol  and  ether,  to  which  is  added  hydrochloric 
acid.  This  mixture  dissolves  fi-ee  succinic  acid.  Salkowski  *  mentions  the  fol- 
lowing peculiarities  of  succinic  acid  for  the  purpose  of  identification  :  It  forms 
four-sided  needles,  its  melting  point  is  182,  it  is  readily  soluble  in  water  and 
also  in  alcohol,  and  entirely  soluble  in  ether.  If  heated  in  a  glass  tube  the  acid 
melts  and  sublimes,  being  partly  changed  to  anhydrous  succinic  acid.  When 
heated  on  platinum  the  acid  folliculizes  and  forms  vapors  which  tend  to  make 
one  cough.  If  neutral  lead  acetate  is  added  to  the  aqueous  solution,  lead  suc- 
cinate, a  hea^sy  crystalline  precipitate,  appears. 

Demonstration  of  Paralbumin  (Pseudomucin  in  Ovarian  Cysts). — Salkow- 
ski gives  the  following  rules :  1.  A  few  drops  of  an  alcoholic  solution  of  rosolic  acid 
are  added  to  a  small  quantity  (about  25  c.c.)  of  the  fluid,  which  is  heated  to 
boiling,  and  very  dilute  sulphuric  acid  (tenth-normal  solution)  is  added  drop  by 
drop  until  a  yellowish  tinge  indicates  that  the  reaction  of  the  fluid  is  acid.  The 
solution  is  again  heated  to  boiling  and  filtered.  If  paralbumin  is  present,  the 
filtrate  will  be  clouded.  2.  The  same  quantity  of  the  cyst  fluid  is  precipitated 
with  three  times  its  volume  of  95  per  cent,  alcohol,  filtered,  washed  several  times 
with  alcohol,  and  then  shaken  up  in  a  mixture  of  one  volume  of  hydrochloric 
acid  and  three  volumes  of  water.  The  tube  is  then  heated  over  a  wire  net  to 
boiling,  allowed  to  cool,  and  Trommer's  test  performed  with  a  portion  of  the 
fluid  without  filtrating.  After  boiling,  a  specimen  is  cooled  off"  by  placing  the  test 
tube  in  water.  Should  paralbumin  or  mucin  be  present,  a  precipitate  of  red 
copi^er  oxid  will  form.  For  the  purpose  of  differentiating  paralbumin  (pseudo- 
mucin) fi'om  mucin,  it  should  be  remembered  that  the  former  cannot  be  precipi- 
tated from  the  cyst  fluid  by  means  of  the  acetic  acid. 

Salkowski' s  Test  for  Urea  in  Cysts  of  the  Urinary  System. — One  hun- 
dred cubic  centimeters  of  the  fluid  are  carefully  neutralized  with  acetic  acid 
and  then  poured  into  400  c.c,  of  95  j^er  cent,  or  absolute  alcohol.  After  it 
has  been  shaken  and  stirred  and  has  stood  for  several  hours,  the  coagulum  is 
washed  off"  with  alcohol  and  the  extract  evaporated  over  a  low  flame.  The  resi- 
due is  treated  several  times  with  absolute  alcohol,  and  the  extract  evaporated 
to  dryness.  A  few  drops  of  nitric  acid  are  added  to  the  residue  after  it  has 
cooled  off",  and  it  is  then  allowed  to  stand  in  a  cool  place  for  twenty-four  hours. 
As  a  general  thing  the  nitric  acid  produces  only  a  cloudiness  at  first,  due  to  the 
fatty  acids  derived  from  the  soaps  which  are  almost  always  present.  Little  by  little 
nitrate  of  urea  is  thrown  down  as  a  crj^stalline  precipitate.  This  is  characterized 
by  the  shape  of  the  crystal  (Fig.  13),  and  also  by  the  fact  that  when  the  water 
is  drawn  off"  with  filter  paper,  the  crystal  decomposes  energetically  or  undergoes 
sudden  combustion.     Provided  the  quantity  of  nitrate  of  urea  is  sufficient,  the 

^  Traces  of  urea  also  occur  in  exudates  and  transudates. 

^  Handbuch  der  physiologisch-pathologisch-chemischen  Analyse,  6th  ed.,  1893,  p.  52. 

^  Practkum  d.  physiol.  u.  pafhol.  Chanie,  2d  ed.,  1900. 


EXPLORATORY  PUNCTURES  IN  DISEASED  CONDITIONS.     725 

remaining  portion  may  be  utilized  to  obtain  urea  itself,  which  is  tested  for  with 
the  familiar  reaction  for  this  purpose,  i 

Demonstration  of  Pancreatic  Ferments  in  Pancreatic  Cysts. — For  the 
purpose  of  demonstrating  the  tryptic,  diastatic,  and  fat-splitting  actions  of  fluid 
obtained  by  puncture,  reference  is  made  to  the  procedures  on  pp.  421  and  425. 

PUNCTURE  OF  THE  SPLEEN. 

Puncture  of  the  spleen,  such  as  is  recommended  in  typhoid  in  order  to  demon- 
strate typhoid  bacilli  microscopically  in  the  material  obtained  and  by  means  of 
culture,  is  not  without  danger.  The  small  wound  in  the  spleen  in  itself  is  of  no 
particular  importance,  but  the  capsule  may  be  considerably  torn  by  the  aspira- 
tory  excursions,  as  has  been  shown  repeatedly  on  autopsy.  This  has  often  led  to 
severe  hemorrhage  and  peritoneal  symptoms.  The  author  warns  against  jjuncture 
of  the  spleen,  especially  since  we  have  at  the  present  time  in  Widal's  serum  test 
a  method  much  more  simple  and  far  less  dangerous.  In  any  case,  care  should  be 
taken  to  perform  the  puncture  rapidly  and  to  see  that  the  patient  does  not  breathe 
during  the  act. 

EXPLORATORY  PUNCTURE  IN  APPENDIQTIS. 

This  method  in  suitable  cases  is  devoid  of  danger  and  may  be  of  practical 
value.  It  is  self-evident  that  it  cannot  be  applied  in  cases  of  diffuse  resistance, 
especially  when  deep  and  when  intestines  intervene.  There  is  little  chance  in 
these  cases  of  obtaining  pus,  so  that  the  procedure  would  be  useless,  to  say  the 
lea.st,  if  not  dangerous.  When,  however,  there  is  a  well-defined  tumor,  over 
which  the  percussion  note  is  dull,  an  exploratory'  puncture  may  be  performed 
without  danger.  Under  these  conditions  one  is  sure  to  i^ass  through  alreaty 
infected  tissue,  so  that  the  risk  of  infection  is  unimportant.  One  may  in  this  way 
favor  external  napture  of  an  abscess,  as  the  author  has  personally  obseiwed.  it 
may,  however,  happen,  even  in  cases  where  the  percussion  note  is  dull  over  a 
tumor,  that  the  needle  passes  through  compressed  intestines  lying  between  the 
abdominal  wall  and  the  tumor  mass.  But  this  does  no  great  harm,  as  is  shown 
by  the  cases  of  puncture  performed  for  therapeutic  reasons  in  meteorism.  The 
author  would  not,  however,  have  it  understood  that  he  recommends  exploratoiy 
puncture  in  appendicitis  as  a  necessary  and  desirable  routine  measure  for  determ- 
ining pus.  On  the  contrary,  he  considers  that  the  procedure  is  unnecessaiy  for  one 
of  experience.  He  believes  that  the  method  has  a  didactic  value  chiefly  for  those 
physicians  who  are  not  familar  with  the  nature  of  appendicitis  and  who  believe 
that  all  cases  of  appendicitis  suppurate.  It  may  also  serve  to  show  that  Cjuite 
extensive  atrophies  may  be  present  in  very  innocent-appearing  cases.  Besides 
this,  exploratory  puncture  may  be  of  a  certain  amount  of  value  in  demonstrating 
pus  to  people  who  otherwise  refuse  operation.  The  negative  result,  of  course, 
proves  nothing. 

LUMBAR  PUNCTURE. 

Lumbar  puncture  attained  diagnostic  importance  for  the  first  time  in  the 
hands  of  Quincke.  This  author  showed  that  it  was  very  easy  to  enter  the  spinal 
column  and  the  dura  mater  by  means  of  a  small  aspirating  needle  introduced 
between  the  vertebral  arches.  Fig.  273  represents  the  arrangement  of  the  lum- 
bar vertebrje  of  a  child  twelve  years  of  age,  and  shows  that  the  interval  indicated 
by  the  shaded  area  is  quite  sufficient  for  this  procedure.  The  spinal  cord  reaches 
only  to  the  second  lumber  vertebrje,  so  that  it  escapes  injury.  There  is  also  little 
danger  of  injuring  the  cauda  equina,  because  the  fibers  are  .sufficiently  movable 
to  escape  the  cannula,  and  injury  to  a  few  fibers  would  not  be  ])roductive  of  any 
serious  trouble.  The  technic  is  as  follows  :  The  patient  is  placed  on  his  side  and 
the  body  bent  forward  as  much  as  possible,  so  as  to  increase  the  distance  between 
the  arches.      It  is  not  well  to  try  lumbar  puncture  with  the  patient  sitting  up — 

^  See  Salkowski,  Practicum  d.  Physiol,  u.  Pathol.  Chemie,  2d  ed.,  1900,  p.  1G2. 


726 


EXPLOBATOBY  PUNCTUBES  AND  HABPOONINO. 


Fig.    273— Lumbar     vertebra    of 
twelve-year-old  child. (Quincke). 


at  least  when  performed  for  therapeutic  reasons — as  certain  disadvantages  have 
been  observed  due  to  the  change  of  pressure.  Quincke  recommended  that  the 
puncture  be  performed  between  the  second  and  third  or  third  and  fourth  lumbar 
vertebrae. 

Subsequent  experience  has  shown  that  the  space  between  the  fifth  lumbar 
vertebra  and  the  sacrum  serves  just  as  well  and  may  even  be  preferable,  as  the 

morphologic  constituents  of  the  cerebral  spinal 
fluid,  such  as  pus  cells,  blood,  and  tubercle  ba- 
cilli, tend  to  gravitate  toward  the  lowest  portion 
of  the  dural  sac,  and  might  escape  observation 
should  the  puncture  be  performed  higher.  The 
fluid  at  times  runs  clear  at  first,  to  become  cloudy 
later.  For  the  purpose  of  avoiding  error,  it  is  well 
to  count  the  vertebrae  not  only  from  the  seventh 
cervical  spine  down,  but  from  the  sacrum  up. 
The  needle,  to  which  an  aspirating  syringe  is  at- 
tached, is  introduced  under  the  usual  antiseptic 
precautions  in  a  chosen  space,   and,  according  to 

V\^^^  ^jjnr'  —^  .^^■'  Quincke,  a  few  millimeters  from  the  median  line, 

<~~v_-=«»a(&r«»=^  V  /  so  as  to  avoid  the  dense  ligamentum  interspinosum. 

The  point  of  the  needle,  however,  is  directed  to- 
ward the  median  line.  According  to  Quincke,  the 
distance  to  the  dural  sac  in  a  child  two  years  of 
age  is  about  2  cm. ,  and  in  an  adult  4  to  6  cm.  It 
is  just  as  well  to  introduce  the  needle  in  the  me- 
dian line,  and  it  would  appear  to  the  writer  that 
this  procedure  is  somewhat  easier,  because  of  the 
topographic  relation.  It  should  be  remembered  that  in  a  child  the  spinal  proc- 
esses are  short,  whereas  in  an  adult  they  are  longer  and  are  directed  somewhat 
downward.  It  therefore  follows  that  in  children  the  needle  may  be  introduced 
midway  between  the  spinous  processes,  whereas  in  adults  it  is  best  to  keep  close 
to  the  lower  margin  of  the  upper  jsrocess.  In  adults  it  may  be  also  necessary, 
if  the  needle  is  introduced  in  the  median  line,  to  direct  the  point  slightly  ujjward. 
Lumbar  puncture  is  of  diagnostic  importance  in  two  ways  :  It  enables  one, 
first,  to  determine  the  pressure  of  the  cerebrospinal  fluid;  and  secondly,  to  deter- 
mine its  peculiarties.  It  is  self-evident  that  the  pressure  of  the  cerebrospinal 
fluid  is  immediately  influenced  by  removal  of  a  portion  of  it,  so  that  tests  to 
determine  pressure  should  be  performed  before  drawing  off"  any  of  the  fluid.  An 
approximate  idea  of  the  pressure  may  be  obtained  by  allowing  the  fluid  to  squirt 
out  through  the  needle  after  removing  the  aspirating  syringe.  If  the  pressure  is 
low  the  fluid  appears  drop  by  drop  ;  if  higher,  the  drops  come  faster;  and  if 
extreme,  the  fluid  may  escape  in  a  stream.  If  the  pressure,  however,  is  to  be 
measured  accurately,  the  above  experiment  should  not  be  performed.  The  sim- 
plest and  most  accurate  way  is  to  attach  the  needle  by  means  of  a  tube  filled  with 
a  1  per  cent,  solution  of  carbolic  acid,  to  a  small  mercury  manometer  of  1  mm. 
caliber.  The  pressure  is  estimated  in  the  usual  way.  The  portion  of  mano- 
meter above  the  level  of  the  quicksilver,  forming  the  connection  between  it  and 
the  carbolic  acid  tube,  must,  of  course,  also  be  filled  with  the  fluid.  If  correct 
results  are  to  be  obtained,  the  manometer  must  be  filled  with  mercury  to  the  zero 
point,  and  must  be  held  in  such  a  manner  that  this  point  is  on  a  level  with  the 
point  of  the  aspirating  needle,  which  is  possible  with  ordinary  manometers  only 
when  the  connecting  tube  is  of  considerable  length.  The  use  of  a  small  mano- 
meter has  the  advantage  that  when  the  mercury  column  rises,  only  a  small 
amount  of  fluid  is  drawn  from  the  dural  sac,  whereas  the  manometers  of  greater 
caliber  and  the  ordinary  water  manometers  have  the  disadvantage  of  withdrawing 
enough  fluid  from  the  dorsal  sac  to  diminish  the  pressure  materially.  On  the 
other  hand,  water  manometers  have  the  advantage  of  making  larger  excursions 
with  low  pressure.     This,  however,  does  not  offset  the  above  disadvantage. 

As  regards  the  dural  pressure  under  physiologic  and  pathologic  conditions,  it 


EXPLORATORY  PUNCTURES  IN  DISEASED  CONDITIONS.     727 

may  be  said  that  in  the  dorsal  position  it  is  60  to  100  mm.  of  water  (5  to  7.3 
mm.  Hg.)  under  normal  conditions,  and  200  to  800  mm.  of  water  (15  to  60  mm. 
Hg.)  in  pathologic  conditions,  such  as  meningitis  and  tumor  of  the  brain. 

After  determining  the  pressure,  a  specimen  of  cerebrospinal  fluid  may  be 
removed  for  the  purjjose  of  examination.  It  should  be  remembered  that  it  is 
not  justifiable  in  case  of  simple  exjjloratory  puncture  to  remove  large  quantities 
of  the  fluid,  because  of  the  dangers  that  supervene  when  the  pressure  is  reduced 
below  60  to  80  mm.  of  water.  These  dangers  have  led  certain  authors  to  desist 
entirely  from  the  therapeutic  use  of  lumbar  puncture. 

The  fluid  is  either  withdrawn  by  aspiration  or  allowed  to  trickle  out  through 
the  tubes  of  its  own  accord.  This  latter  procedure  has  the  advantage  of  with- 
drawing the  fluid  gradually,  and  of  allowing  one,  by  holding  the  tube  at  a  cer- 
tain level,  to  prevent  the  pressure  approaching  the  danger  line — i.  t.,  below 
80  mm.  This  may  readily  be  accomplished  by  holding  the  open  end  of  the  tube 
80  mm.  above  the  site  of  the  puncture. 

So  far  as  the  peculiarities  of  the  fluid  are  concerned,  it  will  be  found  that 
under  normal  conditions  it  is  colorless,  water-clear,  and  of  a  specific  gravity  only 
a  little  above  1000  (1003).  Under  such  conditions  it  contains  very  little  albu- 
min and  shows  no  distinct  nucleo-albumin  reaction  (p.  711).  An  increase  of  the 
specific  gravity  will  indicate  meningitis,  although  a  normal  sj^ecific  gravity  may 
be  present  in  this  disease.  Lenhartz  claims  that  more  than  0. 25  per  cent,  of 
albumin  also  indicates  meningitis;  although  the  same  author,  in  exceptional 
cases  of  cerebral  tumor  and  apoj^lexy,  has  found  albumin  up  to  1.5  to  2.25  jser 
cent.  The  macroscopic  ajapearance  of  the  fluid  is  of  considerable  importance. 
A  cloudy  fluid  indicates  inflammation,  as  does  also  the  presence  of  numerous 
white  blood-corpuscles  on  microscopic  examination.  These  are,  as  a  rule,  the 
cause  of  the  cloudiness.  On  the  other  hand,  the  fluid  may  remain  perfectly 
clear  in  cases  of  inflammation,  especially  in  tuberculosis,  and  even  in  purulent 
cerebrospinal  meningitis.  Marked  cloudiness  jjroduced  by  white  blood-  cor23Us- 
cles  is  in  favor,  generally  speaking,  of  purulent  and  against  tuberculous  menin- 
gitis. The  degree  of  cloudiness  may  under  certain  circumstances  serve  to  distin- 
guish between  brain  abscess  and  cerebral  meningitis,  or  to  establish  a  diagnosis 
of  a  combination  of  the  two,  a  point  which  may  be  of  value  in  determining  the 
advisability  of  operative  interference.  A  clear  fluid  in  these  cases  is  against,  and 
a  cloudy  fluid  in  favor  of,  iiurulent  meningitis.  In  case  of  meningeal  hemor- 
rhage and  pachymeningitis  hemorrhagica,  the  fluid  has  been  found  blood-stained, 
a  point  which  may  be  of  differential  diagnostic  importance  in  connection  with 
spontaneous  cerebral  hemorrhages  and  softening,  although,  of  course,  an  intra- 
cerebral hemorrhage  perforating  the  ventricle  would  be  liable  to  cause  a  hemor- 
rhagic cerebrospinal  fluid.  In  tumors  of  the  cord  and  meninges,  one  should 
observe  whether  the  fluid  contains  tumor  cells,  although  we  have  no  jDOsitive 
information  of  their  being  found  in  such  cases,  and  a  case  examined  by  the 
author  with  this  in  view  furnished  negative  results.  Still  the  jjossibility  of  find- 
ing cells  analogous  to  those  found  in  pleuritic  and  jjeritoneal  exudates  should  be 
borne  in  mind. 

It  is  of  great  importance  for  the  purpose  of  diagnosis  to  examine  a  dry  prep- 
aration of  the  cerebrospinal  fluid  for  bacteria.  In  epidemic  cerebrosjjinal  men- 
ingitis Weichselbaum' s  Diplococcus  intracellularis  will  be  found.  This  was 
formerly  confounded  with  Frankel's  pneumococcus,  although  there  is  little 
resemblance  between  them,'  the  former  being  more  closely  related  morjshologi- 
cally,  and  so  far  as  culture  is  concerned,  to  the  ordinary  staphylococci. 

Furthermofe,  the  frequent  occurrence  of  polyarticular  inflammation  of  the 
joints  in  cerebral  meningitis  is  in  favor  of  a  closer  relationship  between  the 
meningeal  bacteria  and  staphylococci,  for  there  can  be  no  doubt  that  many  cases 
of  polyarticular  inflammation  are  due  to  coccus  infection.  In  tuberculous  men- 
ingitis it  is  quite  surprising  that  tubercle  bacilli  are  found  in  the  puncture  fluid 

'  H.  Jager,  Zeits.  f.  Ilyg.,  vol.  xix.,  p.  351  This  work  contains  photographs  of  the 
Diplococcus  intracellularis. 


728  EXPLORATORY  PUNCTURES  AND  HARPOONING. 

in  over  50  per  cent,  of  the  cases.  They  are  found  most  easily  after  allowing  the 
fluid  to  settle  for  some  time  until  a  coagulum  appears,  from  which  a  dry  prepara- 
tion is  made  (see  p.  593).  In  cases  where  no  coagulum  forms  the  fluid  must  be  cen- 
trifuged  for  some  time,  so  that  the  bacteria  will  settle  through  the  lower  layers. 
Should  the  fluid  contain  nucleo-albumen,  for  instance  (p.  711),  it  is  well  to  pre- 
cipitate this  with  acetic  acid,  then  centrifuge,  and  hunt  for  the  tubercle  bacilli 
in  the  isolated  precipitate.  (See  Examination  of  the  Sputum  according  to 
Ilkewitsch,  p.  596.) 

HARPOONING* 

For  the  purpose  of  obtaining  small  pieces  of  deep-seated  tissue  for  the  pur- 
pose of  examination,  harpoon-like  instruments  have  been  introduced  through  a 
cannula  and  then  projected  beyond  the  protecting  sheath,  to  be  subsequently 
drawn  back  into  the  cannula  with  a  portion  of  the  tissue  desired.  As  a  rule, 
harpooning  is  unnecessary,  as  it  is  usually  possible  to  obtain  sufficient  tissue  for  an 
examination  by  using  the  ordinary  aspirator  in  the  manner  explained  on  p.  208. 
At  any  rate,  the  harpoon  will  be  used  only  in  cases  where  the  aspirate  fails  or 
where  larger  particles  are  desired  for  the  purpose  of  making  microscopic  sections. 
These  harpoons  may  be  obtained  from  an  instrument  maker,  or  they  may  be 
improvised  by  cutting  a  notch  in  the  stilet  of  an  ordinary  trocar.  Care  should 
be  taken  not  to  have  the  notch  in  the  stilet  so  deep  that  there  is  danger  of  the 
bob  breaking  off".  Harpooning  is  a  much  more  severe  procedure  than  the 
exploratory  puncture,  because  for  safety  it  is  essential  that  the  harpoon  be  of  a 
certain  thickness.   Generally  speaking,  harpooning  has  been  justly  given  up. 


RONTOEN-BAY  EXAMINATIONS. 


729 


RONTGEN-RAY    EXAMINATIONS. 

The  editors  consider  it  advisable  to  insert  a  few  illustrations  which 
will  show  some  of  the  more  typical  results  of  «-ray  examination  in 
cases  where  this  method  may  aid  in  arriving  at  a  diagnosis. 


re's.  C>T| 
o  ^       J^ 

■Sag  I 

■"   cuts. 

re  T  V< 

3  K  M  a 

n  o  reTS 

(T)  r+  ^*  o 


C  c  c  -: 


GC   (^    ps 

5;.  ^3 


5   O   CD 


?2B 

o  -  re 


re  as. 


re 


gp  B 

is  re's' 
M  o  3 

s-re<* 


730 


E  OXTGEX-BA  Y  EX  A  MIX  A  TIOXS. 


It  is  hardly  within  the  scope  of  this  book  to  do  more  than  to  explain 
the  illustrations  as  briefly  as  possible.     For  all  other  information  in  regard 


Fig.  275.— Normal  ar-ray  of  lumbar  region.  Plate  on  back.  In  order  to  detect  a  renal  calculus 
the  plate  should  show  good  definition  in  the  lumbar  vertebree  and  well-defined  transverse  proc- 
esses with  detail  in  the  soft  parts.  The  patient's  bowels  should  be  thoroughly  evacuatea,  and 
the  diaphragm  immobilized  by  the  pressure  cylinder  or  a  swathe.  In  tnis  plate  the  observer  can 
make  out  the  oblique  lines  marking  the  muscular  masses.  An  absolute  outline  line  of  the 
kidneys  can  often  be  defined  in  a  perfect  plate.  Here  there  is  so  much  detail  of  soft  parts  it  is 
almost  impossible  to  see  the  kidney.  This  plate  should  be  contrasted  with  Figs.  276  aud  277 
(Massachusetts  General  Hospital). 


RONTOEN-RAY  EXAMINATIONS.  731 

to  the  technic,  instruments,  methods,  and  diagnostic  value  to  be  attached 
to  the  findings,  we  refer  to  text-books  and  to  the  periodicals  devoted  to 


Fig.  276.— Calculus  in  right  ureter.  Before  a  diagnosis  of  renal  or  ureteral  calculus  is  made, 
several  plates  should  be  taken  and  the  findings  should  agree.  Two  plates  taken  on  this  case : 
calculus  removed  (Dr.  John  Elliott's  case,  Massachusetts  General  Hospital). 


732  RONTGEN-RAY  EXAMINATIONS. 

the  subject.     In  our  opinion  the  method  is  useful  only  when  its  results 
confirm  those  of  various  other  methods  of  examination.     In  a  case  of 


Fig.  277.— Renal  calculus  (right  kidney).  The  density  of  the  shadow  of  this  stone  indicates 
that  it  is  either  phosphatic  or  oxalate.  Uric  acid  stones  east  a  very  faint  shadow  owing  to  their 
organic  composition  (Dr.  S.  J.  Mixter's  case,  Massachusetts  General  Hospital). 

aneurism  of  the  arch  of  the  aorta,  or  in  a  case  of  renal  or  bladder  cal- 
culus, we  may  sometimes  obtain  evidence  of  as  much  or  more  value 
than  that  from  any  other  source. 


RONTGEN-RAY  EXAMINATIONS. 


733 


Fig.  278.— Left  pneumothorax,  showing  dislocation  of  the  heart  and  compression  of  the  hing. 
Black  square  is  a  lead  marker  at  the  level  of  the  nipple  :  A,  shadow  of  the  cardiac  apex ;  L,  com- 
pressed  lung  (Dr.  J.  J.  Minot,  Massachusetts  General  Hospital j. 


734 


E  ONTGEN-RA  Y  EX  A  MINA  TIONS. 


The  orthodiagraph,  a  recently  devised  instrument,  is  worth  mention- 
ing.     It  promises  to  add  valuable  help  in  more  accurately  determining 


Fig.  279.— Vesical  calculus  (marked  by  arrow). 

the  outlines  of  the  heart  and  the  arch  of  the  aorta.  The  instrument 
has  not  been  employed  long  enough  to  warrant  criticism,  but  its  utility 
seems  assured. 


E  ONTO  EK-RA  Y  EX  A  MINA  TIONS. 


735 


Fig.  280. — Chronic  tuberculosis  of  both  lungs :  An  abscess  cavitj'  in  left  upper  lobe  connect- 
ing with  esophagus  (A— A).  The  multiple  foci  of  tuberculosis  are  well  shown  in  this  plate  (Dr. 
E.  G.  Cutler's  case,  Massachusetts  General  Hospital). 


Fig.  281.— Hernia  of  diaphragm.    Note  line  of  diaphragm  about  third  interspace  of  the  right  lung. 


736 


RONTGEN-EA Y  EXAMINATIONS. 


RONTGEN-RA  Y  EXAMINATIONS. 


737 


The  illustrations  have  all  been  made  by  Mr.  Walter  Dodd,  at  the 
Massachusetts  General  Hospital  in  Boston,  and  we  wish  to  take  this 


Fig.  283.— Large  aneurism  of  arch  of  aorta  (Massachusetts  General  Hospital) 

opportunity  of  acknowledging  our  indebtedness  to  him,  and  to  the  cour- 
tesy of  the  various  physicians  whose  cases  he  photographed. — Ed.] 


47 


738  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


EXAMINATION   OF  THE   NERVOUS   SYSTEM. 

Although  the  technical  aids  to  the  examination  of  the  nervous 
system  are  usually  simple  and  require  but  brief  notice,  it  is  more  import- 
ant in  this  department  of  internal  medicine  than  in  any  other  to  con- 
duct the  examination  in  accordance  with  a  definite,  logical  plan.  The 
complex  functions  of  the  nervous  system  make  such  a  plan  essential  in 
order  that  no  symptoms  may  be  overlooked,  and  that  the  symptoms 
may  be  so  grouped  as  to  suggest  the  diagnosis.  Such  systematic  pro- 
cedure takes  time ;  but  it  is  quite  simple  and,  in  fact,  often  easier  than 
in  other  forms  of  disease,  since  the  examiner  needs  less  technical  skill. 
The  reason  why  the  beginner  finds  the  diagnosis  of  nervous  diseases  so 
difficult  is  because  he  is  not  familiar  with  those  anatomic  and  physiologic 
facts  which  are  absolutely  essential  for  the  accurate  interpretation  of 
clinical  cases. 

GENERAL  PART, 

I.  PSYCHICAL  EXAMINATION. 

The  clinician  now  and  then  observes  in  his  patient  mental  disturb- 
ances which  belong  exclusively  to  the  domain  of  psychiatry.  For  a 
comprehensive  method  of  examination  in  such  a  case,  it  is  advisable  to 
consult  text-books  upon  that  subject.  In  this  volume  we  shall  describe 
only  psychical  disturbances  which  occur  so  frequently  in  clinical  medi- 
cine as  to  be  typical.  These  include  the  various  grades  of  depression 
or  irritative  disorders  of  consciousness,  delirium,  and  disturbances  of 
intelligence  and  memory. 

DEPRESSED  DISTURBANCES  OF  CONSCIOUSNESS. 

The  term  somnolence  (sleepiness  or  hebetude)  is  applied  to  the  mildest 
grade  of  a  depressive  disturbance  of  consciousness.  This  merges  im- 
perceptibly into  lethargy  or  stupor,  and  finally  into  coma,  or  absolute 
loss  of  consciousness. 

These  depressive  disturbances  of  consciousness  are  observed  not  only 
in  brain  diseases,  but  also  in  all  sorts  of  general  affections  :  1 .  In  any 
lethal  illness,  a  short  time  before  death.  2.  At  the  height  of  infectious 
febrile  diseases,  though  such  diseases  rarely  produce  complete  loss  of 
consciousness.  3.  In  uremia,  and  then  generally  accompanied  by  con- 
vulsions. 4.  In  diabetic  coma.  The  gradual  onset  is  here  very  char- 
acteristic ;  the  loss  of  consciousness  usually  becomes  complete,  and  the 
breathing  deep,  slow,  and  labored  (see  p.  91).  5.  In  cases  of  poison- 
ing, especially  with  alcohol,  morphin,  chloroform,  chloral  hydrate,  coal 
gas.  6.  In  epileptic  attacks.  7.  In  many  hysteric  attacks.  8.  In 
focal  lesions  of  the  brain  of  sudden  onset,  hemorrhage,  softening  (shock, 
stroke),  in  traumatic  cerebral  lesions  (laceration,  concussion),  in  the 
different  varieties  of  meningitis,  and  in  the  later  stages  of  brain  tumors. 

The  disturbance  of  consciousness  noted  in  hyderia  is  distinctive.  If  complete, 
it  is  ordinarily  called  lethargy.     It  can  be  differentiated  from  the  comatose  con- 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  739 

ditions  observed  in  severe  brain  diseases  (apoplexy,  uremia,  etc.)  because  it  simu- 
lates normal  sleep  so  perfectly.  Presumably  it  has  the  same  psychologic  genesis 
as  that  torpor  of  the  cerebral  cortex  which  we  call  sleep.  The  function  of  the 
cortex  only  is  interrupted,  so  that  those  phenomena  accompanying  other  vari- 
eties of  coma  and  depending  upon  infracortical  disturbances,  such  as  stertorous 
or  interrupted  breathing,  cyanosis,  involuntary  evacuations  of  feces  and  urine, 
etc.,  are  lacking.  The  hysteric  condition  of  lethargy  differs  from  normal  sleep 
in  that  the  former  arises  and  persists  under  conditions  which  would  prevent 
or  interrupt  the  latter.  Quite  a  series  of  transitional  forms  may  occur  in  the 
hysteric  between  lethargy  (hysteric  unconsciousness)  and  alert  consciousness — 
e.  g.,  somnambulism,  in  which  a  person  without  any  subsequent  recollection  may 
perform  all  kinds  of  complicated  actions,  influenced  apparently  by  no  ordinary 
motives,  but  by  constraining  ideas.  During  the  somnambulistic  condition,  the 
memory  frequently  seems  to  be  cognizant  of  what  has  occurred  in  previous 
attacks,  whereas  in  the  interval  everything  relating  to  the  somnambulistic  con- 
dition is  effaced  from  consciousness  (dual  personality).  These  transitions  between 
absent  and  present,  or,  better,  between  waking  and  sleeping  consciousness,  may 
be  produced  artificially  in  certain  persons  by  hypnotic — i.  e.,  suggestive — influ- 
ence, and  are  therefore  called  hypnotic  conditions.  Wundt  regards  them  as  limita- 
tions of  consciousness  ;  in  other  words,  certain  anatomic  substrata  in  the  brain 
are  sleeping — i.  e.,  inhibited — whereas  other  areas  functionate  much  more  actively, 
and,  in  consequence  of  their  isolation,  oftentimes  in  peculiar  fashion.  A  motor 
phenomenon  frequently  connected  with  hysteric  disturbances  of  consciousness  is 
the  so-called  catalepsy  or  cataleptic  muscular  rigidity  described  upon  p.  751.  Such 
hysteric  (hypnotic)  conditions  associated  with  cataleptic  rigidity  are  ordinarily 
designated  as  catalepsy,  although  the  latter  expression  should  really  be  limited  to 
the  condition  of  the  motor  system,  and  not  include  that  of  the  consciousness. 

IRRITATIVE  DISTURBANCES  OF  CONSCIOUSNESS. 

Delirium  is  practically  the  only  one  of  these  irritative  disturbances 
which  concerns  the  clinician.  It  means  a  dream-like,  cloudy  state  of 
consciousness,  generally  associated  with  deranged  ideas,  in  which  the 
intellectual  capacity  is  altered  in  a  morbid,  irritative  way.  It  does  not 
preclude  a  depressive  condition  in  other  provinces  of  consciousness,  and 
so  delirious  patients  may  at  the  same  time  exhibit  stupor.  Delirium  is 
frequently  accompanied  by  hallucinations  and  illusions.  We  distinguish 
a  noisy  from  a  quiet  delirium.  The  highest  grade  of  the  former  is  the 
so-called  maniacal  delirium.  In  muttering  delirium  the  patient  lies 
quietly  in  bed  and  continually  mutters  to  himself.  Delirium  may  be 
observed  in  any  severe  general  condition ;  it  is  especially  frequent  in 
fever,  and  then  it  nearly  always  denotes  a  severe  sickness.  But  we 
should  remember  that  children  become  delirious  more  readily  than  adults, 
just  as  in  fever  their  temperatures  run  higher.  Many  acute  brain  dis- 
eases manifest  active  delirium. 

The  irritative  disturbances  of  consciousness  depressive  in  nature  which  accom- 
pany hysteria  and  which  occur  especially  in  the  so-called  "hysteria  major"  are 
essentially  a  variety  of  delirium,  and  should  be  attributed  partly  to  the  influence 
of  inhibition,  as  a  result  of  dejiressive  conditions  of  other  districts  of  con- 
sciousness. 

The  characteristic  delirium  of  alcoholism  (delirium  tremens)  is  for 
the  most  part  a  very  noisy,  maniacal  form,  and  is  almost  always  asso- 
ciated with  hallucinations.  The  patient  sees  black  forms,  mice,  bugs, 
snakes,  wires  running  through  the  air,  a  policeman,  etc.     These  appear- 


740 


EXAMISATION   OF  THE  NERVOUS  SYSTEM. 


ances  have  been  attributed  to  the  presence  of  scotomata  in  the  visual 
field  ;  but  if  this  explanation  were  correct,  the  condition  would  be  one 
of  illusions,  or  of  errors  in  sight,  not  of  real  hallucinations.  The  typi- 
cal tremor  which  almost  always  accompanies  delirium  tremens  may 
decide  the  diagnosis. 

Most  cases  of  quiet  delirium  which  are  noticed  in  patients  seriously 
ill  and  which  are  accompanied  w4th  the  so-called  carphologia  or  floccil- 
lation  render  the  prognosis  rather  grave.  The  patient  lies  completely 
oblivious  of  his  environment,  contmually  picking  at  the  bedclothes,  or 
making  motions  with  his  fingers  as  if  he  would  pick  off  flakes  or  scales. 
Carphologia,  a  symptom  which  generally  precedes  death  only  by  a  short 
time,  prol3ably  depends  upon  hallucinations. 

DISTURBANCES   OF  THE  INTELLIGENCE. 

These  may  be  independent  of  any  of  the  disturbances  of  conscious- 
ness, although  they  are  frequently  associated  with  them.  The  patient's 
history  or  a  previous  acquaintance  with  him  is  all  there  is  to  aid  the 


Fig.  284.— Cretinismus  fDr.  F.  C.  Shattuck, 
Massachusetts  General  Hospital). 


Fig.  2^").— Cretinismus.  Same  case  as  Fig.  284 
after  treatment  (Dr.  F.  C.  Shattuck,  Massachu- 
setts General  Hospital). 


physician  in  appreciating  the  milder  grade  of  disturbances  of  the  intel- 
ligence. On  the  contrary,  the  severer  grade  {stupidity)  and  the  highest 
grade  (imbecility)  are  evident  enough  from  the  facial  expression  and 
deportment  of  the  patient.  ■ 

Any  of  the  incurable  maladies  may  be  accompanied  by  the  milder 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  741 

disturbances  of  the  intelligence — e.  g.,  heart  disease,  nephritis.  Severe 
disturbances — i.  e.,  marked  stupidity  or  distinct  mental  disease — on  the 
contrary,  point  with  much  probability  to  disease  of  the  brain,  and,  if 
we  except  imbecility,  they  point  to  brain  tumor,  paralytic  dementia,  mul- 
tiple sclerosis,  or  the  after-effects  of  acute  focal  lesions  of  the  brain,  such 
as  hemorrhage  and  softening.  In  other  cases  imbecility  is  the  expression 
of  a  congenital  or  early  acquired  cerebral  anomaly  [idiocy  or  cretinism). 
The  disturbance  of  intelligence  which  is  observed  in  myxedema,  spon- 
taneous or  operative  (such  as  after  removal  of  a  goiter),  deserves  special 
mention.  This  condition  is  either  very  closely  related  to  or  identical 
with  cretinism.  Such  patients  exhibit  sometimes  mild  mental  disturbance, 
such  as  slowness  of  thought ;  sometimes  however,  a  much  more  serious 
trouble  bordering  on  real  imbecility. 

DISTURBANCES    OF    MEMORY. 

Memory  is  frequently  appreciably  impaired  in  old  but  otherwise  quite 
healthy  persons.  In  other  cases  it  may  be  affected  under  the  same  con- 
ditions as  the  intelligence.  In  fact,  after  acute  lesions  of  the  brain 
(hemorrhage  and  softening)  a  w^eakness  or  even  sometimes  a  complete 
loss  of  the  memory  is  very  often  noticed,  and  frequently  it  persists, 
although  the  intelligence  is  not  necessarily  affected.  The  so-called  trau- 
matic neuroses  are  very  often  accompanied  by  a  failing  memory. 

n.  EXAMINATION    OF   MOTILITY. 

I.  PARALYSIS. 

To  demonstrate  paralysis  the  examiner  requests  the  patient  to  per- 
form voluntary  motions  either  without  or  against  resistance.  If  par- 
alysis of  the  muscles  exists,  such  a  movement  is  either  not  performed 
at  all  (complete  paralysis)  or  more  slowly  and  less  completely  than  nor- 
mally (incomplete  paralysis,  paresis,  motor  weakness).  We  easily  recog- 
nize severe  paralysis  or  even  motor  weakness  in  this  way.  In  many 
instances  the  posture  of  the  body  at  rest  is  in  itself  so  distinctive  that 
we  need  no  attempt  at  motion  to  appreciate  the  complete  loss  of  power. 
For  example,  a  paralysis  of  the  eye  muscles  is  often  evident  from  the 
abnormal  position  of  the  eyeball ;  facial  paralysis  from  the  asymmetry 
of  the  face ;  paralysis  of  the  arm  from  the  dropping  and  dangling  of 
the  arm ;  peroneal  paralysis  from  the  drooping  of  the  tip  of  the  foot 
(equinovarus) ;  a  musculospinal  paralysis  from  the  wrist-drop  ;  an  ulnar 
paralysis  from  the  characteristic  claiv-like  position  of  the  fingers  (exten- 
sion of  the  proximal  phalanges  and  flexion  of  the  terminal  phalanges) ; 
a  median-nerve  paralysis  from  the  abduction  and  extension  of  the  thumb, 
simulating  the  ape  hand.  We  must,  however,  always  combine  inspec- 
tion with  an  attempt  to  secure  voluntary  movements,  since  to  make  a 
diagnosis  it  is  necessary  not  only  to  determine  a  paralysis,  but  also 
exactly  to  localize  it,  and  so  we  must  test  separately  the  functions  of  the 
individual  muscles  and  muscle  groups.  The  cranial  nerve  supply  will  be 
found  ujjon  pp.  826—883  ;  the  nerve  supply  of  the  muscles  of  the  remainder 


742 


EXAMmjiTION  OF  THE  NERVOUS  SYSTEM. 


of  the  body  upon  pp.  910-914.  If  the  paralysis  is  unilateral  and  not  very 
marked  the  examination  is  made  easier  by  comparing  the  healthy  with 
the  aifected  side.  In  this  way  we  can  demonstrate  in  hemiplegia,  for 
example,  a  weakness  of  the  trapezius  muscle,  as  well  as  of  the  respira- 
tory and  abdominal  muscles  of  the  paralyzed  side,  although  otherwise  it 
might  easily  escape  the  examiner's  notice.  The  rapidity,  the  force,  and 
the  excursion  of  the  movement  should  all  be  noted.  An  excellent 
method  for  detecting  a  very  slight  one-sided  paresis  of  an  arm  or  a  leg 
is  to  have  the  patient  raise  both  extremities  as  quickly  as  possible  at  the 
same  time.  The  paretic  arm  or  leg  will  then  be  plainly  seen  to  remain 
behind  the  healthy  member,  and  to  fall  more  quickly  from  the  raised 
position,  even  in  cases  where  in  testing  the  power  by  movements  against 


Fig.  286.— Right  hemiplegia,  organic  ;  excessive  flexion  of  the  right  forearm  upon  the  arm. 


opposition  we  can  scarcely  appreciate  any  abnormality.     AV^e  can  utilize 
the  hand  dynamometer  to  test  the  strength  of  the  hand. 

A  mechanical  liDiitation  of  movement  in  a  joint,  or  j^ain  incident  to  its  move- 
ment, sometimes  makes  the  movement  weak,  inefiectual,  or  almost  lacking,  and  so 
is  responsible  for  an  erroneous  diagnosis  of  motor  paralj'sis  or  paresis.  Therefore, 
before  assuming  the  presence  of  a  motor  weakness  we  should  particularly  examine 
for  such  a  condition  of  affairs.  Of  course,  patients  will  have  to  be  believed  in 
regard  to  the  influence  of  pain  upon  mobility,  although  they  are  often  very  unsat- 
isfactory in  their  statements.  They  will  acknowledge  that  they  feel  pain,  but 
deny  that  it  is  responsible  for  the  interference  of  motion.  Frequently  they  are 
firmly  convinced  of  the  existence  of  a  paralysis  until  the  pain  subsides  under 
treatment  and  permits  perfect  motion.  In  such  a  case  some  unappreciated  limi- 
tation of  motion  probably  exists,  depending  upon  pain.  If  the  limitation  of 
motility  persists  longer  than  the  painful  irritation,  the  so-called  hysteric  paralyses 
often  result. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


743 


Fig.  287.— Left  hemiplegia,  organic  (combined  flexion  of  the  left  thigh  and  trunk);  inability 
of  the  left  leg  to  remain  in  contact  with  the  floor  while  the  patient  attempts  to  sit  up  or  lie  down 
with  folded  arms.    The  legs  should  be  slightly  separated. 

[Babinski   has  called  attention  to  several  aids  in  differentiating  an 
organic  from  an  hysteric  hemijjlegia.     Three  of  these  are  well  illustrated 


Fig.  288.— Left  hemiplegia,  organic;  sign  of  the  platysma.    The  paralysis  of  the  platysma  upon 

the  left  side  is  evident. 

in  the  following  cuts  (Figs.  286,  287  and  288)  copied  from  his  article.^ 
—Ed.] 

'  Gaz.  des  Hop.,  1900,  No.  52,  p.  521. 


744  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

2.  PHENOMENA    OF    MOTOR    IRRITATION. 
(«)  Clonic  Convulsions  or  Contractions;  Qonic  Spasms. 

By  these  we  mean  involuntary  muscular  contractions  repeated  in 
shocks  or  series,  generally  with  considerable  force  and  rapidity,  and  con- 
trasted with  voluntary  contractions  badly  co-ordinated.  Thus,  in  spite 
of  the  great  expense  of  power,  there  often  results  only  very  slight  move- 
ment, because  antagonistic  muscles  are  working  in  opposition.  An  epi- 
leptic attack  and  the  typical  uremic  and  eclamptic  spasms  are  types  of 
the  clonic  convulsion. 

Clonic  convulsions  are  never  occasioned  by  peripheral  excitation  of 


Fig.  289.— Hvsteria  ;  blepharospasm.    Contrast  these  two  pictures  with  the  picture  of  ptosis  (Fig. 
320)  (Neurologic  Department,  Massachusetts  General  Hospital). 

motor  nerves.  An  irritative  center  whose  action  may  be  compared  to 
that  of  a  Leyden  jar  seems  to  be  essential  to  set  off  the  shock-like 
explosions.  Clonic  contractions  are  practically  always  occasioned  either 
by  a  direct  or  by  a  reflex  irritation  of  a  motor  center,  whether  it  be  the 
nucleus  or  the  psychmotor  center  of  the  cortex. 

{h)  Tonic  Convulsions;  Tonic  Spasms  or  Cramps. 

By  tonic  convulsions  are  understood  long-continued  rigid  convulsions 
of  muscles  which  may  change  suddenly  and  lead  to  prolonged  change 
of  position  or  tension  of  the  muscles  implicated.  Tonic  convulsions, 
may,  under  some  circumstances,  be  associated  with  or  even  transformed 
into  the  clonic  variety.  Tetanus  is  the  type  of  a  tonic  convulsion. 
Tonic  .convulsions  originate  in  most  cases  from  irritation  of  some  center, 
and  generally  reflexly  from   a   nucleus,   as,    for    instance,    in    tetanus, 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


745 


strychnia  tetanus,  tetany,  and  the  rigidity  of  the  neck  and  back  in 
meningitis.  The  well-known  cramp  of  the  gastrocnemius  which  is 
observed  in  health  and  in  choleraic  conditions,  but  whose  genesis  is 
still  obscure,  belongs  to  this  group. 

(c)  Contractures. 
When  a  joint  becomes  more  or  less  permanently  fixed  from  contrac- 
tion of  the  muscles  around  it,  so  that  active  or  passive  movements  are 
difficult  or  impossible,  the  condition  is  called  contracture.  The  increased 
tension  of  the  muscle  may  depend  upon  increased  tonus — i.  e.,  an  active 
(although  reflex)  contraction — so-called  active  or  irritative  contracture; 


Fig.  290.— Same  patient,  showing  an  attempt  to  open  left  eye.    Note  the  associated  movements  of 
the  muscles  supplied  by  other  branches  of  the  facial  nerve  (see  pp.  750  and  863). 

or  it  may  depend  merely  upon  a  nutritive  shortening  of  the  muscle, 
passive  contracture. 

Active  contractures  are  very  closely  related  in  their  origin  to  tonic 
convulsions,  and  are  to  be  distinguished  from  the  latter  only  by  being 
more  permanent.  In  contrast  with  passive  contracture,  active  contracture 
disappears  during  ether  or  chloroform  narcosis  ;  it  ordinarily  diminishes 
during  a  warm  bath.  Even  without  narcosis,  active  contracture  may  be 
overcome  sottietimes,  though  not  always.  Such  contractures  offer  a  some- 
what elastic  resistance  to  passive  movements  ;  they  are  practically  always 
associated  with  increase  in  the  corresponding  tendon  reflexes ;  every 
brusque  attempt  to  overcome  the  contracture  reflexly  increases  the  ten- 
sion ;  the  muscles  exhibit  no  signs  of  degeneration  ;  and  the  contractures 
exhibit  spontaneously  a  certain  slow  change  or  even  a  gradual  transition 
to  tonic  convulsions. 


746 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


Passive  contractures,  on  the  contrary,  are  decidedly  resistant  to  pas- 
sive movements.  They  are  influenced  neither  by  narcosis  nor  by  warm 
baths,  and  they  are  ordinarily  associated  with  diminution  of  the  tendon 
reflexes.     If  overcome  by  force,  which  is  only  possible  by  a  tearing  of 

tissue,  they  may  disappear  for  a  long  time. 
This  is  a  very  rare  occurrence  with  active 
contractures,  except  the  hysteric.  For  the 
differentiation  of  active  and  passive  con- 
tractures, Crocq  recommends  the  applica- 
tion of  the  Esmarch  bandage,  which,  like 
narcosis,  has  no  effect  upon  passive  con- 
tractures, but  causes  the  active  ones  to 
disappear. 

Active  contractures  may  occur  whenever 
the  muscle  tone  is  increased.  Since  the 
muscle  tone  is  of  reflex  origin,  this  comes, 
on  the  one  hand,  from  involvement  of  the 
reflex  inhibitory  fibers,  situated  perhaps  in 
the  pyramidal  tracts,  and,  on  the  other 
hand,  from  increased  irritability  of  the 
reflex  centers.  Curiously  enough,  active 
contractures  fix  the  upper  extremities  in 
a  position  of  flexion,  and  the  lower  ex- 
tremities in  extension.  This  agrees  with 
the  physiologic  ascendancy  of  the  muscles  in  question  over  their  antago- 
nists, and  with  the  predominance  of  extensor  paralysis  in  the  upper 
extremities.  To  explain  the  varying  relations  of  the  flexor  and  ex- 
tensor muscles  in  active  contractures,  Mann^  assumes  that  the  reflex 


Fig.  291. — Tetany  in  an  infant 
eleven  months  of  a'ge  (Dr.  Gannett, 
Massachusetts  General  Hospital). 


Fig.  292.— Tetany  in  an  infant  eleven  months  of  age  (Dr.  Gannett,  Massachusetts  General 

Hospital). 

inhibitory  fibers  for  the  flexors  run   with   the   psychomotor  fibers  of 

the  extensors,   and  the  inhibitory   fibers   for   the  extensors   with   the 

motor  fibers  for  the  flexors,  or,  which  the  author  thinks  more  prob- 

^  Monats.f.  Psychiatrie  u.  Neurologic,  vol.  iv.,  1898. 


PLATE  J2. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  747 

able,  are  identical  with  them.  This  supposition  coincides  very  well 
with  the  facts  demonstrated  by  Sherrington  and  Herring  (Physiologic 
Congress  in  Cambridge,  1892),  that  cortical  stimulation  of  a  muscle 
exerts  an  inhibitory  influence  upon  its  antagonists.  In  consequence  of 
this,  lesion  of  the  pyramidal  tract,  causing  a  preponderance  of  the 
paralysis  in  one  muscle  group  leads  to  the  preponderance  of  the  con- 
tracture in  its  antagonist.  Still,  a  simple  interruption  of  the  reflex 
inhibitory  tracts  does  not  seem  sufiicient  to  explain  the  original  of  well- 
marked  contractures.  Muscle  tonus  and  tendon  reflexes,  which  pass 
along  the  same  reflex  paths,  are  generally  increased  in  mere  interference 
of  spinal  cord  conduction  with  a  lesion  of  the  reflex  inhibitory  tracts 
(see  p.  782)  ;  but  an  actual  contracture  appears  only  when  a  descending 
degeneration  of  the  pyramidal  tracts  is  superadded.  For  some  unknown 
reason,  only  descending  degeneration  seems  to  be  able  to  cause  active 
contractures.  Perhaps  it  may  be  explained  by  assuming  that  the  lower 
end  of  the  inhibitory  paths  — L  e.,  the  pyramidal  tracts — even  when 
separated  from  the  source  of  the  inhibition  (the  central  apparatus),  still 
succeeds  in  causing  a  certain  inhibitory  influence  upon  the  muscle  tone, 
an  influence  which  disappears  entirely  only  when  the  tract  is  degenerated 
down  to  its  lowest  termination  in  the  motor  ganglion  cells  of  the  ante- 
rior horns.  When  active  contractures  depend  upon  an  anatomic  lesion, 
and  are  not  purely  functional  as  in  hysteria,  they  furnish  an  important 
sign  for  the  diagnosis  of  descending  secondary  degeneration  of  the  pyra- 
midal tracts,  both  in  the  brain  and  in  the  spinal  cord  {cerebral  hemorrhage, 
softening,  tumors,  transverse  myelitis,  cervical  hypertrophic  pachymen- 
ingitis, syringomyelia,  compression  of  the  spinal  cord,  etc.).  The  contrac- 
tures may  arise  in  a  similar  way  from  primary  systemic  degeneration  of 
the  pyramidal  tracts  {spastic paraplegia,  amyotrophic  lettered  sclerosis,  etc.). 
The  mechanism  of  hysteric  contractures  is  not  yet  fully  understood,  nor 
is  the  early  (at  times  almost  instantaneous)  occurrence  of  contractures 
of  the  paralyzed  extremities  (contractura  prsecox). 

Passive  contractures  occur  wherever  the  insertions  of  a  muscle  are 
permanently  approximated,  so  that  the  muscle  is  gradually  shortened  in 
a  nutritive  sense.  This  occurs  in  mechanical  fixation  of  joints  by 
bandages  which  have  been  applied  for  a  long  time  in  surgical  aifections, 
and  in  localized  atrophic  paralyses — e.  g.,  infantile  paralyses.  In  the 
latter  unparalyzed  antagonists  dislocate  the  affected  limb  permanently 
in  their  own  direction,  and  thereby  shorten  themselves,  in  the  nutritive 
sense.  There  is  still  another  type  of  passive  contracture  which  arises 
from  contracting  connective  tissue  which  gradually  takes  the  place  of  a 
paralyzed  and  degenerating  muscle  and  overcomes  the  tonus  of  the 
weaker  antagonists.  Here,  of  course,  the  contracture  is  not  in  the 
direction  of  the  preserved,  but  in  that  of  the  affected,  muscles. 

The  result  of  contractures  is  the  fixation  of  parts  which  we  see  so  frequently 
in  certain  paralyses.  These  deformities  have  been  variously  named  according  to 
the  anomalous  position  of  the  limbs.  For  example,  equinovarus  in  peroneal 
paralyses,  claw-hand  in  ulnar  paralysis  (Fig.  293),  the  ape  hand  in  median  par- 
alysis, the  preacher' .s  hand  in  pachymeningitis  cervicalis  hypertrophica.  Special 
pathology  should  be  consulted  for  more  details. 


748  EXAMIXATIOX  OF  THE  XEBVOUS  SYSTEM. 

(d)  Fibrillary  Twitching  (Better  CHaracterized  as  "Fascicular")* 

These  are  brief  cbronic  contractions,  not  of  an  entire  muscular 
belly,  but  of  mere  individual  groups  of  muscle  fibers.  Outside  of  the 
small  muscles  of  the  hand  and  face,  these  contractions  do  not  produce 
an  actual  locomotion  of  the  insertion  of  the  muscle,  but  merely  a  pecu- 
liar trembling  or  wave-like  rhythmic  vibration  of  the  muscular  mass. 
The  cause  of  fibrillar}^  twitching  is  not  yet  explained.  It  appears  in 
paretic  and  atrophied  muscles,  particularly  when  of  nuclear  or  sub- 
nuclear  origin  [in  sjyinal  neuritis,  muscular  atrophy,  and  bulbar  paraly- 
sis).    It  may  also  occur  even  without  paresis  or  atrophy — e.  g.,  in  the 


Fig.  293.— Claw -hand  of  ulnar  paralysis. 

traumatic  neuroses.  A  certain  diagnostic  significance  is  often  attributed 
to  this  phenomenon  because  it  is  an  impossible  symptom  to  simulate ; 
but  we  must  be  ver^^  guarded  in  drawing  conclusions,  because  the  action 
of  cold  upon  the  naked  body  of  many  healthy  individuals  may  cause 
fascicular  contractions. 

(e)  Tremor    (Trembling). 

Bv  tremor  we  mean  rapid  and  rhythmic  muscular  contractions 
which  are  relatively  but  .-lightly  pronounced.  They  produce  movement 
of  the  insertions  of  the  affected  muscle  or  the  skeletal  parts,  thus  differ- 
ing from  fascicular  contractions.  There  are  transition  forms  between 
donic  spasms  and  tremor,  as  well  as  between  fibrillary  contractions  and 
tremor.  We  distinguish  between  intention  tremor,  which  arises  only 
with  purposeful  movement,  and  tremor,  which  persists  during  rest.  The 
intention  tremor  is  typically  observed  in  multiple  sclerosis.  It  was 
formerly  regarded  as  a  paralytic  tremor,  since  it  was  assumed  that  the 
disturbed  conduction  transformed  the  voluntary  impulse  into  a  suc- 
cession of  rhythmic  impulses  (from  which,  as  physiology  teaches,  the 
voluntary  tetanic  contraction  is  constructed),  and  that  the  muscle  lost 
the  greater  portion  of  the  separate  stimuli.  From  recent  experience  it 
would  seem  that  this  view  can  no  longer  be  maintained.  The  author 
has  observed  that  in  cases  of  multiple  sclerosis,  where  the  increased 
tendon  reflexes  lead  to  clonic  tendon  reflexes  (ankle  clonus,  knee  clonus, 
wrist  clonus,  etc.),  the  intention  tremor  is  often  synchronous  with  the 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  749 

clonus.  This  would  certainly  indicate  that  the  tremor  of  multiple 
sclerosis  is  nothing  else  than  a  clonic  tendon  or  muscle  reflex  which  is 
excited  and  maintained  by  the  tension  which  the  muscle  experiences 
during  the  intended  movement.  The  tremor  of  multiple  sclerosis  is 
consequently  a  spastic  phenomenon,  as  is  also  true  of  the  majority  of 
tremors.  This  conception  of  the  intention  tremor  of  multiple  sclerosis 
explains  why  it  may  gradually  assume  the  character  of  those  less 
regular  arrhythmic  contractions  which  appear  during  the  course  of  vol- 
untary movements  and  make  them  simulate  ataxia.  The  so-called  rest 
tremor  is  not  dependent  on  voluntary  movement,  but  occurs  also  during 
rest.  In  fact,  it  may  be  present  only  during  rest,  and  may  sometimes 
be  voluntarily  controlled.  This  variety  of  tremor  is  one  of  the  char- 
acteristics of  paralysis  agitans.  It  is  a  spastic  phenomenon,  the  cause 
of  which  is  located  above  the  circuit  of  the  tendon  reflexes,  and  has 
nothing  to  do  with  an  increase  of  these  reflexes. 

To  avoid  overlooking  tremor  of  any  sort,  we  should  observe 
patients  both  at  rest  and  during  purposeful  movements,  as  well  as  in 
positions  of  the  body  which  require  muscular  action — e.  g.,  horizontal 
projection  of  the  forearm  and  hands  with  the  fingers  spread. 

The  characteristics  of  the  well-known  tremors  are  as  follows : 

1.  The  peculiarity  of  intention  tremor  in  multiple  sclerosis  is  that  it 
ceases  during  repose  and  ttiat  it  is  very  slight  at  the  beginning  of  the 
movement,  then  gradually  becomes  more  extensive  and  rapid  until  it 
seriously  interferes  with  the  accomplishment  of  the  attempted  move- 
ment. The  excursions  are  frequently  so  large  and  the  rhythm  of  the 
oscillations  so  irregular  that  the  tremor  resembles  ataxia ;  but  the 
attempted  movement  always  keeps  at  least  to  its  general  direction. 
The  tremor  of  multiple  sclerosis  is  usually  more  pronounced  in  the 
upper  extremities. 

2.  The  tremor  in  paralysis  agitans  is  relatively  slow,  persists  dur- 
ing repose,  is  usually  somewhat  lessened  by  purposeful  movements,  and 
is  inhibited,  often  for  a  considerable  time,  by  a  very  strong  voluntary 
impulse.  The  rate  of  the  oscillations  is  usually  5  or  6  in  the  second.  The 
tremor  is  generally  noticed  first  in  the  hands,  in  which  it  is  especially 
distinctive.  It  often  resembles  certain  fine  intention  mov^ements  like 
the  rolling  of  a  pill  between  the  thumb  and  forefinger.  There  is  rarely 
any  tremor  of  the  head  in  paralysis  agitans,  but  to  this  rule  there  are 
exceptions. 

3.  In  senile  tremor  there  are  4  to  6  oscillations  in  the  second.  In 
less  marked  cases  it  is  an  intention  tremor ;  in  more  marked  cases  it 
also  continues  during  rest.  The  head  and  frequently  the  lower  jaw,  as 
well  as  the  upper  extremities,  are  the  seats  of  this  variety  of  tremor. 

4.  The  tremor  of  exophthalmic  goiter  and  of  other  neuroses  (hjB- 
teria)  is  usually  fine  and  rapid  (8  to  9  oscillations  to  the  second).  It 
can  generally  be  recognized  most  easily  in  the  hands  when  they  are 
extended  horizontally  with  the  fingers  apart.  Purposeful  movements 
of  the  hands  sometimes  increase  it. 

5.  ToxiG    tremor  may  assume  varied  forms    in  alcoholics,  morphin 


750  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

habitues,  in  those  poisoned  by  mercury  and  lead,  as  well  as  in  acute  and 
chronic  nicotin-poisoning.  Alcoholic  tremor  is  characterized  by  early 
involvement  of  the  lips,  as  well  as  of  the  hands.  It  is  most  pro- 
nounced during  purposeful  movements,  and  ordinarily  disappears  after 
taking  a  large  quantity  of  alcohol.  The  toxic  tremors  are,  as  a  rule, 
rapid. 

It  should  be  borne  in  mind  that  in  addition  to  these  varieties  tremor 
may  under  some  circumstances  occur  in  health — e.  g.,  after  vigorous 
bodily  exercise,  from  mental  excitement,  intense  cold,  etc.  Diagnostic 
stress  can  therefore  be  attributed  to  the  occurrence  of  a  tremor  only 
after  these  physiologic  conditions  are  excluded. 

(/ )  Choreic  and  Athetoid  Movements. 

Choreic  movements,  or  chorea,  are  involuntary  (often  very  extensive), 
muscular  contractions,  which  are  not  like  clonic' convulsions,  absolutely 
without  co-ordination,  despite  their  lack  of  purpose  or  rule  in  co-ordi- 
nation. They  can  be  differentiated  from  voluntary  movements  by 
their  bizarre  character  and  their  aimlessness.  In  pronounced  chorea, 
the  entire  body  is  thrown  into  constant  motion,  so  that  any  attempt  at 
purposeful  movements  is  often  entirely  fruitless.  Chorea  of  the  facial 
muscles  is  exhibited  by  grimaces ;  chorea  of  the  breathing,  voice,  and 
speech  muscles  by  the  choreic  articulation,  which  may  render  speech 
quite  incomprehensible.  Choreic  movements  are  most  pronounced  in 
the  neurosis  chorea,  in  which  they  constitute  the  principal  symptom. 
Symptomatically,  choreic  movements  occur  in  the  form  of  hemichorea 
in  some  cases  of  hemiplegia,  especially  with  lesions  of  the  posterior 
part  of  the  internal  capsule,  and  the  optic  thalamus  (chorea  post-  or  pre- 
hemiplegia). 

Athetosis  may  be  regarded  as  a  variety  of  chorea.  When  the  invol- 
untary movements  occur  slowly  and  very  regularly,  the  condition  is 
called  athetosis.  Its  significance  is  not  essentially  distinct  from  that 
of  ordinary  symptomatic  chorea.  Posthemiplegic  athetosis,  involving 
the  muscles  of  the  hand  and  fingers,  is  the  most  frequent  form. 

The  muscle  unrest  observed  in  Friedreich's  or  hereditary  ataxia  is 
diagnostically  an  important  symptom.  French  authors  speak  of  it  not 
unfittingly  as  "  instabilite  chor^iforme."  It  also  belongs  to  the  symp- 
tomatic conception  of  chorea. 

{(f)  Associated  Movements. 
These  are  to  a  certain  extent  physiologic.  They  depend  upon  the 
fact  that  intense  motor  impulses  which  escape  inhibition  are  switched 
off  to  neighboring  or  more  distant  muscle  territories.  Pathologic  asso- 
ciated movements  are  noticed  especially  when,  through  some  interrup- 
tion of  conduction,  the  impulse  of  the  will  cannot  be  transmitted  in  a 
physiologic  direction.  A  weakening  of  the  physiologic  associated 
movements  in  the  territory  supplied  by  the  facial  nerve  is  sometimes 
of  service  in  suggesting  the  existence  of  a  paresis  of  this  nerve  quite 
early  in  its  involvement. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  751 

Striimpell  has  described  a  special  form  of  associated  movement  as  "tibial 
phenomenon";  it  consists  of  a  contraction  of  the  tibialis  anticus  during  adduc- 
tion of  the  leg.  This  phenomenon  is  observed  in  spastic  paralysis,  and  is 
regarded  by  Striimpell  as  indicative  of  an  anatomic  lesion  in  the  pyramidal  tract. 
According  to  Mann,  this  phenomenon  may  also  be  reversed,  the  leg  being  adducted 
when  the  tibialis  anticus  contracts.  Other  associated  movements  occurring  with 
lesions  in  the  pyramidal  tract  are,  according  to  Striimpell,  extension  of  the  great 
toe  during  extension  of  the  leg;  the  so-called  radial  phenomenon,  which  consists 
of  extension  at  the  wrist  during  flexion  of  the  fingers;  and  a  pronation  of  the 
hand  which  follows  the  elevation  of  the  forearm  from  a  dependent  position,  the 
palm  having  been  directed  anteriorly.  As  a  symptom  of  a  lesion  in  the  pyram- 
idal tract,  Babinski  describes  an  associated  movement  occurring  particularly  in 
hemiplegia,  which  consists  of  the  elevation  of  the  paralyzed  thigh  when  the 
reclining  patient  sits  up  or  simply  attempts  to  assume  a  sitting  posture. 

In  reference  to  the  associated  movements  of  the  eyeball  in  facial  paralysis, 
which  have  been  described  as  Bell's  phenomenon,  the  reader  is  referred  to  p.  863 
et  seq. 

(h)  Forced  Movements* 

These  movements,  which  are  sufficiently  characterized  by  their 
name,  are  highly  co-ordinated,  and  so  constituted  that  they  can  be 
simulated. 

They  are  especially  typified  by  most  of  the  hysteric  spasms,  laugh- 
ing and  crying  spasms,  "arc  de  cercle,"  "grands  mouvements,"  and 
"  attitudes  passionelles,"  as  well  as  by  many  phenomena  of  convulsive 
tic.  The  forced  movements,  lateral  positions,  rolling  and  manege  move- 
ments of  patients  with  lesions  of  the  median  cerebellar  peduncle  belong 
to  the  same  category. 

A  peculiar  form  of  forced  movement  is  the  so-called  forced  laughing  which 
occurs  as  one  of  the  characteristic  symptoms  of  multiple  sclerosis.  The  laughter 
of  these  patients,  whether  it  be  spontaneous  or  the  result  of  external  stimuli,  is 
spasmodic  and  uncontrollable  ;  it  apparently  arises  in  the  ordinary  psychologic 
way,  and  then,  according  to  the  statements  of  the  patient,  takes  on  all  of  the 
characteristics  of  a  pure  somatic  spasm.  The  fact  that  the  forced  laughing  of 
multiple  sclerosis  is  associated  with  a  spasmodic  condition  of  the  musculature 
and  increased  muscle  and  tendon  reflexes  would  naturally  lead  us  to  suppose  that 
the  slight  motor  stimulation  and  tension  of  the  laughing  muscles  always  pro- 
duced by  the  suggestion  of  laughter-exciting  objects  or  ideas,  together  with  the 
increased  reflex  activity  of  the  laughing  muscles,  is  sufficient  to  throw  the  laugh- 
ing mechanism  into  increased  and  continued  spasmodic  action. 

(i)  Catalepsy;   Cataleptic  Rigidity  (Flexibilitas  Cerea). 

By  catalepsy  is  understood  a  peculiar  state  of  the  motor  system  not 
yet  explained,  in  which  the  limbs  seem  to  be  fixed  and  to  present  to 
passive  motion  a  moderate  dough-like  resistance,  retaining  for  a  longer 
or  shorter  period  the  position  given  them.  Catalepsy  can  be  differen- 
tiated from  active  contractures  by  the  fact  that  the  parts  do  not  resume 
their  former  position  after  they  have  been  forcibly  changed.  This  cata- 
leptic condition  of  the  muscles  occurs  in  the  hysteric,  in  hypnosis  (see 
p.  739),  in  the  psychosis  designated  katatonia,  and  sometimes  in  brain 
tumors  leading  to  stupor  [especially  those  implicating  the  corpus  cal- 
losum. — Ed.]  . 


752  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

(k)  Myotonia. 
This  is  a  rare  condition  of  the  muscles  which,  as  yet,  has  been  ob- 
served only  in  Thomsen's  disease  (myotonia  congenita).  In  this  affec- 
tion the  muscles  appear  normal  during  repose,  but  when  voluntary 
movements  are  attempted  assume  a  characteristic  tension  which  hinders 
the  movements.  The  tension  then  gradually  diminishes,  enabling  the 
movements  to  proceed  in  an  approximately  normal  way.  (See  later, 
Myotonic  Reaction,  p.  815). 

3.  ATAXIA;    DISTURBANCE    OF    CO-ORDINATION  AND   SO-CALLED 
CEREBELLAR  ATAXIA. 

To  facilitate  better  comprehension  of  this  section,  it  is  advisable  to 
read  first  the  section  upon  Examination  of  Complicated  Sensory  Func- 
tions, p.  766  et  seq. 

Ataxia  means  absence  or  disturbance  of  the  co-ordination  necessary 
to  the  accomplishment  of  purposeful  movements.  Co-ordination  is  the 
effectual  distribution  of  voluntary  impulses  to  the  groups  of  muscles 
which  must  act  harmoniously  in  each  intended  movement.  Ataxic 
movements  are  inco-ordinated  or  badly  co-ordinated  movements. 

Ataxia  shows  itself  clinically  by  movements  which  are  not  neces- 
sarily curtailed  in  power,  but  which  accomplish  a  result  different  from 
the  one  expected.  Ataxic  movements  produce  an  impression  of  inse- 
curity ;  they  either  overshoot  the  mark,  or,  conversely,  do  not  reach  it 
or  reach  it  in  a  roundabout  way  with  loss  of  time.  The  movements  of 
a  child  making  his  first  attempt  at  walking  present  the  best  picture  of 
ataxia  ;  he  is  not  yet  "  master  of  his  muscles."  Ataxia  is  to  be  demon- 
strated clinically  by  observing  how  a  patient  performs  voluntary  move- 
ments. If  the  ataxia  is  pronounced  it  may  be  evident  in  the  simplest 
movements,  because  even  these  require  co-ordination  of  various  muscle 
groups.  If  less  marked,  it  may  be  noticed  only  in  attempts  at  more 
complicated  and  finer  movements.  Ataxia  of  the  lower  extremities  is 
usually  most  noticeable  in  the  patient's  gait.  A  pronounced  ataxia 
gait  presents  a  peculiar  clinging,  swinging,  frequently  stamping  char- 
acter. Ataxia  of  the  upper  extremities  may  be  tested  by  having  the 
patient  attempt  to  touch  an  object — e.  g.,  his  nose  with  the  index  finger. 
If  he  is  ataxic  he  will  either  be  unable  to  do  so,  or  he  will  succeed  only 
after  several  trials.  In  a  similar  way  the  lower  extremities  may  be 
tested  for  ataxia.  Ataxia,  both  of  the  upper  and  lower  extremities,  is 
usually  increased  when  the  patient's  eyes  are  closed  and  he  is  thus 
deprived  of  the  aid  furnished  by  the  sense  of  sight  in  correcting  his 
movements. 

Ataxia  appears  typically,  and  by  far  the  most  frequently,  in  tabes 
dorsalis,  in  hereditary  tabes  or  so-called  Friedreich' s  disease,  in  lesions  of 
the  motor  cortex  (cortical  ataxia),  in  polyneuritis,  especially  in  'polyneu- 
ritis alcoholica,  and  rarely  in  multiple  sclerosis. 

In  each  case  the  ataxia  may  arise  from  a  different  cause.  It  seems 
to  be  certain  that  in  children  co-ordination  is  learned  essentially  by  the 
sensory  control   of  the  completed  movements.      A   child  congenitally 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  753 

anesthetic  and  blind  would  never  learn  to  perform  co-ordinate  move- 
ments. Sensory  control  is  necessary  for  the  acquisition  of  co-ordination, 
and  probably  likewise  for  its  preservation,  although  perhaps  not  in  the 
fullest  measure.  We  may  therefore  say  that  the  disturbances  of  sensi- 
bility which  occur  contemporaneously  with  ataxia  have  a  direct  bearing 
upon  the  occurrence  of  the  latter.  This  is  especially  plausible  in  tabes 
dorsalis,  in  which  sensory  disturbances  are  the  rule.  It  is  self-evident 
that  the  sensibility  of  the  skin  is  of  much  less  importance  than  that  of 
the  deeper  parts — the  joints  and  the  muscles — which  aid  us  so  efficiently 
in  determining  changes  of  position  of  the  extremities.  (See  Testing  the 
Appreciation  of  Passive  Movements,  p.  767  etseq.).  Therefore  it  fol- 
lows that  ataxia  need  not  accompany  a  pronounced  cutaneous  anesthesia, 
provided  the  perception  of  passive  movements  is  not  aifected. 

In  many  examples  of  ataxia,  however,  we  cannot  determine  any 
very  extensive  disturbances  of  the  deep  sensibility  of  the  extremities,  so 
that  we  must  search  elsewhere  for  the  explanation.  Many  authors 
(especially  v.  Leyden  and  Goldscheider)  assume  correctly,  as  the 
author  thinks,  that  the  disturbances  of  sensibility,  especially  in  tabes, 
are  frequently  overlooked,  because  sufficiently  accurate  methods  of 
examination  are  not  employed  to  disclose  the  slight  degrees  which  are 
present.  In  fact,  it  is  conceivable  that  very  insignificant  disturbances 
of  sensibility  of  joints,  tendons,  and  muscles  are  quite  capable  of  up- 
setting that  fine  control  which  is  regulated  by  unknown  centripetal 
impulses  and  which  persists  during  movement  only  for  an  instant,  and 
yet  are  so  slight  that  they  might  be  entirely  overlooked  during  a  rough 
test.  It  should  be  borne  in  mind  that,  by  means  of  the  mechanism 
described  upon  p.  767,  the  sensation  of  innervation  for  the  percep- 
tion of  passive  movements  of  the  extremities  may  also  be  utilized. 

Even  after  excluding  these  cases  with  sensory  disturbances  which  are 
rather  insignificant  and  difficult  to  demonstrate,  there  still  remain  other 
cases  in  which  such  an  explanation  does  not  apply,  and  for  which, 
therefore,  we  must  work  out  some  other  of  the  explanations  which 
follow  deductively  from  the  theory  of  ataxia. 

Co-ordination,  as  we  have  seen,  is  accomplished  to  a  certain  extent 
after  the  manner  of  a  reflex,  using  the  word  reflex  in  its  broadest  sense. 
Peripheral  stimulation  incites  the  central  organs  to  transmit  throughout 
the  duration  of  the  movement  just  the  appropriate  amount  of  motor 
stimulation  to  each  muscular  district  concerned.  Obviously,  such  a 
procedure  may  be  damaged  either  in  the  sensory  limb  of  the  reflex  arc, 
in  the  psychomotor  center,  in  its  immediate  neighborhood  where  the 
centripetal  stimulation  is  transferred  to  the  center,  or,  finally,  in  the 
motor  limb  of  the  reflex  arc.  Injury  of  any  one  of  these  components 
will  probably  produce  ataxia. 

In  the  so-called  cortical  or  central  ataxias  which  are  observed  in 
fiDcal  lesions  of  the  motor  convolutions  unaccompanied  by  sensory  dis- 
turbances, we  must  assume  that  the  cortical  centers  have  lost  their 
capacity  of  carrying  out  normally  co-ordinated  representations  of  move- 
ments and  imjjulses.     We  cannot,  however,  exclude  the  possibility  of 

48 


754  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

such  ataxias  arising  from  an  imperfect  conduction  of  the  centripetal 
sensory  impulses  to  the  motor  center,  for  an  imperfect  conduction  is 
quite  possible,  even  if  the  sensory  appreciation  itself  seems  normaL 
Whenever  an  ataxia  of  cortical  origin  is  also  associated  with  sensory 
disturbances  for  the  appreciation  of  passive  movements,  the  latter  diffi- 
culty alone  is  quite  sufficient  to  account  for  the  ataxia,  just  as  it  is  in 
tabes.  In  such  cases  the  only  distinction  from  tabes  would  be  that  in 
the  cortical  variety  the  sensory  path  would  be  affected  much  nearer  to 
the  motor  center  than  to  the  periphery.  As  a  rule,  these  cortical 
ataxias  are  not  very  pronounced,  at  least  in  so  far  as  they  depend  upon 
an  extensive  lesion  of  the  motor  cortex,  because  if  the  cortical  lesion  is 
very  large  the  picture  of  the  paralysis  overshadows  that  of  the  ataxia. 
(Consult  p.  763  in  regard  to  the  character  and  recognition  of  the  ataxia 
due  to  disturbances  of  the  representations  of  movement.) 

A  lesion  in  the  motor  limb  of  the  "  co-ordination  arc "  may  also 
produce  ataxia,  as  is  well  shown  by  the  cases  of  motor  polyneuritis 
without  sensory  disturbances.  It  is  clear  that  a  co-ordinated  impulse 
can  accomplish  its  proper  action  only  when  the  conduction  is  perfect, 
even  down  to  the  muscles.  If  certain  ramifications  of  the  motor  con- 
duction are  affected  by  serious  obstructions,  the  co-ordinated  impulse  is 
naturally  curtailed  and  ataxia  must  result.  Under  these  conditions  a 
certain  degree  of  motor  paralysis  would,  from  the  nature  of  things,  be 
present,  and  many  authors  are  inclined  to  exclude  such  an  ataxia  with 
paresis  from  the  true  ataxias,  and  to  call  it  a  pseudo-ataxia.  The 
author  does  not  consider  this  justifiable.  The  characteristics  of  these 
cases  may  be  exactly  the  same  as  of  those  of  other  origin,  and  even  the 
theoretic  difference  exists  only  in  a  different  localization  of  the  inter- 
ruption of  conduction  within  the  aforesaid  reflex  arc.  Moreover,  we 
must  assume  an  interruption  of  conduction  also  both  in  ataxias  of  sen- 
sory origin  and  in  the  cortical  or  central  ataxias,  independent  of  sensory 
disturbances.  Besides,  in  cases  of  polyneuritic  ataxia  the  paralysis  is 
sometimes  very  much  in  the  background  or  can  hardly  be  observed  at 
all.  To  be  sure,  such  a  paralysis  could  always  be  detected  if  we  were 
able  to  test  the  motor  power  of  each  muscle  individually  ;  but  this  is 
not  possible,  because  in  general  we  can  test  muscles  only  as  groups. 
Hence  slight  paresis  of  individual  muscles  may  readily  escape  our 
notice,  although  it  suffices  to  explain  the  ataxia.  Ataxia  may  even  be 
caused  by  mere  diminution  in  the  tone  of  certain  groups  of  muscles, 
from  peripheral  disturbances  of  conduction  which  cause  retarded  action 
of  these  muscles. 

The  above  explanation  postulates  co-ordination  as  a  complicated 
reflex  which  is  centered  in  the  cortex.  In  opposition  to  this  conception, 
Cyon  has  attempted  to  localize  the  co-ordinating  reflex  center  in  the 
spinal  cord.  His  hypothesis  not  only  fails  to  explain  cortical  ataxia, 
but  is  also  opposed  to  our  idea  of  the  simplicity  and  elementary  nature 
of  the  spinal-cord  reflexes.  Yet  it  must  be  acknowledged  that,  inas- 
much as  it  determines  muscle  tonus,  the  spinal  cord  does  play  some 
part  in  co-ordination,  because  a  muscular  action  takes  place  promptly 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  755 

and  securely  only  when  the  muscle  at  the  beginning  of  its  contraction 
possesses  a  sufficient  degree  of  tension. 

Our  hypothesis,  nevertheless,  does  not  admit  of  a  special  co-ordi- 
nating center  in  the  brain  distinct  from  the  motor  centers  of  the  cortex, 
and  from  this  a  centrifugal  co-ordinating  tract  descending  through  the 
cord.  Many  authors,  however,  have  assumed  this.  The  truth  is  that 
all  our  knowledge  of  the  function  of  the  cerebral  cortex,  especially  our 
views  upon  motor  aphasia  and  the  results  of  stimulating  the  motor 
cortex  in  animal  experiments,  shows  that  the  cortex  is  the  motor  organ 
of  highest  development,  and  that  it  sends  out  impulses  which  have  been 
already  co-ordinated.  If,  however,  as  is  practically  certain,  the  psycho- 
motor or  pyramidal  tract  transmits  co-ordinated  impulses  as  a  direct 
radiation  from  the  cortical  motor  center,  it  is  quite  incomprehensible 
what  there  is  for  special  co-ordinating  centers  and  co-ordinating  tracts 
to  do.  The  theory  that  the  degeneration  of  the  posterior  column  in 
tabes  involves  a  special  centrifugal  co-ordinating  tract,  and  so  leads  to 
ataxia,  is  thus  disproved,  even  if  we  disregard  wholly  the  fact  that  the 
posterior  columns  are  nothing  but  prolongations  of  the  sensory  roots, 
a  fact  which  has  been  proved  both  anatomically  and  experimentally. 
As  a  matter  of  fact,  this  theory,  opposed  to  the  attribution  of  ataxia 
uniformly  to  disturbances  of  sensibility,  was  advanced  only  to  explain 
cases  of  tabes  in  which  ataxia  was  found  presumably  without  sensory 
disturbances.  But  even  if  we  disregard  the  probability  of  having  over- 
looked slight  disturbances  in  sensibility  of  the  deeper  parts  (especially 
emphasized  by  v.  Leyden),  these  cases  are  easily  explained  by  assuming 
that  the  ataxia  depends  either  upon  involveineut  of  the  representations 
of  movement  in  the  motor  cortex  or  upon  lesions  of  the  peripheral 
motor  tracts.  Pathologic  changes  have  been  found  both  in  the  cortex 
(Jendrassik,  see  p.  764)  and  in  the  peripheral  nerves  of  tabetic  patients. 
As  has  been  mentioned,  ataxia  may  also  depend  upon  a  disturbance  of 
muscle  tonus.  This  latter,  which  is  ordinarily  very  striking  in  tabes, 
can  readily  be  explained  by  the  lesions  of  the  reflex  collaterals  and  of 
the  posterior  columns,  even  without  any  sensory  disturbance.  We 
know  that  the  fibers  of  the  pyramidal  tracts  subdivide  in  the  cord  into 
"  collaterals,^^  just  as  the  sensory  fibers  of  the  posterior  columns  do,  and 
that  these  '^collaterals"  are  first  connected  with  the  ganglion  cells  of 
the  anterior  horns  by  means  of  "  terminal  arborizations."  Hence  we 
must  accept  the  fact  that  ataxia  may  ensue  from  partial  lesions  of  the 
pyramidal  tract  in  the  neighborhood  of  the  "  collaterals,"  as  the  result 
of  an  imperfect  distribution  of  the  motor  impulses. 

So-called  "  cerebellar  ataxia "  requires  special  mention,  as  sympto- 
matically  it  does  not  agree  with  the  picture  of  ataxia  described  above, 
nor  can  it  be  explained  in  the  same  way.  It  may  be  described  as  a 
characteristic  reeling,  both  in  walking  and  standing,  AA'hich  is  observed 
especially  in  patients  with  cerebellar  tumors,  particularly  when  the 
worm  is  involved.  This  staggering  gait,  resembling  that  of  a  drunken 
person,  is  quite  different  from  the  gait  of  the  true  tabetic.  It  results 
from  the  disturbance  of  equilibrium  which  occurs  in  cerebellar  diseases, 


756  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

and  is  attributed  to  the  relation  of  the  cerebellum  to  the  semicircular 
canals.  We  assume  that  this  connection  is  established  by  the  median 
acoustic  roots  crossing  over  in  the  vestibular  nerve.  Cerebellar,  as  con- 
trasted with  true,  ataxia  is  associated  with  vertigo,  and  for  the  most 
part  is  noticed  only  while  the  patient  is  walking  or  standing ;  whereas, 
while  he  is  lying  in  bed,  the  movements  of  the  legs,  as  well  as  those 
of  the  arms,  appear  quite  normal. 

There  is,  however,  sometimes  a  distinct  uncertainty  in  the  movements  of  the 
arms  and  legs  even  in  bed,  which  is  suggestive  of  tabes  dorsalis.  This  will  be 
understood  if  we  remember  that  scarcely  any  extensive  movement  of  the  extremi- 
ties is  possible  without  some  more  or  less  vigorous  participation  of  the  sense  of 
equilibrium  on  the  part  of  the  cerebellum  in  order  to  correct  the  altered  relations 
of  gravity.  The  changed  muscle  tonus  which  is  almost  always  demonstrable  in 
these  cases  may  also  play  a  pai't  in  this  true  ataxia  of  cerebellar  disease.  This 
association  of  change  of  muscle  tonus  with  cerebellar  affections  has  been  explained' 
by  the  work  of  Luciani,  which  shows  that  the  muscle  tonus  is  diminished  by 
extirpation  of  the  cerebellum.  It  has  previously  been  pointed  out  that  a  dimin- 
ished muscle  tonus  may  jDroduce  ataxic  phenomena.  We  consequently  see  that 
the  so-called  cerebellar  ataxia  is  made  up  of  two  components — the  disturbance 
of  equilibrium  and  actual  ataxia. 

The  gait  is  similarly  affected  when  centripetal  stimulations  are  not 
transmitted  normally  to  the  cerebellum,  for  these  are  essential  to  its 
role  as  the  organ  of  equilibrium — e.  g.,  in  eye-mnsde  paralysis,  and  in 
affections  of  the  organs  of  hearing  which  lead  to  vertigo,  especially  in 
affections  of  the  sanicircyular  canals  (Meniere's  disease).  The  same 
thing  is  seen  in  hereditary  ataxia,  in  which  it  is  probably  due  to  the 
loss  of  the  centripetal  impulses  conveyed  to  the  cerebellum  through  the 
direct  cerebellar  tract  and  the  tract  of  Gowers. 

m.  GENERAL  DISCUSSION  OF  THE  METHODS  OF  TESTING 
THE  SENSIBILITY. 

The  method  of  testing  the  higher  senses  will  be  described  in  the 
part  devoted  to  the  special  examination  of  the  cranial  nerves.  Here 
we  mention  merely  the  testing  of  the  common  sensibility,  especially  of 
the  trunk  and  extremities.  The  w^ork  of  M.  Burchardt,  referred  to 
upon  p.  760,  should  be  consulted  in  regard  to  the  simulation  of  sen- 
sory paralysis,  and  also  p.  760,  concerning  the  impossibility  of  simu- 
lating certain  results  obtained  by  testing  the  pressure  sense  wdth  v. 
Frey's  "irritation  hairs." 

SENSORY  PARALYSIS. 

Complete  abolition  of  the  sensibility  of  a  definite  part  of  the  body 
is  called  anesthesia;  a  mere  diminution  of  sensibility,  hypesthesia.  In 
all  examinations  for  sensory  defect  it  is  important  to  have  the  patient 
shut  his  eyes,  in  order  to  exclude  any  visual  control  of  the  results, 
intentional  or  otherwise. 

The  examination  is  complicated  because  it  includes  the  determina- 
tion of  the  relations  of  very  different  sensory  functions. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


757 


(a)  Examination  of  Simple  Sensory  Functions. 

Method  of  Testing-  Tactile  and  Pressure  Sensibility. — 

Tactile  and  pressure  sensibilities  are  in  a  way  identical.  The  estima- 
tion of  pressure  sensibility  is  nothing  more  than  a  quantitative  estima- 
tion of  the  sensation  of  touch.  Conversely,  the  examinatiou  of  tactile 
sensibility  furnishes  a  merely  qualitative  estimation  of  the  pressure 
sense.  Among  other  things  in  favor  of  this  conception  is  the  circum- 
stance that  both  senses  are  localized  at  identical  points  of  the  skin,  the 
so-called  pressure  points  (see  below). 

Tactile  sensibility  is  tested  by  touching  the  patient's  skin  lightly 
with  the  tip  of  the  finger,  or,  in  finer  tests,  by  means  of  a  dry  camel's- 
hair  brush,  and  ascertaining  whether  he  feels  the  touch 
or  not ;  if  so,  what  he  feels  and  where  he  feels  it. 
Anesthetic  spots  can  then  be  marked  upon  the  skin 
with  a  dermatographic  pencil  (p.  164),  and  the  re- 
sult afterward  transferred  to  a  diagram  of  the  body. 
By  means  of  this  test  we  can  sometimes  determine  a 
complete  loss  of  tactile  sensibUity  over  a  considerable 
area ;  in  other  cases  we  can  gather  from  the  patient's 
statements  that  he  appreciates  the  touch,  but  less 
plainly  than  normal,  showing  only  a  slight  diminu- 
tion of  tactile  sensibility.  The  comparative  exami- 
nation of  different  symmetric  parts  of  the  body  is 
here  of  the  greatest  importance.  (In  regard  to  the 
significance  of  so-called  tactile  hyperesthesia  or,  bet- 
ter, hyperalgesia,  compare  the  section  on  Sensory  Ir- 
ritative Phenomena,  p.  769  et  seq.) 

Pressure  sensibility  or  perception — i.  e.,  the  quan- 
titative appreciation  of  the  sense  of  touch — can  be 
tested  accurately  only  when  the  skin  has  a  firm  sub- 
cutaneous support — e.  g.,  over  the  ulna  and  radius. 
The  part  to  be  examined  must  itself  be  firmly  sup- 
ported. Otherwise,  to  appreciate  the  pressure,  a  pa- 
tient would  make  use  of  his  muscular  power- — i.  e., 
the  innervation  sense  (see  p.  762  etseq.) — and  the  re- 
sults would  no  longer  be  correct.  Gross  disturbances 
may  be  recognized  accurately  by  simply  touching  the  patient's  skin  with 
the  finger-tip,  varying  the  amount  of  pressure  and  having  him  describe 
what  he  feels.  For  more  exact  quantitative  determination,  small  objects 
of  the  same  bulk  but  of  different  weight,  or,  still  more  accurately,  the 
ho,resthesiometer  (Euleuberg's,  Fig.  294)  may  be  employed.  This  is  a 
simple  instrument  in  which  a  pelot  (ci)  working  upon  a  spring  is  applied 
with  varying  degrees  of  pressure  to  the  skin,  and  the  grams  of  pressui-e 
employed  can  be  read  upon  the  scale.  By  means  of  this  instrument 
we  can  determine,  on  the  one  hand,  the  minimal  amount  of  pressure 
which  can  be  appreciated  as  differing  from  a  mere  touch,  and,  on  the 
other  hand,  the  size  of  the  pressure   difference  that  can  be  felt — /.  e., 


Fig.  294.— Eulenburg's 
baresthesiometer. 


758  EXAJIIXATIOy  OF  THE  NERVOrS  SYSTEM. 

how  much  the  indicator  moves  before  the  patient  can  be  sure  that  the 
pressure  has  been  increased. 

V.  Frey  ^  has  found  that  the  value  of  the  pressure  appreciation  depends  essen- 
tially upon  the  size  of  the  area  pressed  upon  and  upon  the  rapidity  of  the  pressure. 
The  second  factor  can  neither  be  exactly  estimated  nor  regulated  by  simple 
clinical  methods,  hence  the  results  of  the  above  method  are  approximate  only.  In 
any  case  they  are  of  value  only  if  the  deviations  from  the  normal  are  quite 
striking.  It  is  at  all  events  desirable,  in  order  to  establish  such  deviations,  that 
both  the  patient  and  a  normal  control  individual  be  examined  exactly  in  the  same 
way  — i.  e,  with  corresijonding  areas  of  skin  and  equal  rapidity  of  pressure. 

In  regard  to  the  difierences  of  the  value  of  the  pressure  appreciation,  Weber 
found  that,  normally,  differences  of  weight  of  1  :  30  can  be  distinguished  by  the 
palmar  surface  of  the  third  i3halanx  of  the  index  finger  (excluding  the  balancing 
movement — /.  e.,  with  the  finger  lying  upon  the  table).  This  relation  remains 
almost  the  same,  according  to  Fechner's  psychophysical  law,  if  we  alter  the 
absolute  size  of  the  burden  within  wide  limits.  The  rapidity  of  the  pressure 
probably  influences  these  conditions.  Although  neglected  by  Weber,  it  should 
be  taken  into  account  in  making  comparative  tests.  His  estimates  are  based  upon 
quick  pressure.  In  consideration  of  the  insuificient  data  upon  the  physiologically 
normal  values,  it  is  advisable  for  clinical  jjurposes  to  make  control  tests  upon  the 
corresponding  cutaneous  areas  of  a  healthy  individual  under  absolutely  identical 
conditions  (the  same  pressure  surface  and,  as  nearly  as  possible,  the  same  rapidity 
of  touch).  If  the  affection  is  unilateral,  it  is  possible  to  test  the  pressure  sense  by 
a  simple,  unobjectionable  method.  Equal  weights  (of  identical  surface  and 
material)  are  placed  as  slowly  as  possible  upon  symmetric  parts  of  the  skin,  and 
the  patient,  with  closed  eyes,  determines  whether  one  of  the  weights  seems 
heavier  than  the  other.  Unsymmetric  cutaneous  areas  vary  so  decidedly,  even 
physiologically,  in  the  refinement  of  their  pressure  sense,  that  it  is  not  safe  to 
employ  the  above-mentioned  method  of  comparison  except  with  the  greatest  care. 

So-called  Pressure  Points  ;  v.  Prey's  Irritation  Hairs. — The  quantitative 
estimate  of  the  pressure  sense  has  been  placed  upon  an  apparently  more  secure 
basis,  since  we  have  known  (Blix,  Goldscheider)  that  the  pressure  sense  is  not  scat- 
tered diffusely  in  the  skin,  but  that  it  depends  upon  localized  organs.  The  pro- 
jections of  the  latter  upon  the  surface  of  the  skin  are  called  "pressure  points,"  and 
their  anatomic  substratum,  according  to  v.  Frey,^  consists  of  nerve  fibers  arranged 
around  the  coronary  hair  follicles.  The  pressure  points  are  distributed  in  widely 
differing  numbers  to  the  different  parts  of  the  skin.  The  enumeration  of  the 
hairs  practically  determines  the  number  of  pressure  points,  because  a  pressure 
point  lies  in  the  projection  of  each  hair  follicle,  and  about  95  per  cent,  of  the 
skin  surface  is  covered  with  hair.  As  a  matter  of  fact,  there  are  some  pressure 
points  between  the  hairs  and  upon  hairless  places — e.  g. ,  they  are  specially  numer- 
ous in  the  palm  of  the  hand  and  in  the  sole  of  the  foot.  (On  the  palm  of  the 
hand,  according  to  v.  Frey,  there  are  at  least  100  pressure  points  to  each  J  sq.  cm.) 
These  isolated  pressure  points  are  the  only  receptors  of  tactile  and  pressure  per- 
ceptions. A  slight  touch  or  pressure  cai'eftilly  localized  between  them  either 
cannot  be  appreciated  at  all,  or  can  be  appreciated  only  when  the  skin  is  so 
deformed  by  the  pressure  that  neighboring  pressure  points  are  affected,  v.  Frey 
claims  that  the  existence  of  localized  pressure  points  thus  renders  possible  a 
strictly  localized  testing  of  the  pressure  perception,  and  his  examination  seems  to 
furnish  much  more  trustworthy  results  than  superficial  testing.  In  testing  pres- 
sure points,  we  first  determine  the  location  of  the  points  and  then  estimate  their 
ability  to  discriminate  pressure,  v.  Frey's  irritation  hairs  accomplish  both  pur- 
poses most  efficiently.  They  are  short  spears  of  hair  of  varjdng  stiffness,  glued 
at  right  angles  into  the  end  of  a  wooden  handle.     Human  hairs  are  employed 

^  V.  Frey,  "  Untersuchungen  ueber  die  Sinnesfunctionen  der  mensclilichen  Haut." 
Abhandlungen  der  mathem.-pht/sischen  Classe  der  konigl.  sacks.  Akademie  der  Wissent^chaften, 
vol.  xiii.,  No.  3,  Leipzig,  1896.  =  Ibid. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  759 

for  weak  stimulation,  and  horses'  hairs  for  strong  stimulation.  Hairs  have  two 
advantages  for  the  mechanical  irritation  of  the  skin.  In  the  first  place,  they  act 
upon  yer}'  small  surfaces  of  the  skin — L  e, ,  they  are  sharply  localized — and,  in 
the  second  place,  the  intensity  of  the  irritation  can  be  graded.  To  estimate  the 
hair's  irritation  value,  we  first  determine  the  amount  of  weight  in  one  scale  of  a 
delicate  chemical  balance  which  the  hair  can  lift  by  exerting  pressure  with  its  end 
upon  the  other  scale.  The  power  of  the  hair,  a  term  which  v.  Frey  applies  to 
the  weight  raised  by  the  hair,  is  a  constant  factor  for  each  irritation  hair,  because 
a  pressure  sufiicient  to  balance  a  heavier  weight  would  bend  the  hair  and  conse- 
quently destroy  its  power.  By  means  of  such  irritation  hairs  the  pressure  points 
can  not  only  be  mapped  out,  but  also  sharply  localized  and  quantitatively  stimu- 
lated. The  irritability  or  pressure  susceptibility  of  a  certain  pressure  point  is  to 
be  estimated  by  determining  the  weakest  hair  which  can  be  felt  at  that  point. 
With  hairs  of  different  thicknesses  the  cross-section  as  well  as  the  power  influences 
the  variation  in  the  irritation  value,  and  v.  Frey  has  found  that  the  irritation 
value  is  proportional  to  the  product  of  the  power  by  half  the  cross-section.  This 
product  he  calls  the  tension  value.  It  also  measures  the  pressure  irritation  value 
of  the  hair.  v.  Frey  found  the  mean  susceptibility  of  the  pressure  points  he 
examined  to  equal  a  tension  value  of  1.44  grammillimeters. 

The  power  of  any  hair  will  also  depend  upon  its  length,  since  a  long  hair  will 
be  bent  by  less  force  than  a  short  one,  and  it  is  upon  this  principle  that  v.  Frey's 
esthesiom'eter  has  been  constructed.  The  instrument  consists  essentially  of  a 
strong  irritation  hair  (horsehair),  which  can  be  pushed  out  of  a  sheath  to  a  greater 
or  less  distance,  and  whose  length  can  be  read  in  millimeters  from  a  scale  on  the 
sheath.  The  millimeter  scale  is  gauged  empirically  by  estimating  the  power  of 
the  projecting  portion  (by  means  of  a  delicate  chemical  balance)  for  every  fifth  or 
tenth  division  of  the  scale.  The  instrument  is  manufactured  by  Zimmennan,  of 
Leipzig.  The  thickness  of  the  hair  must  also  be  measured  in  order  to  determine 
accurately  the  pressure  value  of  the  instrument  for  a  definite  length  of  hair. 
Half  its  cross-section  multiplied  by  the  power  gives  the  tension  value  of  the  hair, 
which,  as  mentioned  above,  is  identical  here  with  the  irritation  value.  The 
examination  of  the  j^ressure  sense  should  be  conducted  as  follows:  The  positions 
of  the  pressure  points  are  first  localized  with  stronger  irritation,  and  then  their 
susceptibility  to  pressure  estimated  with  weaker  irritations.  As  yet  no  clinical 
experience  has  been  tabulated  with  this  method,  but  it  would  seem  to  the  writer 
to  possess  considerable  utility,  although  less  for  examining  anatomic  lesions  of 
the  nervoiLS  system,  wherein  only  the  grosser  disturbances  are  of  diagnostic  value, 
than  for  the  examination  of  neurasthenic  and  hysteric  symptoms,  for  the  investiga- 
tion of  the  action  of  drugs  upon  the  sensory  nervous  system,  and  the  like. 

V.  Frey  believes  that  by  means  of  this  method  v/e  can  demonstrate  the  oscil- 
lating character  of  the  pressure  sense — i.  e.,  the  periodical  increase  and  decrease 
of  the  perception,  and  even  its  fatigue.  The  method  may  therefore  perhaps 
obtain  a  similar  significance  as  the  demonstration  of  the  fatigue  of  the  visual  field 
in  neurasthenia  and  hysteria.  As  contrasted  with  the  latter  test  (visual  field), 
the  results  obtained  by  means  of  the  irritation  hairs  can  in  no  way  be  simulated, 
because  the  patient  is  unable  to  orient  himself  concerning  the  pressure  points  that 
are  being  stimulated,  v.  Frey  states  that  the  mean  irritability  of  the  pressure 
points  over  the  entire  body  is  about  equal.  This  is  interesting  and  important  for 
the  clinical  utility  of  the  method.  The  local  variability  of  the  acuteness  of  the 
pressure  sense  seems  to  depend  more  upon  the  number  of  pressure  points.  The 
rapidity  of  applying  the  irritation  hairs  has  but  little  influence,  yet  it  is  better  to 
do  it  as  slowly  as  possible. 

Method  of  Testing  the  Cutaneous  Sensibility  to  Pain. — 

By  pricking  a  patient  with  a  pin,  we  determine  whether  the  prick  as 
well  as  the  tonch  is  felt  and  properly  localized.  The  anesthetic  or 
hyperesthetic  spots  are  then  marked  upon  the  body  and  later  transferred 
to  a  diagram.     In  this  test  special  attention  should  be  paid  to  deter- 


760  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

mining  any  delay  in  transmission  of  the  impression,  such  as  is  so 
common  in  tabes  dorsalis  and  peripheral  neuritis.  A  good  plan  is  to 
have  the  patient  call  out  the  word  "now"  the  instant  he  appreciates 
the  touch,  and  the  word  "  prick  "  the  instant  he  appreciates  the  prick. 
A  distinct  interval  often  elapses  between  the  two.  v.  Frey's  ^  researches 
attribute  this  difference  to  the  increase  of  a  physiologic  peculiarity  of 
pain  perception,  which,  in  so  far  as  it  is  mechanically  discharged, 
always  possesses  a  distinct  latent  stage,  which  does  not  exist  in  tactile 
perception.  It  is  a  well-known  fact  that  the  pain  caused  by  stubbing 
the  naked  toe  becomes  more  severe  after  the  lapse  of  an  instant.  The 
accentuation  of  the  pain  sense,  the  painful  after-sensation,  and  the  repe- 
tition of  a  painful  impression  (successive  polyesthesia)  dependent  upon 
a  slight  prick  are  all  related  to  this  delay  and  occur  under  similar  con- 
ditions. Simultaneous  polyesthesia  is  a  different  phenomenon,  and 
probably  depends  upon  an  irradiation  or  a  reflex  perception  (see  p.  774 
et  seq.).  In  this  variety  several  pin  pricks  are  simultaneously  perceived 
at  neighboring  spots  instead  of  one  single  pin  prick.  The  examination 
with  the  pin  prick  can  be  made  easier  by  comparing  different  parts  of 
the  body. 

Testing    the    Sense  of  Pain    by  Means  of   Irritation  Hairs ;    Pain 

Points. — V.  Frey  ^  has  recently  demonstrated  tliat  the  api^reciation  of  pain, 
like  that  of  touch,  is  not  diffused  over  the  skin,  but  is  localized  at  circumscribed 
points,  the  so-called  pain  points.  The  territory  between  these  points  is  insensitive 
to  pain.  Ordinary  experience  with  pin  pricks  at  first  makes  this  seem  para- 
doxical, until  we  recall  that  any  sharp  mechanical  irritation  of  the  skin  sufficient 
to  excite  pain  causes  a  deformity  upon  every  side.  To  demonstrate  the  pain 
points,  V.  Frey  has  employed  the  irritation  hairs  described  upon  p.  758.  The 
pain  points  are  very  thickly  distributed,  so  that  very  fine  hairs  are  selected,  in 
order  to  avoid  the  skin  deformity  which  would  otherwise  prevent  an  isolated 
irritation;  they  must,  however,  possess  relatively  considerable  strength  (see 
p.  758),  so  V.  Frey  sharpened  the  horsehairs  by  means  of  a  scalpel  under  a  lens. 
Experience  shows  that  for  demonstrating  pain  points  they  are  superior  to  needles, 
because  they  do  not  injure  the  skin.  Such  pointed  irritation  hairs,  if  possessed 
of  sufficient  "power,"  cause  pain,  which  proves  that  the  painful  irritation  of  the 
skin  from  needle  pricks  does  not  depend  upon  the  injury  as  such.  If  we  sharpen 
the  hair  we  can  employ  the  esthesiometer  (described  on  p.  769)  to  test  the  pain 
points.  Only  by  employing  these  irritation  hairs  can  we  be  positive  that  a  painful 
impression  is  produced  immediately  at  a  definite  spot,  without  any  trace  of  a  pre- 
ceding sensation  of  touch,  v.  Frey  has  further  found  that  the  irritation  value  of  a 
hair  for  testing  the  sense  of  pain  is  equal  to  the  product  of  its  power  (see  p.  759) 
and  the  square  of  its  touching  surface — i.  e. ,  its  point.  He  calls  this  varying  power 
of  irritation  which  decides  the  degree  of  pain  the  pressure  value  of  the  irritation 
hair,  in  contrast  with  the  tension  value,  which,  according  to  p.  759,  measures  the 
sense  of  touch.  He  has  not  yet  estimated  the  median  pressure  value  of  the  pain 
points,  but  it  varies  between  20  and  150  quadrimillimeter  grams.  The  number 
of  the  pain  points  varies  in  different  parts  of  the  body  between  100  and  200  to 
each  square  centimeter.  With  this  great  profusion  of  pain  points  it  is  easy  to 
understand  why  we  have  only  learned  recently  that  pain  perception  is  localized  in 
points.  The  intra-epithelial  free  nerve  terminations  of  the  skin  are  thought  to 
he  situated  in  the  anatomic  substrata  of  the  pain  points  ;  they  are  therefore 
located  more  superficially  than  the  end  organs  of  the  sense  of  touch. 

V.  Frey's  researches,  as  we  have  seen,  prove  that  actual  pain-percipient  organs 

'  Loc.  cit,  p.  242.  ^  Loc.  cit. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  761 

exist  in  the  skin.  They  are  interesting  theoretically  because  they  show  that 
pain,  a  phenomenon  which  otherwise  we  should  have  considered  purely  patho- 
logic, has  been  to  a  certain  extent  anticipated  by  Nature  and  has  been  endowed 
with  physiologic  organs.  Its  importance  can  be  easily  understood,  because  the 
perception  of  pain  in  the  skin  protects  the  organism  from  impending  dangers 
(transmitted  pressure  or  actual  injury)  just  as  does  the  pressure  sense.  Whether 
the  deeper  organs  also  possess  special  pain  nerves  is  not  yet  known.  At  all 
events,  according  to  the  statements  made  above,  the  very  remarkable  richness  of 
the  cutaneous  pain  nerves  and  the  great  distress  that  follows  cutaneous  injuries 
seem  quite  natural  from  a  teleologic  point  of  view. 

Method  of  Testing  the  Cutaneous  Thermal  Sensibility. 

— A  sufficiently  accurate  and  very  convenient  method  of  testing  the 
sense  of  heat  and  cold  consists  in  breathing  upon  the  patient's  skin 
with  the  mouth  wide  open  and  again  with  it  nearly  closed.  In  the 
former  case  a  sense  of  warmth,  in  the  latter,  of  cold,  will  be  appre- 
ciated distinctly  and  so  characterized  by  healthy  individuals.  If  any 
abnormality  exists,  its  location  can  be  represented  upon  a  chart  of  the 
body.  We  can  estimate  the  degree  of  disturbance  more  accurately  by 
touching  the  skin  alternately  with  test  tubes  filled  with  cold  and  warm 
water,  and  determining  at  what  temperatures  the  water  can  still  be  dis- 
criminated as  cold  and  warm.  By  this  method  we  can  estimate  at  the 
same  time  the  so-called  indifferent  zone  of  the  temperature  sense — 
i.  e.,  the  areas  in  which  the  tubes  produce  an  impression  neither  of 
warmth  nor  of  cold.  These  results  are  valuable  only  when  symmetric 
parts  of  the  body  are  compared,  or  when  the  results  are  compared  with 
those  from  a  healthy  individual  over  corresponding  cutaneous  areas. 
This  method  is  more  useful  than  that  of  estimating  the  minimum  dif- 
ference of  temperature  which  can  be  appreciated,  because  it  furnishes 
conclusions  about  the  relations  of  the  nerves  for  warmth  as  distin- 
guished from  those  for  cold.  Such  a  discrimination  is  necessary, 
because  we  know  that  the  organs  of  warmth  and  cold  sensation  are 
anatomically  distinct  (warmth  and  cold  points),  and  that  warmth  and 
cold  perception  may  be  affected  independently  of  each  other.  State- 
ments about  the  minimum  temperature  difference  are  of  little  value, 
because  this  difference  may  vary  considerably  according  to  the  degree 
of  the  temperature  used.  Fechner's  psychophysical  law  (see  p.  758)  is 
of  no  use,  because  the  ordinary  thermometer  scales  are  divided  only 
arbitrarily,  and  not  according  to  the  iabsolute  temperatui^es.  Especial 
instruments  for  testing  the  temperature  sense  may  be  desirable  for 
physiologic  purposes,  but  they  are  superfluous  for  clinical  needs,  espe- 
cially if  the  principles  of  examination  described  here  are  followed. 

An  examination  of  the  temperature  sense  is  much  simplified  and 
entirely  accurate  if  the  disturbances  are  unilateral.  Objects  identical 
in  size,  shape,  and  substance,  and  of  the  same  temperature  are  gently 
and  slowly  placed  upon  symmetric  areas  of  the  skin,  and  the  patient, 
with  eyes  closed,  tells  the  examiner  upon  which  side  the  object  feels 
warmer  or  colder.  This  method  is  of  less  value  for  differentiating  dis- 
turbances which  are  not  unilateral,  because  non-symmetric  areas  do 
not  have  the  same  temperature  sensibility  even  physiologically. 


762  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

We  are  indebted  to  the  studies  of  Blitz  and  Goldscheider  for  the  demonstra- 
tion that  the  temperature  sense  depends  upon  the  existence  of  localized  end 
organs  in  the  skin  which  are  specialized  for  detecting  heat  and  cold.  [Only 
a  few  physiologists  and  experimental  psychologists  accept  these  conclusions 
of  Blitz  and  Goldscheider. — Ed.]  The  warmth  and  cold  points  coincide  neither 
with  the  pressure  points  nor  with  the  pain  points.  Their  relations  have  thus 
far  been  of  no  clinical  significance.  Should  it  be  necessary  in  any  case  to  deter- 
mine the  warmth  and  cold  points,  Goldscheider's  method  is  the  simplest.  It 
consists  in  touching  the  skin  with  the  slightly  pointed  end  of  a  metallic  cylinder 
varyingly  heated.  The  end  organs  of  the  temperature  sense — i.  e.,  the  anatomic 
substrata  of  the  warmth  and  cold  points — are  not  yet  known. 

Method  of  Testing  the  Sensation  of  Innervation,  or  the 
So-called  Sense  of  Strength ;  Judgment  of  the  Conception 
of  Movement. — By  inuervation  sensibility  is  meant  the  ability  to 
estimate  the  measure  of  voluntary  movement  impulses.  One  speaks 
of  this  capacity  as  the  sense  of  strength  in  so  far  as  by  means  of 
muscular  power  it  serves  to  distinguish  differences  in  weight.  The 
designation  power  sense  or  sense  of  strength  is  really  incorrect,  because 
neither  a  separate  sense  nor  special  sensory  nerves  take  part  in  this 
function.  It  is  much  more  plausible  to  assume  that  the  innervation 
sense  differs  from  the  actual  sensory  function  by  having  its  origin 
in  the  motor  centers  and  not  in  the  periphery.  Probably  the  rep- 
resentation of  movement  becoming  a  reality — i.  e.,  by  carrying  out  the 
activity  of  the  will — is  identical  with  the  innervation  sense.  The 
expression  strength  sense  or  "  power  "  sense  can  be  justified  only  by  its 
brevity  and  comprehensiveness.  In  reality  the  examination  of  this 
function  might  be  considered  quite  as  well  under  motility  as  under 
sensibility. 

An  entirely  isolated  test  of  the  sense  of  strength  is  difficult,  strictly 
speaking  impossible,  because  the  tactile  sense  simultaneously  stimulated 
by  the  lifted  weight  is  bound  to  influence  the  result.  For  practical 
purposes  the  test  is  performed  in  this  way  :  Different  weights  are  hung 
in  a  cloth  sling  looped  about  the  hand,  forearm,  or  foot,  lifted  by  the 
patient,  and  then  discriminated.  At  the  same  time  the  normal  rela- 
tions are  best  preserved  by  practising  the  same  experiment  upon  control 
persons  with  healthy  nerves — e.  g.,  upon  the  examiner.  By  this 
method  we  are  able  to  determine  not  only  the  absolute  estimation  of 
weight,  but  also  the  estimation  of  differences  in  weight  which  in 
pathologic  cases  are  thought  to  be  either  too  small  or  too  large.  The 
results  are  of  diagnostic  value  only  when  they  are  very  striking, 
because  people's  ability  to  differentiate  weights  by  the  innervation  sense 
varies,  and  is  to  a  great  extent  influenced  by  practice. 

In  this  examination  two  devices  may  be  employed  to  aid  in  excluding  the 
pressure  sense.  One  is  to  make  the  sling  holding  the  weight  very  broad,  so  that 
it  will  extend  over  as  large  an  area  of  skin  as  possible,  and  so  reduce  the  pressure 
sensation  below  the  value  for  which  Fechner's  psychophysical  law  holds.  A  slight 
increase  then  in  the  weight  will  not  influence  the  pressure  sense.  The  other 
device,  supposing  we  wish  to  estimate  the  strength  sense  of  the  arm,  is  to  hold 
the  sling  with  the  strongest  possible  pressure  with  the  hand.  Here,  conversely, 
the  strong  hand  pressure  has  the  effect  of  making  the  sensation  of  pressure  so 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  763 

strong  that,  according  to  Fechner's  law,  a  slight  addition  of  weight  will  not 
appreciably  increase  the  sense  of  pressure,  but  only  the  fatigue  of  the  muscles. 
E.  H.  Weber  has  made  use  of  the  latter  device  for  testing  the  strength  sense.  He 
found  that  the  strength  sense  of  the  arm  could  appreciate  differences  of  weight 
of  1  :  40,  whereas  the  pressure  sense  alone  of  the  fingers  appreciated  differences 
of  1  :  30  (see  p.  758).  His  researches  also  showed  that  a  combination  of  the  pres- 
sure and  the  strength  sense  furnishes  no  more  accurate  results  than  the  strength  sense 
alone.  The  principle  of  this  test  can  also  be  applied  to  the  lower  extremities  by 
fastening  the  sling  which  carries  the  weight  to  the  thigh  by  means  of  a  strongly 
tied  knot. 

The  strength  sense  can  also  be  tested  by  means  of  Eulenburg's  baresthesi- 
ometer  (see  p.  757,  Fig.  294).  As  in  testing  the  pressure  sense,  the  part  to  be 
examined — e.  g. ,  the  terminal  phalanx  of  the  fingers  or  toes — must  be  supported 
artificially  and  not  by  muscular  action. 

Even  excluding  the  influence  of  the  pressure  sense,  the  results  of 
these  tests  do  not  always  furnish  direct  conclusions  upon  the  "  innerva- 
tion" or  "strength  sense."  The  discrimination  of  weight  may  be 
affected  by  disturbances  of  innervation  sense  which  are  localized  in  the 
psychomotor  centers  and  by  motor  pareses,  because  in  such  cases  an 
especially  vigorous  impulse  of  the  will  is  required  to  lift  a  weight. 
Whether  to  credit  a  disturbance  in  the  discrimination  of  weight  to  an 
actual  involvement  of  the  "  innervation  sense  "  or  to  an  error  in  judg- 
ment due  to  motor  paresis  must  be  determined  from  the  results  of  an 
examination  such  as  we  have  described  above,  and  especially  from  the 
condition  of  the  motility.  Actual  affections  of  the  innervation  sense 
must  be  attributed  to  functional  or  anatomic  lesions  in  the  neighbor- 
hood of  the  motor  cortex. 

The  innervation  sense,  in  so  far  as  it  is  tested  as  a  sense  of  strength, 
always  refers  to  the  entire  group  of  muscles  which  together  exercise 
the  necessary  co-ordination  for  lifting  a  weight,  and  any  disturbance 
detected  must  affect  equally  the  entire  group  of  muscles  in  question. 
Now,  in  lesions  of  the  psychomotor  center  and  in  lesions  of  the  periph- 
eral motor  fibers  a  case  is  conceivable  in  which  the  disturbance — i.  e., 
the  disproportion  between  the  conductor  of  the  motor  impulses  and  the 
size  of  the  innervation,  affects  only  individual  muscles  of  the  group 
ordinarily  acting  together.  In  such  cases  the  trouble  should  be  consid- 
ered less  a  disturbance  of  the  sense  of  strength  than  one  of  co-ordina- 
tion, in  that  one  muscle  receives  too  much  innervation  for  the  accom- 
plishment of  purposeful  movement,  the  others  too  little.  On  reflection 
it  will  be  seen  that  here  we  are  in  reality  only  considering  the  two  cases 
of  ataxia  alluded  to  on  p.  753  et  seq. — namely,  cortical  ataxia  from  dis- 
turbances of  the  co-ordination  impulses  or  of  the  representations  of 
movement,  and  an  ataxia  from  partial  motor  paralysis  (so-called  pseudo- 
ataxia).  In  the  cortical  form  the  ataxia  depends  upon  the  actual  dis- 
turbance of  the  innervation  sense,  and  with  it  also  of  the  representation 
of  movements  ;  in  partial  motor  paralysis,  on  the  contrary,  while  the 
innervation  sense,  as  such,  is  correct,  the  impulses  transmitted  to  the 
muscle  are  quantitatively  incorrect,  and  therefore  the  resulting  ataxia 
simulates  a  falsification  of  the  innervation  sense.  Before  attributing 
the  ataxia  in  any  given  case  to  perversion  of  the  innervation  sense  or 


764  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

of  the  representation  of  movement,  every  other  possible  cause  of  ataxia 
must  be  excluded — e.  g.,  other  disturbances  of  motility,  disturbances 
of  the  sensibility  of  passive  movements,  and  anomalies  of  the  muscular 
tone.  If  the  examination  discloses  abnormalities  of  the  muscular  sense, 
the  diagnosis  will  be  strengthened.  Yet  this  is  not  necessary.  Just 
this  kind  of  cortical  ataxia  has  sometimes  been  noted  in  focal  lesion  of 
the  motor  cortex.  But  even  in  tabes  dorsalis,  should  an  actual  ataxia 
appear  without  any  disturbance  of  sensibility,  this  cortical  ataxia  may 
possibly  play  a  part,  because,  according  to  Jendrassik's  researches,  this 
disease  presents  in  common  with  general  paresis  a  degeneration  of  the 
tangential  fibers  of  the  cerebral  cortex. 

The  So-called  Sense  of  l/ocation,  Better  Described  as 
the  Ability  to  I/Ocali^e  Sensations. — There  is  no  special  sense 
of  location,  for  every  sensory  representation  has  its  own  place — i.  e.,  it 
is  localized  or  referred  to  a  certain  part  of  the  body.  Physiologic 
psychology  claims  that  each  conscious  impression  produces  a  so-called 
local  sign,  depending  upon  the  fiber  from  which  it  is  discharged.  These 
local  signs  become  indistinct  if  the  intensity  or  distinctness  of  the  im- 
pression itself  has  suifered.  However,  we  scarcely  notice  any  disturbed 
localization  provided  the  impressions  themselves  are  perfectly  intact. 
On  the  other  hand,  indistinct  impressions  and  inexact  localizations  go 
hand  in  hand.  The  so-called  associated  or  reflex  impressions  (see  p. 
774),  together  with  the  indistinctness  of  the  local  signs,  are  much  more 
apt  to  be  the  cause  of  inexact  localization  in  diminished  sensibility. 
Such  reflex  impressions  arise  quite  readily  in  interruption  of  sensory 
conduction  from  the  lateral  dislocation  of  the  impulses  through  the 
collaterals  of  the  sensory  tract. 

Slight  disturbances  of  the  location  of  sensation  are  sometimes  observed  in 
parts  in  wliicb  the  paralysis  is  purely  motor.  They  are  due  to  the  absence  of  the 
daily  exercise  of  localization  and  of  the  continued  refreshing  of  localization  by 
movement,  and  are  explained  by  the  fact  that  the  actual  conception  of  space  and 
the  sensation  of  localization  are  acquired  ontogenetically  through  motility  only, 
and  consequently  require  motility  for  their  intact  preservation. 

The  power  of  localizing  sensation  is  best  investigated  by  applying  the  touchj 
pain,  and  temperature  tests  to  the  area  to  be  investigated,  the  patient  having  his 
eyes  closed,  and  then  requiring  him  to  open  his  eyes  and  locate  with  his  finger 
the  spot  at  which  he  experienced  the  particular  sensation  ;  or,  if  this  be  impos- 
sible on  account  of  motor  disturbances,  to  describe  its  location.  The  distance 
between  the  point  irritated  and  the  point  indicated  by  the  patient,  expressed  in 
centimeters,  indicates  the  degree  of  the  error  in  localization.  Absolute  values 
for  the  normal  error  in  localization  cannot  be  given,  since  they  are  subject  to 
great  individual  variations  and  are  markedly  influenced  by  practice.  It  is  conse- 
quently best  to  compare  the  investigated  area  with  the  opposite  healthy  one,  or, 
if  this  be  impossible,  with  the  same  region  in  another  person  of  similar  physical 
and  mental  characteristics.  In  view  of  the  influence  of  practice,  only  marked 
errors  in  localization  are  of  diagnostic  importance. 

The  So-called  Muscle  Sense  or  Muscular  Sensibility. — 

What  we  have  described  above  as  the  innervation  sense  is  often  con- 
fused, under  the  common  title  of  Muscle  Sense,  with  the  appreciation  of 
active  and  passive  movements,  to  be  described  later.     Such  a  special 


EXAMINATION   OF  THE  NERVOUS  SYSTEM.  765 

muscle  sense  does  not  really  exist,  and  the  obscure  term  leading  to  a 
misconception  should  therefore,  once  for  all,  be  dropped. 

Method  of  Testing  Bone  Sensibility;  the  So-called 
Sensation  of  Vibration. — M.  Egger^  was  the  first  to  demonstrate 
the  feasibility  of  testing  the  sensibility  of  the  bones  by  applying  a 
vibrating  tuning-fork  to  them.  The  examination  was  suggested  by  the 
extreme  sensitiveness  of  periosteal  lesions.  If  we  set  a  C  tuning-fork 
of  132  vibrations  or  an  ordinary  A  tuning-fork  of  440  vibrations  upon 
the  surface  of  a  bone,  the  person  examined  normally  perceives  a  char- 
acteristic whizzing  or  trembling  sensation.  Egger  has  demonstrated 
that  this  perception  in  pathologic  cases  is  entirely  independent  of  the 
absence  or  presence  of  cutaneous  sensitiveness,  and  has  proved  that  it 
is  actually  peculiar  to  the  osseous  system.  It  may  be  retained  with  a 
diminished  cutaneous  sensibility  or  lost  when  the  latter  is  normal, 
despite  the  fact  that  the  vibrations  are  naturally  transmitted  to  a  con- 
siderable distance.  Egger  found  that  this  sensation  of  whizzing  was 
strictly  localized,  so  that  under  pathologic  conditions  the  tuning-fork 
was  appreciated  at  one  spot  of  a  bone  and  not  at  a  neighboring  spot. 
He  also  demonstrated  a  hyperesthesia  of  the  bones,  for  they  could 
appreciate  the  vibration  of  a  high  tuning-fork  (vibrating  2048  times), 
although  this  normally  is  not  perceptible.  Bone  anesthesia  occurs  espe- 
cially frequently  in  the  ataxic  stage  of  tabes.  The  occurrence  of 
disturbances  in  the  appreciation  of  active  and  passive  movements  is, 
however,  independent  of  the  bone  sensibility.  In  many  cases  of  tabes, 
and  especially  in  the  initial  stage,  tuning-fork  vibrations  produce  a 
sensation  of  burning  as  well  as  of  whirring  (hyperalgesia  of  the  bones). 
In  the  trophic  changes  of  the  joints  and  bones  in  tabes,  the  disturbances 
in  bone  sensibility  are  mostly  localized  in  the  vicinity  of  the  aifected 
parts.  Disturbances  in  bone  sensibility  also  occur  in  syringomyelia, 
and  mostly  in  the  diffuse  areas  of  anesthesia  so  characteristic  of  this 
disease.  In  Brown-Sequard's  unilateral  paralysis,  the  osseous  sensibility, 
like  that  for  passive  movements,  and  in  contrast  to  the  cutaneous  sensi- 
bility, suffers  upon  the  same  side  as  the  motor  disturbance.  In  cerebral 
hemi-anesthesia,  bone  anesthesia  is  localized  upon  the  paralyzed  side, 
although  it  is  ordinarily  incomplete  upon  the  head.  Bone  sensibility 
varies  in  hysteric  anesthesias.  Frequently,  though  not  constantly,  the 
bones  share  in  the  anesthesia.  In  hysteric  conditions,  the  bone,  as 
well  as  the  cutaneous,  sensibility  not  uncommonly  suddenly  disappears 
under  the  influence  of  the  tuning-fork  vibrations.  Bone  anesthesias 
sometimes  of  equal,  sometimes  of  less,  extent  than  the  sensory  disturb- 
ance of  the  skin,  are  also  found  in  transverse  lesions  of  the  spinal  cord. 
In  the  latter  case,  the  bones  of  the  lower  end  of  the  leg  are  ordinarily 
most  affected.  From  the  pathologic  findings  Egger  believes  that  the 
tracts  for  bone  sensibility  take  an  uncrossed  course  in  the  gray  matter. 

Egger's  supposition  that  the  vibrations  of  the  tuning-fork  are  per- 
ceived only  through  the  bones  has  recently  been  shown  by  Goldscheider  2 

1  Jour,  de  Physiol,  et  de  Pathol,  gen.,  vol.  i.,  No.  3,  1899. 

2  Berliii.  klin.  Woch.,  1904,  No.  14. 


766  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

to  be  erroneous.  The  soft  parts  are  also  susceptible  to  these  vibrations, 
but  not  to  so  great  a  degree,  owing  to  their  less  ability  to  vibrate 
synchronously.  Goldscheider  found,  in  contrast  to  Egger,  that  the 
perception  of  tuning-fork  vibrations  is  partly  dependent  also  upon  the 
condition  of  cutaneous  sensibility.  One  way  in  which  he  proved  this 
was  by  anesthetizing  the  skin  with  cocain.  The  cutaneous  sensibility 
and  the  osseous  sensibility  to  tuning-fork  vibrations  may  be  separately 
tested  by  pressing  the  tuning-fork  softly  against  the  part  for  the  former, 
and  firmly  for  the  latter.  In  the  first  instance  the  vibrations  remain 
upon  the  surface,  while  in  the  second  they  are  conducted  to  the  deeper 
parts  through  the  compressed  skin.  Goldscheider  calls  the  perception 
of  the  vibrations  of  the  tuning-fork  the  sensation  of  vibration,  and 
regards  it,  not  as  a  specific  sensation,  but  as  an  expression  of  the  sensa- 
tion of  rhythmic  interrupted  irritation  of  the  nerves  that  are  responsible 
for  the  sensations  of  contact  or  pressure.  In  spite  of  his  objections  to 
the  conception  of  Egger,  Goldscheider  regards  the  test  with  the  firmly 
applied  tuning-fork  as  the  best  procedure  for  the  estimation  of  osseous 
sensibility. 

(6)  Examination  of  Complicated  Sensory  Functions. 

Method  of  Testing  the  Perception  and  the  Judgment 
of  Active  Movements  of  the  Extremities. — Even  with  closed 
eyes  a  healthy  person  has  a  very  exact  knowledge  of  every  change  of 
posture  of  his  extremities,  and  graduates  his  motor  impulses  accord- 
ingly. These  perceptions  of  movement  depend  primarily  upon  the 
innervation  sense  (see  p.  763  et  seq.) — i.  e.,  upon  the  judgment  of  the 
impulses  of  contraction  which  the  individual  muscles  receive  in  a  certain 
position,  and,  secondarily,  upon  the  sensibility  of  the  deeper  portions 
of  the  extremities — i.  e.,  of  the  muscles,  joints,  tendon  sheaths — and 
even  of  the  skin.  The  skin  is,  of  course,  compressed  and  stretched 
differently  in  every  change  of  posture.  So  this  performance  does  not 
depend  merely  upon  a  single  sensory  function,  but  upon  the  cerebral 
reception  of  several  sensory  impressions  aided  by  the  innervation  sense, 
which  belongs  in  reality  to  motility.  Affections  of  the  appreciation 
and  judgment  of  active  movements  are  therefore  encountered  as  often  in 
sensibility  disturbances  from  peripheral  interruption  of  conduction  as  in 
lesions  of  the  psychomotor  centers  or  tracts,  causing  an  impaired 
judgment  of  the  effect  of  the  will  impulses.  Yet,  when  the  cause  of 
the  affection  lies  upon  the  motor  side,  the  sensibility  of  the  deeper  parts 
can  to  a  certain  extent  perform  vicariously  the  function  of  the  impaired 
judgment  of  the  condition  of  muscular  contraction ;  and,  conversely, 
when  the  defect  lies  upon  the  sensory  side,  the  innervation  sense  can 
equalize  a  certain  part  of  it.  It  appears  that  this  vicarious  performance 
of  one  function  by  another  is  possible,  and  varies  somewhat  with  the 
individual. 

To  test  the  appreciation  of  active  movement,  we  direct  the  patient 
either  to  describe  as  accurately  as  possible  a  position  of  his  extremities, 
which    he  voluntarily  assumes    and  alters  while  his  eyes  are  closed, 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  767 

or  to  touch  with  an  extremity  an  object  whose  position  he  has 
noted  before  he  closed  his  eyes,  employing  the  shortest  and  most 
direct  movement  possible.  In  the  latter  experiment  any  disturbance 
of  the  function  in  question  is  manifested  by  the  ataxic  character  of  the 
movement  and  by  its  lack  of  certainty.  This  test,  then,  is  like  that 
for  ataxia.  But  although  absence  of  ataxia  proves  that  the  patient 
judges  his  voluntary  movements  correctly,  nevertheless,  if  ataxia  is 
demonstrated,  we  require  further  evidence  to  decide  that  it  is  accom- 
panied by  a  failure  in  the  appreciation  or  judgment  of  active  movements. 
The  latter  function  may  be  absolutely  preserved  and  the  patient  may  be 
perfectly  cognizant  of  the  ataxic  peculiarity  of  his  movements,  yet  be 
unable  to  execute  them  co-ordinately  if  the  motor  elaboration  of  his 
movement  impulses  is  defective.  We  need  the  most  accurate  analysis 
possible,  and  a  consideration  of  all  the  conceivable  causes  of  ataxia,  in 
order  to  decide  whether  the  ataxia  proves  faulty  judgment  of  the  patient's 
own  movements.  Should  the  muscular  tone  (p.  754)  be  normal  and  no 
sign  of  motor  weakness  be  apparent  (p.  753)  we  must  attribute  the 
ataxia  to  a  defective  judgment  of  active  movements.  Then  we  must 
decide  whether  such  an  affected  judgment  depends  upon  an  actual  dis- 
turbance of  sensibility  or  of  the  innervation  sense — i.  e.,  a  faulty  repre- 
sentation of  movement  (p.  762).  If  the  former,  the  appreciation  of 
passive  movements  will  also  be  affected.  As  we  have  already  men- 
tioned, this  is  the  commonest  cause  of  ataxia.  It  is  also  worth  noting 
that  an  intelligent  patient,  simply  by  his  own  observation,  can  often 
decide  correctly  whether  his  ataxia  should  be  attributed  to  faulty 
judgment  of  movements  or  to  a  faulty  motor  conduction.  If,  how- 
ever, he  attributes  the  difficulty  to  the  former  cause,  ordinarily  he  can- 
not determine  whether  an  actual  disturbance  of  sensibility  or  of  the 
innervation  sense  is  at  fault.  Upon  this  point  the  results  obtained 
from  testing  the  appreciation  of  passive  movements  must  decide.  Actual 
disturbances  of  sensibility  are  the  usual  causes  of  the  ataxia  in  tabes 
dorsalis,  but  a  disturbance  in  the  innervation  sense  or  in  the  represen- 
tation of  movements  may  cause  ataxia  in  cortical  afPections,  without  any 
true  disturbance  of  sensibility. 

Method  of  Testing  the  Appreciation  of  the  Position  and 
of  Passive  Movements  of  the  ^Extremities  (in  Brief,  Postural 
Perception). — In  estimating  a  passive  change  in  position  of  the 
limbs,  the  innervation  sense  is  of  no  assistance.  We  judge  of  it  purely 
in  a  sensory  way  by  employing  the  sensibility  of  the  deeper  parts, 
muscles,  fasciae,  joints,  etc.  Theoretically  considered,  the  appreciation 
and  judgment  of  active  movements  must  be  easier  than  that  of  passive 
movements,  because  the  former  utilizes  more  aids.  Therefore,  even 
where  the  appreciation  of  active  movement  is  intact,  that  of  passive 
movements  must  still  be  tested  for.  It  is  done  in  this  way  :  The 
patient,  with  closed  eyes,  is  asked  either  to  describe  passive  changes 
of  position  in  his  extremities,  or  to  imitate  them  with  another  extremity 
whose  innervation  has  not  been  involved.  This  will  scarcely  be  pos- 
sible if  the  appreciation  of  passive  movements  is  affected.     Yet  it  is  to 


768  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

be  noted  that  under  some  circumstances  the  patient  can  compensate 
moderate  disturbances  by  informing  himself  of  the  position  of  his 
extremities  through  the  appreciation  of  muscular  contractions  by  means 
of  the  innervation  sense.  In  this  way  many  observers  explain  the  fact 
that  the  estimation  of  passive  alterations  of  posture  is  comparatively  well 
preserved  in  moderate  sensory  disturbances  of  the  extremities,  although 
this  gives  us  no  right  to  assume  that  the  sensibility  of  the  deeper  parts  has 
escaped.  To  obtain  clear  results  in  such  cases  we  must  demand  of  the 
patient  a  practically  complete  muscular  relaxation.  In  most  cases  dis- 
turbances in  the  appreciation  of  posture  show  themselves  without  any- 
thing further  by  an  ataxia,  because  of  the  failure  of  the  essential  sensory 
control  of  the  movements.  Hysteric  disturbances  of  sensibility  present 
an  exception  to  this  rule  ;  in  them  the  appreciation  of  posture  can  be  com- 
pletely lost  without  the  appearance  of  ataxia.  This  can  be  explained 
by  the  nature  of  hysteria ;  because  here  the  disturbance  lies  in  the  most 
central  organs  of  consciousness,  so  that  the  intelligent  appreciation  of 
passive  changes  of  position  is  annulled,  but  not  the  control  of  move- 
ments, which  is  supplied  by  the  sensory  impulses  further  down. 

Disturbances  in  the  appreciation  of  passive  movements  are  observed 
principally  in  tabes  dorsalis,  where,  as  mentioned  repeatedly  above, 
they  furnish  a  sufficient  explanation  of  the  ataxia.  It  is  not  rare  to 
meet  such  disturbances  in  diseases  of  the  motor  area  of  the  cortex, 
apparently  because,  for  the  purpose  of  co-ordination,  the  sensory  fibers 
which  subserve  the  appreciation  of  posture  are  anatomically  related  to 
the  psychomotor  centers.  The  above-mentioned  disturbances  in  the 
perception  of  posture  which  occur  in  hysteria  belong,  in  a  broader  sense 
of  the  word,  as  most  hysteric  symptoms  do,  to  cortical  implication. 

Method  of  Testing  tne  Touch  Perception  (the  Stereog- 
nostic  Sense). — Touch  perception — i.  e.,  the  recognition  of  the  form 
of  objects  by  their  surface — is  by  no  means,  as  is  sometimes  supposed, 
merely  a  function  of  the  tactile  and  pressure  sensation.  Its  popular 
title,  feeling  sensation  or  feeling  sense,  is  therefore,  in  the  strict  sense  of 
the  word,  incorrect.  In  handling  an  object  we  first  employ  the  touch 
and  pressure  sense,  then  the  appreciation  of  the  active  movements  essen- 
tial to  feeling  the  object,  further  the  perception  of  the  position  of  the 
fingers  encircling  it,  and  finally  the  sensation  of  temperature,  to  recognize 
the  material  of  which  it  consists  (metal,  wood,  etc.).  Here  again  it  is  a 
question  of  very  complicated  perception  worked  out  in  the  brain  with 
various  aids,  but  in  no  way  the  product  of  a  single  specific  sensibility. 
This  conception  makes  it  clear  how,  even  when  the  examination  of  the 
simple  sensory  functions  (touch,  perception,  etc.)  shows  no  disturbance 
at  all,  the  stereognostic  recognition  of  objects  may  be  disordered  in  cere- 
bral disease — i.  e.,  in  lesions  of  the  motor  cortex,  whose  relation  to  the 
innervation  sense  and  to  the  judgment  of  active  and  passive  movements 
and  of  the  position  of  the  extremities  has  already  been  mentioned — as 
well  as  in  peripheral  motor  paralysis,  which  prevents  a  correct  appre- 
ciation of  the  innervation  sense. 

To  test  the  stereognostic  sense  we  ask  the  patient,  with  closed  eyes, 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  769 

to  name  various  small  objects  placed  in  his  hand.  This  function  is 
only  slightly  developed  in  the  feet,  yet  a  healthy  individual  can  recog- 
nize larger  objects  even  with  them.  Objects  placed  upon  the  back  can 
be  recognized  only  when  they  are  very  large  and  characteristic.  This 
clearly  demonstrates  that  the  stereognostic  sense  is  not  essentially  aided 
by  the  cutaneous  sensibility,  as  the  old  name,  "  feeling  sense,"  would 
lead  us  to  believe.  As  is  well  known,  the  stereognostic  sense  is  very 
acutely  developed  in  the  mouth,  where  it  depends  considerably  upon 
the  perception  of  the  active  movements  and  of  the  position  of  the 
tongue. 

(c)  Observations  upon  the  Technique  of  Testing  Sensibility. 

In  the  foregoing  description  the  author  has  refrained  intentionally 
from  describing  the  instrumental  methods  which  are  claimed  to  possess 
special  accuracy  in  testing  sensibility.  Perhaps  some  readers  may  miss 
them,  as,  for  instance,  the  examination  for  localizing  the  sensation  of 
touch,  or  for  testing  the  feeling  crises  with  Weber's  touch  compass,  or 
with  Sieveking's  esthesiometer,  the  examination  of  the  temperature 
sense  with  the  various  peculiarly  constructed  thermo-esthesiometers, 
etc.  He  is  convinced  that  none  of  these  instruments  aids  clinical 
observation  to  any  extent,  because,  in  the  first  place,  our  diagnosis  must 
depend  upon  the  grosser  changes  which  can  be  demonstrated  by  the 
simple  methods  described  above,  and  because,  in  the  second  place,  we 
either  do  not  know  the  physiologic  normal  for  such  instruments,  or  else 
the  normal  varies  so  much  according  to  the  individuality  that  even  the 
apparent  exactness  of  the  results  may  lead  to  marked  diagnostic  falla- 
cies. Their  apparent  exactness  is  really  fancied,  because  each  method 
has  so  many  sources  of  error  that  even  the  very  great  skill  which  is 
attainable  by  but  few  physicians  will  not  obviate  them.  Everyone  who 
has  had  any  experience  with  the  Weber's  compass  w-ill  agree  wdth  the 
author.  Neither  has  he  mentioned  the  electrical  methods  of  testino' 
sensibility,  because  in  the  present  state  of  knowledge  these  will  hardly 
be  of  much  service  to  the  diagnosis.  As  a  matter  of  fact,  we  do  not 
really  know  what  we  are  testing  for  by  this  method,  as  it  has  not  been 
studied  enough  physiologically,  v.  Frey's  method  of  testing  with  irri- 
tation hairs  should,  however,  be  of  real  service  in  the  future. 

2.   PHENOMENA  OF  SENSORY  IRRITATION. 

Paresthesia. — By  paresthesias  are  understood  subjective  sensa- 
tions— i.  €.,  sensations  corresponding  to  no  correlation  in  the  external 
world — which  are  not  actually  painful,  but  which  without  any  sharp 
boundary  often  merge  into  pain.  They  are  sufficiently  well  character- 
ized by  such  names  as  "furry,"  "  tickling,"  "  cmirUng  of  anti<,"  and 
"falling  asleep"  The  buzzing  character  and  the  comj^lete  dissociation 
of  these  sensations  (the  latter  especially  characterizes  the  sensation  of 
fur  or  crawling  of  ants)  depend,  according  to  the  research  of  v.  Frey, 
upon  the  oscillatory  character  of  the  nerve  stimulation  in  pressure  sen- 
sation.    This  can  very  easily  be  demonstrated  by  exciting  the  pressure 

49 


770  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

points  by  irritating  hairs  (see  p.  759).  Subjective  feelings  of  warmth 
and  cold  correspond  to  similar  paresthesias  in  the  province  of  the  ther- 
mal nerves ;  those  of  smell,  sight,  hearing,  and  taste,  in  the  territory 
of  the  higher  senses.  Paresthesias  may  arise  from  an  irritation  of  the 
sensory  tracts  at  any  point  of  their  entire  course,  but  they  are  most  fre- 
quently observed  in  lesions  of  the  sensory  roots  downward  and  are 
therefore  localized  in  the  peripheral  nerves.  The  paresthesias  which 
occur  in  spinal  cord  affections,  and  which  are  localized  at  the  intercostal 
nerves  or,  rather,  their  sensory  roots,  are  spoken  of  as  "  girdle  sensa- 
tion."    The  girdle  sensation  frequently  becomes  a  "  girdle  pain." 

Spontaneous  Pains. — In  a  general  way  pain  may  be  subdivided 
into  parenchymatous  and  neuralgic  pains.  In  parenchymatous  pains 
the  sensory  fibers  are  irritated  at  their  terminal  ramifications,  in  neu- 
ralgic pains,  at  the  trunks  of  sensory  or  mixed  nerves,  in  the  sensory 
roots  or  in  the  sensory  centers.  In  the  former  the  terminations  of  the 
sensory  fibers  are  irritated  quite  independently  of  their  origin,  and 
therefore  the  pains  overlap  the  boundaries  of  peripheral  sensory  areas, 
apparently  at  will.  Neuralgic  pains,  on  the  contrary,  according  to  the 
law  of  eccentric  projection,  are  localized  in  areas  that  correspond 
exactly  to  the  peripheral  distribution  of  the  nerve  trunk  or  nerve 
involved.  Pain  may,  however,  be  felt  in  neighboring  nerve  territories 
from  irradiation  of  the  pain  from  the  involved  nerve  into  them.  (See 
p.  774  et  seq.,  Sympathetic  Sensations.)  A  further  difference  between 
these  pains  is  to  be  found  in  their  severity.  Neuralgic  pains  are  gen- 
erally much  more  severe  than  parenchymatous  pains,  for  the  reason  that 
in  the  former  a  much  larger  number  of  fibers  are  painfully  irritated, 
and  ordinarily  at  the  same  moment.  Probably  for  the  same  reason 
remissions  in  a  severe  pain  are  more  decided  in  neuralgic  than  in  par- 
enchymatous pains.  Some  of  these  remissions  can  readily  be  attributed 
to  a  fatigue  of  a  central  pain-percipient  apparatus,  a  fatigue  which 
naturally  occurs  sooner  and  more  pronouncedly  after  intense  irritation 
than  after  weaker  irritation.  Another  distinction  is  that  generally  with 
parenchymatous  pains  the  entire  painful  area  is  sensitive  to  pressure. 
This  is  sometimes  the  case  with  neuralgic  pains  ;  but,  as  a  rule,  only 
that  portion  of  the  nerve  trunk  is  sensitive  to  pressure  which  lies 
superficially  or  upon  a  hard  foundation  (neuralgic  pressure  points). 

The  best-known  example  of  neuralgic  pains  are  the  true  neuralgias, 
which  occur  in  some  instances  in  otherwise  healthy  individuals,  but 
which  in  other  instances  are  indirectly  due  to  disease  (joint  rheuma- 
tism, syphilis,  diabetes,  etc.),  and  the  so-called  lancinating  pains  in  spinal 
cord  diseases,  especially  in  the  initial  stage  of  tabes  dorsalis. 

To  the  parenchymatous  pains  belong  most  of  those  pains  which 
occur  in  organic  disease  of  various  viscera;  many  of  the  diffuse  head- 
aches of  meningitis  and  intracranial  pressure;  toxic,  febrile,  dyspeptic, 
and  anemic  headaches,  as  well  as  migraine  and  most  forms  of  neuras- 
thenic headaches. 

In  most  cases  the  sensation  of  pain,  whether  it  is  of  a  neuralgic  or  par- 
enchymatous character,  is  of  peripheral  origin — i.  e.,  depends  upon  an 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  771 

irritation  of  the  peripheral  sensory  neurons  (of  the  peripheral  nerves  or 
sensory  roots).  It  still  seems  doubtful  whether  pains  may  be  caused 
from  involvement  of  the  conduction  tracts  above  the  sensory  roots  in 
the  spinal  cord.  This  part  of  the  conduction  pathway  has  usually  been 
considered  to  be  purely  esthesodic — i.  e.,  conductory  but  not  irritable. 
On  the  contrary,  eccentrically  projected  pains  can  doubtless  be  pro- 
duced by  lesions  of  the  sensory  tracts  in  the  brain,  especially  of  the 
posterior  part  of  the  internal  capsules.^  It  is  also  certain  that  pains  may 
take  their  origin  from  the  most  central  organs  of  perception.  It  is  to 
this  category  that  the  suggested  and  auto-suggested  pains  and  also  many 
hysteric  pains  belong.  Naturally  these  pains  have  in  their  radiation  the 
character  of  parenchymatous  pains  and  not  neuralgic,  because  the  arrange- 
ment of  the  elements  in  the  central  parts— i.  e.,  the  brain — does  not  corre- 
spond to  the  nerve  trunks,  but  to  the  limits  of  the  organ.  For  instance,  hys- 
teric joint  pains  are  often  improperly  spoken  of  as  articulatory  neuralgia. 

A  peculiar  combination  of  symptoms,  so-called  anesthesia  dolorosa, 
should  be  mentioned  here.  It  consists  of  the  occurrence  of  spontan- 
neous  pains  in  a  portion  of  the  body  which  is  anesthetic  to  external 
stimulation.  Such  conditions  occur  when  a  focus  of  disease,  most  often 
of  the  nerves  or  nerve  roots,  interrupts  the  conductivity  of  peripheral 
stimuli  and  at  the  same  time  causes  irritation  of  the  sensory  fibers. 

Hyperalgesia  (Hyperesthesia) ;  Sensitiveness  to  Pain. — 
By  the  term  hyperesthesia  or,  better,  hyperalgesia,  we  understand  a  con- 
dition of  the  sensory  mechanism  in  which  stimulation  produces  the 
sensation  of  pain  in  a  certain  area  (especially  of  the  skin),  although 
normally  such  stimulation  would  not  be  painful.  The  slightest  touch 
of  the  skin,  moving  the  part,  or  the  mildest  sort  of  thermic  influence 
may  under  such  circumstances  produce  pain.  We  now  recognize  that 
pain  perception  (at  least  cutaneous  pain  perception)  is  a  specific  per- 
formance of  a  definite  kind  of  nerve  fibers  (see  p.  760  et  seq.) ;  hence, 
we  may  regard  hyperalgesia  merely  as  a  supersensitiveness  of  the  pain 
nerves.  We  have  as  yet  no  convincing  demonstration  that  a  vigorous 
stimulation  of  other  sensory  terminations^— e.  g.,  of  touch,  warmth  or 
cold — :can  produce  pain,  because  we  cannot  exclude  a  coincident  impli- 
cation of  the  pain  nerves  in  every  such  vigorous  stimulation.  There- 
fore we  should  substitute  the  expression  hyperalgesia  for  hyperesthesia. 
We  do  not  yet  know  what  defects  of  the  pain-conducting  or  the  pain- 
appreciating  parts  of  the  nervous  system  can  give  rise  to  hyperalgesia  ; 
but  it  is  certain  that  peripheral  as  well  as  central  parts  may  assist  in 
this  hyperalgesia  from  an  associated  involvement  of  the  sensory  fibers 
or  cells.  Such  involvement  produces  slight  injuries  which  are  insuffi- 
cient to  produce  anesthesia,  but  sufficient  to  cause  irritation.  The  best- 
known  examples  are  the  hyperalgesias  in  the  domain  of  neuralgie  nerves 
during  the  early  stages  of  neuritis,  the  zone-like  hyperalgesias  of  the 
upper  borders  of  sensory  disturbances  in  cross-lesions  of  the  spinal  cord, 
and  the  general  hyperalgesia  of  hysteric  or  neurasthenic  patients. 

^  See  the  meager  literature  upon  this  point  in  the  article  by  Alfred  A.  Reichenberg, 
Zeits.f.  Nervenheilk. ,  vol.  xi.,  pts.  5  and  6,  p.  349. 


772 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


Fig.  295.— For  description  see  next  page. 


The  so-called  jjresmre  sensitiveness  (better  described  as  increased  sen- 
sitiveness to  pressure)  is  in  reality  nothing  more  than  a  special  form  ot 
hyperalgesia.  In  the  examination  of  the  nervous  system,  the  pain  sen- 
sitiveness of  the  nerve  trunk  to  pressure  which  occurs  principally  in 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


773 


Fl(i.  296. 

Figs.  295  and  296.— Hyperalgesic  and  radiation  zones  of  the  skin  iu  diseases  of  deeply  situated 
organs.  Zones  on  the  trunk  and  extremities :  Diseases  of  the  heart,  pain  and  hypersthesia 
in  zones,  C3,  A.  A:  tuberculosis  of  the  lungs,  T>i-D,,  particularly  Dn,  D4,  Dr,;  diseases  of  the 
esophagus,  particularly  Dj,  1)^,  Dg;  diseases  of  the  breast,  A,  A;  diseases  of  the  stomach,  Z>7,  A, 
"     -^'  f  -■  ^.  -^i-  -  — , ,„,-_.    r.      r.      ,^        1- _i7  ,• —    T^     i^     r>     T%  ^.  diseases 

ovaries 
(after 
H.  Head). 


774  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

peripheral  neuralgic  and  neuritic  affections  is  of  special  interest.  It  is 
under  some  circumstances  essential  to  examine  into  this  appearance,  even 
where  no  spontaneous  pain  is  present. 

The  hyperalgesic  zones  of  the  skin  in  diseases  of  the  viscera  are 
mentioned  in  the  following  section. 

Sympathetic  or  Reflex  Sensation  ;  Irradiation  of  Pain ; 
Tickling ;  Hyperalgesic  ^ones  of  the  Skin  in  Diseases  of 
the  Deeper  Organs. — So-called  sympathetic  or  reflex  sensation  is 
nearly  related  to  hyperalgesia. 

The  best-known  form  of  this  is  pain  irradiation,  in  which  the  pain 
is  perceived  far  beyond  the  limits  of  the  painfully  irritated  peripheral 
part  (pain  in  the  entire  trigeminal  distribution,  occasioned  by  a  single 
carious  tooth).  This  phenomenon  can  be  explained  only  by  assuming 
that  the  painful  stimulation  in  the  central  organs  (spinal  ganglia,  gray 
substance  of  the  spinal  cord  or  of  the  brain)  overlaps  or  irradiates  to 
neighboring  tracts  by  means  of  dendrites  and  collaterals,  and  that,  in 
accordance  with  the  law  of  eccentric  projection,  confusion  as  to  the 
origin  of  the  perception  results.  [This  entire  subject  has  been  put 
upon  a  satisfactory  foundation  at  last  by  the  studies  of  Head. — Ed.] 

The  pain  sense  is  not  always  concerned  in  reflexes  either  of  primary  or 
of  secondary  nature  ;  in  fact,  touch  and  temperature  sense  or  the  higher 
senses  can  produce  them,  and  such  sympathetic  sensations  are  not  neces- 
sarily painful. 

As  an  example  of  such  associate  sensation  tickling  may  be  cited. 
This  is  an  irradiating  or  sympathetic  sensation  of  an  oscillating  char- 
acter diffused  over  a  considerable  surface  of  the  skin,  caused  by  a  cir- 
cumscribed skin  stimulation. 

Quincke  ^  has  made  quite  a  complete  collection  of  the  practically  important 
sympathetic  sensations  which  have  been  thus  far  determined  ;  but  only  a  few  of 
the  most  important  will  be  mentioned  :  trigeminal  neuralgia  in  aflfections  of  the 
frontal  sinuses ;  parietal  pain  in  affections  of  the  middle  ear  and  of  the  mastoid 
process  ;  a  tendency  to  cough  from  irritation  of  the  posterior  wall  of  the  audi- 
tory canal  (irradiation  from  the  auricular  branch  of  the  vagus  to  the  other  vagus 
branches)  ;  a  marked  sensation  of  tickling  and  shuddering  in  biting  upon  sand  ; 
painful  sensation  in  the  back  in  swallowing  ;  laryngeal  pain  in  percussing  a  pul- 
monary abscess  (Quincke)  ;  pain  in  the-  left  arm  (rarely  in  the  right)  in  angina 
pectoris  ;  pain  in  the  back  in  stomach  diseases  ;  feeling  of  tickling  in  the  nose 
from  intestinal  worms  ;  pains  in  the  shoulder  in  liver  affections  ;  pains  in  the 
left  shoulder  in  affections  of  the  spleen  ;  pain  in  the  lumbar  region  and  genitalia 
in  bladder  affections  ;  pains  in  the  epigastrium  and  the  stomach  region  in  endo- 
metritis and  during  menstruation  ;  pain  in  the  knees  in  coxitis  ;  simultaneous 
polyesthesia  (p.  760)  in  spinal  cord  affections. 

A  phenomenon  related  to  and  frequently  associated  with  these  sympathetic 
sensations — a  circumscribed  cutaneous  hyperalgesia  depending  upon  diseases  of 
the  deeper  organs — is  of  more  diagnostic  significance.  The  best-known  example 
is  the  sensitiveness  to  pressure  of  the  skin  of  the  precordia  in  heart  disease. 
This  hyperalgesia  is  perhaps  most  satisfactorily  explained  thus  :  The  centripetal 
irritations  proceeding  from  the  diseased  organs  which  escape  direct  perception 
stimulate  by  irradiation  the  neighboring  sensory  parts  of  central  organs.  The 
latter  are  passageways  for  the  sensory  fibers  coming  from  the  areas  of  the  skin  in 

^  Zeits.  f.  klin.  Med.,  vol.  xvii.,1890. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


775 


question.     In  contrast  to  actual  sympathy  or  irradiation,  this  irradiated  stimula- 
tion is  not  strong  enough  to  be  appreciated  by  the  sensorium  as  pain,  but  is 


Nasofrontal  zone 

Maxillary  zone 

Nasolabial  zone 

Mental  zone 


Middle  orbital  zone 

Temporofrontal  zone 
Temporal  zone 


Upper  )  Laryngeal 
Lower  j       ^°°^ 


Middle  orbital  zone 


Temporofrontal  zone 
Temporal  zone 


Sincipital  zone 
Parietal  zone 

Occipital  zone 
Mandibular  zone 

Hyoid  zone 


Upper  I  Laryngeal 
Lower)       ^""^^ 


Fig.  297.— Hyperalgesic  and  radiation  zones  of  the  skin  in  diseases  of  deeply  situated  organs. 
Zones  on  the  head  and  neck:  Nasofrontal  zone,  diseases  of  the  eyes,  nose,  and  upper  incisors: 
middle  orbital  zone,  in  hypermetropy :  temperofrontal  zone,  diseases  of  the  ears  and  heart;  tem- 
poral zone,  in  glaucoma  (after  H.  Head). 


Si  ncipital  zone :  Diseases  of  the  middle  ear. 
Parietal  zone:    Diseases   of  the   ear    and 

stomach. 
Occipital  zone  :  Diseases  of  the  posterior 

half  of  the  larynx  and  certain  abdominal 

viscera. 
Maxillary  zone:  Diseases  of  the  iris  and 

vitreous  body. 
Mandibular  zone:  Diseases  of  the  upper 

molars. 


Nasolabial  zone :  Diseases  of  the  nose  and 
dental  pulp. 

Mental  zone :  Diseases  of  the  incisors  and 
canines. 

Hyoid  zone  :  Diseases  of  the  tonsils,  tongue, 
and  lower  molars. 

Upper  laryngeal  zone :  Diseases  of  the  dor- 
sal surface  of  the  tongue  and  the  wisdom 
teeth. 

Lower  laryngeal  zone :  Diseases  of  larynx. 


merely  sufficient  to  cause  a  superior  stimulation  at  the  junctions  of  the  sensory 
conductions  coming  from  the  skin. 

Fig.  298,  explains  the  process  diagrammatically:  a  Represents  the  diseased 
organ  with  a  centripetal  stimulation  proceeding  to  a  sensory  station,  (b)  for 
example,  in  the  spinal  cord ;  from  there  the  stimulation  can  come  to  the  senso- 


776 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


rium  (c),  either  directly  {b-c)  or  indirectly  (b-d-f),  c,  jumping  to  a  neighboring 
sensory  tract  (e,  /)  .  If  this  process  of  irradiation  produces  a  painful  stimula- 
tion at  d,  a  painful  sympathetic  sensation  will  be  referred  to  the  cutaneous  area 
(e)  ;  whereas  if  it  produces  merely  a  hyperirritable  condition  at  d,  the  cutaneous 
area  (e)  will  merely  present  a  hyperalgesia  to  pressure  and  to  other  stimulations 
not  causing  pain.  Thus,  circumscribed  cutaneous  hyperalgesias,  if  anatomically 
established,  may  under  some  circumstances  possess  the 
same  diagnostic  value  as  actual  sympathetic  sensations. 

Head,  of  London,  has  taken  pains  to  investigate  these 
zones  of  cutaneous  hyperalgesia  in  a  great  number  of 
pathologic  conditions  in  order  to  establish  some  diag- 
nostic relations  to  deep-lying  diseases.  Corresponding 
to  the  above  explanation,  he  found  that  the  hyperalgesic 
zones  were  identical  with  the  zones  to  which  the  irradia- 
tion pains  were  projected  in  the  diseased  organs  in  ques- 
tion. He  tabulated  his  observations  in  the  accompany- 
ing plates'  (Figs.  295,  296,  and  297).  The  separate  zones 
are  shaded  differently.  The  numbers  and  letters  refer  to 
the  segments  of  the  spinal  cord  (designated  according  to 
the  corresponding  spinal  nerves)  whose  stimulation  is  the 
cause  of  the  cutaneous  hyperalgesia  (based  upon  our 
knowledge  of  the  spinal  sensibility  topography  of  the 
skin  (see  p.  922  et  seq.).  Probably  the  affected  organs 
are  also  suj^plied  by  the  same  nerves.  Thus  far  no  sat- 
isfactory anatomic  explanation  has  been  able  to  correlate 
the  localizations  of  hyperalgesic  zones  of  the  head  to 
definite  diseases. 

Though  interesting  theoretically.  Head's  statements 
need  further  confirmation  and  perhaps  modifications. 
Such  relations  of  the  deeper  organs  to  the  surface  of 
the  skin  make  one  appreciate  the  therapeutic  action  of 
counterirritation  to  the  skin,  especially  upon  deep-seated  pains.  It  is  only  fair 
to  suppose  that  the  same  anatomic  tracts  w^hich  conduct  the  cutaneous  hyper- 
esthesias in  diseases  of  the  deeper  organs  can  be  utilized  to  transmit  inhibition 
of  pain  by  vigorous  stimulation  of  the  skin. 


Deep  organ.         Skin. 

Fig.  '298.— Diagram  to  il- 
lustrate skin  liyperalgesias 
and  the  radiation  of  pain  in 
disease  of  deeply  situated 
organs. 


rv.  EXAMINATION  OF  THE  REFLEXES. 

In  testing  reflexes  it  is  advisable  to  distract  the  patient's  attention 
as  much  as  possible  from  the  parts  under  examination,  otherwise  an 
involuntary  inhibition  may  alter  the  reflex.  The  simplest  device  is  to 
direct  him  to  close  his  eyes.  The  fatigue  of  a  reflex  is  sometimes 
responsible  for  mistakes  in  diagnosis.  The  response  to  the  first  tap 
should  be  observed  attentively,  because  it  may  disappear  after  one  or 
two  repetitions.  If  the  first  response  had  not  been  noticed,  the  exam- 
iner would  then  incorrectly  consider  the  reflex  absent.  It  is  therefore 
a  safe  rule  to  observe  each  reflex  quickly  and  accurately,  and  to  utilize 
repeated,  careful  examinations  in  order  to  discriminate  in  any  doubtful 
case,  for  the  reflexes,  like  other  nervous  functions,  often  vary  at  different 
times.  These  precautions  are  especially  valuable  in  testing  the  patellar 
reflex,  which  is  so  important  in  diagnosis. 

^  The  reflexes  belonging  to  the  cranial  nerve  territory  will  be  described  more  fully 
in  the  special  part  devoted  to  examination  of  the  separate  cranial  nerves.  (Concerning 
the  bladder  and  rectal  reflexes,  see  the  section  upon  Examination  of  the  Bladder  and 
Rectal  Functions.)  « 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  Ill 

Ordinarily  the  reflexes  are  local  in  character — t.  e.,  they  take  place 
in  the  region  of  the  body  that  is  irritated.  But  with  an  increase  in  the 
reflex  irritability,  which  may  be  partly  -within  the  normal  physiologic 
limits  and  depend  partly  upon  reflex  stasis  (described  upon  p.  783),  the 
reflexes  may  be  diffused  in  cross  and  longitudinal  directions  to  other 
muscle  areas  and  to  other  extremities.  This  corresponds  to  Pfluger's 
laws  of  reflex  dispersion. 

Increase  of  the  reflexes,  as  well  as  decrease  or  absence  and  qualitative 
abnormalities  (the  so-called  pathologic  reflexes),  are  of  considerable 
importance  for  diagnosis. 

NORMAL  CUTANEOUS  REFLEXES. 

The  cutaneous  reflexes  of  the  upper  extremities  and  of  the  face  are 
very  inconstant.  They  have,  therefore,  no  diagnostic  significance 
except  when  decidedly  increased.  The  following  cutaneous  reflexes 
are  clinically  the  most  important : 

Plantar  Reflex. — Tickling  or  pricking  the  sole  of  a  healthy 
person's  foot  produces  a  plantar  flexion  of  the  toes  (see  Fig.  299).  A 
stronger  irritation  produces  a  dorsal  flexion  of  the  toes,  combined  with 
a  dorsal  flexion  of  the  foot  and  flexion  of  the  knee  and  hip  joints. 

The  cremaster  reflex  is  elicited  when  the  inner  surface  of  the 
thigh  is  irritated  by  scratching  or  pricking,  or  by  stroking  it  quickly 
with  the  handle  of  a  percussion  hammer  or  some  similar  object.  It 
consists  of  a  sudden  contraction  of  the  cremaster  muscle  which  draws 
up  the  testicle.  This  reflex  should  not  be  confused  with  the  slow, 
worm-like  contraction  of  the  tunica  dartos  which  frequently  follows 
uncovering  the  patient,  as  a  result  of  cooling. 

The  inguinal  reflex  (oblique  reflex)  (K.  GeigeP)  can  be  elicited 
in  both  sexes  by  an  irritation  similar  to  that  described  for  the  elicitation 
of  the  cremaster.  It  consists  of  a  contraction  of  the  lower  fibers  of  the 
internal  oblique  muscle  above  and  along  Poupart's  ligament.  Since  the 
cremaster  muscle  is  nothing  but  a  bundle  of  the  internal  oblique  passing 
with  the  testicle  through  the  inguinal  canal,  the  cremaster  reflex  in 
reality  belongs  to  the  inguinal  reflex.  Examination  of  the  latter  in  the 
female  sex  takes  the  place  of  that  of  the  cremaster  reflex. 

The  abdominal  reflex  is  produced  by  tickling,  scratching,  or 
pricking  the  skin  of  the  abdomen.  It  consists  in  a  simultaneous  con- 
traction of  the  transverse  oblique  and  recti  muscles  of  the  abdomen, 
which  produces  a  depression  of  the  abdomen  and  a  pulling  of  the  navel 
toward  the  side  stimulated. 

Several  abdominal  reflexes  should  be  differentiated  upon  each  side 
of  the  abdomen — a  superior,  median,  and  inferior.  Stroking  the 
abdominal  wall  in  a  horizontal  direction  in  the  region  of  the  epigastrium 
or  hypogastrium  causes  reflex  contractions  of  the  abdominal  muscles, 
which  remain  localized  at  approximately  the  height  of  the  stimulation. 
If,  on  the  contrary,  the  entire  length  of  the  abdomen  is  stroked  in  a 
vertical  direction,  the  whole  half  of  the  abdomen  is  contracted,  and  the 
■■*  Deulsch.  med.  WocL,  1892,  vol.  viii.,  p.  166. 


778  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

maximum  of  the  excursion  is  found  at  the  height  of  the  navel.  This  is 
what  we  ordinarily  call  the  abdominal  reflex  (a  poor  term).  With  more 
vigorous  irritation,  horizontal  stroking  of  the  abdomen  can  produce 
the  general  abdominal  reflex. 

The  interscapular  reflex,  which  is  elicited  by  stroking  the  inner 
edge  of  the  scapula,  consists  in  an  adduction  of  the  shoulder-blade.  It 
is  frequently  absent. 

The  gluteal  reflex,  a  contraction  of  the  gluteal  muscles  produced 
by  an  irritation  of  the  skin  about  the  gluteal  region,  is  also  inconstant. 

Anal  Reflex. — Irritation  of  the  skin  of  the  anus,  as  by  a  pin 
prick,  elicits  a  contraction  of  the  sphincter  and  externus.  It  is  often 
absent.  (Consult  p.  784  et  seq.  and  p.  927  et  seq.  in  regard  to  the 
diagnostic  significance  of  abnormalities  of  the  cutaneous  reflexes  and 
their  localization  in  the  spinal  cord  segments.) 

TENDON,  PERIOSTEAL,  AND  JOINT  REFLEXES. 

The  patellar  reflex,  or  the  "knee  phenomenon,"  consists  in  a 
contraction  of  the  quadriceps  muscle  excited  by  a  blow  upon  the  patellar 
tendon.  We  may  employ  the  ulnar  edge  of  the  hand  or,  better,  the 
edge  of  a  firm,  not  too  light  object — e.  g.,  a  percussion  hammer. 

The  Achilles-tendon  reflex  consists  in  a  contraction  of  the  calf 
muscles  excited  by  a  blow  upon  the  Achilles  tendon,  producing  a  flexion 
of  the  foot.  Another  method  of  exciting  this  reflex  is  to  increase  sud- 
denly the  tension  of  these  muscles  by  a  passive  dorsal  flexion  of  the 
foot.  If  the  reflex  is  increased,  the  latter  method  causes  a  series  of 
rapidly  succeeding  plantar  flexions  of  the  foot,  which  often  persist  as 
long  as  dorsally  directed  pressure  is  exerted  upon  the  ball  of  the  foot. 
The  repetition  of  the  flexions  apparently  depends  upon  the  fact  that 
each  contraction  of  the  calf  muscles  increases  the  pressure  upon  the 
plantar  surface,  so  that  the  pressure  acts  later  as  a  renewed  blow.  We 
call  such  an  increase  of  the  Achilles-tendon  reflex  "  the  foot  phenom- 
enon," "  foot-clonus,"  or  "  ankle-clonus." 

The  tendon  reflexes  of  the  upper  extremities  are  extremely  incon- 
stant. In  healthy  individuals  a  flexion  of  the  hand  can  sometimes  be 
obtained  by  striking  the  flexor  tendons  at  the  wrist-joint,  a  bending  of 
the  forearm  from  the  biceps  tendons,  or  an  extension  from  the  triceps 
tendons.  If  the  reflexes  are  increased  a  similar  result  can  be  obtained, 
even  in  the  upper  extremities,  by  striking  almost  any  of  the  tendons. 
Sometimes  an  actual  clonus  can  be  produced  by  vigorously  flexing  the 
hand  dorsally,  "  hand-clonus  "  (analogous  to  ankle-clonus). 

Periosteal  and  joint  reflexes  are  produced  by  striking  various 
bony  prominences  and  joints.  They  are  inconstant  in  health.  The 
best-known  periosteal  reflexes  are  those  of  the  crest  of  the  tibia,  and  of 
the  ulna  and  the  radius  at  the  wrist-joint. 

In  testing  tendon  and  periosteal  reflexes  it  is  especially  important  to 
observe  the  caution  enjoined  above — that  is,  to  distract  the  attention  of 
the  patient  from  the  part  of  the  body  to  be  examined,  since  otherwise 
the  reflex  may  be  inhibited.    A  very  good  plan  is  to  interest  the  patient 


EXAMINATIOIS^  OF  THE  NERVOUS  SYSTEM.  779 

in  some  subject,  and  to  engage  him  in  conversation  while  you  are  test- 
ing. Jendrassik's  device  for  reinforcement  is  often  very  successful  in 
testing  the  tendon  reflexes  of  the  lower  extremities.  The  patient  is 
directed  to  lock  his  fingers  and  pull  strongly,  as  if  tearing  them  apart, 
but  without  separating  them.  Not  infrequently,  however,  this  reinforce- 
ment does  the  opposite  to  what  it  usually  accomplishes — i.  e.,  it  weakens 
or  inhibits  the  patellar  reflex — probably  because,  instead  of  actually  con- 
centrating his  entire  attention  and  effort  upon  the  fingers,  the  patient 
renders  the  muscles  of  his  lower  extremities  tense  by  associated  move- 
ment, and  so  inhibits  the  patellar  reflex.  Another  precaution  that 
should  always  be  taken  is  to  be  sure  that  the  muscles  concerned  in  the 
reflex  are  thoroughly  relaxed.  This  is  especially  important  in  testing 
the  patellar  reflex.  For  the  latter  the  sitting  posture  is  most  desirable, 
with  the  leg  to  be  examined  crossed  and  hanging  limply  over  the  other. 
In  bedridden  patients  the  leg  is  supported  below  the  knee  by  the  hand 
of  the  examiner  in  semiflexion. 

CONSTANCY-!  e.,  FREQUENCY-OF  OCCURRENCE  OF  THE  NORMAL  SPINAL 

REFLEXES. 

Of  the  above-described  reflexes  there  are  only  a  few  which  are  really  constant, 
and  even  these  not  absolutely.  Many  are  even  present  only  in  a  minority  of  cases. 
According  to  the  researches  of  Pflasterer,  the  reflexes  are  found  as  follows: 

Males. 
Epigastric  reflex  (upper  abdominal  wall  reflex),  present  in  62  per  cent.^ 


Abdominal  reflex  (middle  abdominal  wall  reflex), 

Cremaster  reflex, 

Plantar  reflex. 

Interscapular  reflex. 

Gluteal  reflex. 

Periosteal  reflex  of  the  anterior  tibial  edge. 

Periosteal  reflex  of  the  lower  end  of  the  bones  of  the  forearm. 

Patellar  reflex, 

Achilles  tendon  reflex, 

Biceps  tendon  reflex, 

Triceps  tendon  reflex. 


99 
66 
98 
15 

28 

5 

29 

98 
57 
47 


Females. 

Present.  Absent.  Unilateral.            Doubtful. 

Plantar  reflex 88  11                         1 

Abdominal  reflex   ....  92  7                        •  •                          1 

Interscapular  reflex  ...  13  86                          1                         .  . 

Gluteal  reflex 11  89 

RECENT  VIEWS  CONCERNING  THE  ORIGIN  OF  THE  REFLEXES. 

'  Formerly  it  was  believed  that  the  spinal  cord  was  the  center  of  all 
reflexes.  This  view  was  based  upon  the  results  of  animal  experiments 
and  upon  the  observation  that  most  transverse  lesions  of  the  cord  were 
associated  with  increase  of  the  reflexes.  Modern  neuropathologists, 
however,  following  the  teaching  of  Bastian,  endeavor  to  dethrone  the 
cord  from  its  position  as  a  reflex  organ.  Bastian  and  others  have  shown 
that  all  the  reflexes  were  found  to  be  completely  abolished  in  some  cases 
in  which  there  is  complete  transverse  lesion  of  the  spinal  cord.     It  was 

>  Cited  by  K.  Geigel,  Deuhch.  med.  Woch.,  1892,  No.  8,  p.  166. 


780  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

therefore  argued  that  no  transverse  lesion  could  be  complete  if  the 
reflexes  in  the  region  innervated  below  the  injury  either  persisted  or 
were  increased.  A  few  such  observations,  however,  prove  nothing, 
because  the  part  of  the  spinal  cord  situated  below  the  obstruction  might 
be  affected  in  such  cases  bv  inhibition  or  bv  a  diminished  blood-supply 
conditioned  by  lesion  of  the  spinal  arteries.^  In  order  to  determine 
whether  the  reflexes  of  clinical  importance  have  their  centers  in  the 
spinal  cord,  it  is  much  more  essential  to  inquire  whether  there  have 
been  cases  with  persistent  reflexes  of  the  lower  extremities  in  which  a 
careful  anatomic  examination  has  shown  postmortem  complete  cross- 
section  of  the  spinal  cord.  In  recent  years  such  cases,  absolutely  free 
from  question,  have  been  described,^  and  show  beyond  question  that  the 
tendon  reflexes,  at  least,  are  independent  of  nervous  mechanism  beyond 
the  spinal  cord.  Similar  results  have  been  proved  by  the  persistence 
of  the  tendon  reflexes  after  decapitation  (Laborde).^  Hence  it  is  plainly 
incorrect  to  maintain  that  all  reflexes  require  the  aid  of  the  brain.*  The 
discussion  has  been  valuable  in  more  accurately  determining  the  merits 
of  the  earlier  conception,  which  argued  that  all  reflexes  took  place  in  the 
spinal  cord,  and  homologous  portions  of  the  brain  stem.  In  this  con- 
nection Jendrassik  has  formulated  a  theory  of  the  reflexes  which  is  based 
upon  clinical  evidence  and  which  is  worthy  of  careful  study.  [See  also 
upon  this  subject,  Collins  and  Friinkel,  "Muscle  Tonus  and  Tendon 
Phenomena,"  Medical  Record,  Dec.  12,  1903.— Ed.] 

According  to  Jendrassik  there  are  spinal  and  cerebral  reflexes,  as  ^vell  as  a 
combination  of  the  two — i.  e. ,  reflexes  requiring  both  cerebral  and  sjaiual  centers 
for  their  normal  performances. 

I.  Spinal  Reflexes. — This  division  includes  feiidoji,  periosteal,  and  joint  re- 
flexes. Their  characteristics  are  as  follows:  1.  They  are  generally  discharged 
from  parts  which  possess  little  sensation.  2.  The  reflex  is  associated  with  no  par- 
ticular feeling.  3.  The  discharge  takes  place  by  means  of  a  simple  mechanical 
irritation,  sncii  as  a  blow,  etc.  4.  The  intensity  of  the  reflex  depends  upon  the 
intensity  of  the  irritation,  not  upon  its  duration.  5.  The  reflexes  are  quite  as 
easily  excited  in  ourselves  as  in  others.  6.  The  latent  time  of  the  reflex,  corre- 
sponding to  its  origin  in  the  spinal  cord,  is  the  shortest.  7.  The  ensuing  movement 
is  a  very  simple  one  and  serves  a  recognizable  purjiose.  8.  Making  other  niuscles 
tense  increases  the  reflex  (reinforcement  method  of  Jendrassik  ;  see  description  on 
p.  779).  9.  Slowing  of  these  reflexes  never  occurs  pathologically.  10.  Psychical 
inferences  have  no  effect  upon  these  reflexes  aside  from  distraction  of  attention, 
■which  increases  them. 

II.  Cerebral  Reflexes.— These  are  to  a  large  extent  the  cutaneous  reflexes. 
The  scapular,  abdominal,  cremaster,  gluteal,  plantar,  eyelid,  palatal,  conjunctival, 
and  anal  reflexes  belong  to  this  group.  Their  characteristics  are  as  follows  : 
1.  They  are  discharged  from  sensitive  spots  which  are  not  ordinarily  accustomed 
to  a  light  touch  (tickling).  2.  The  liberation  is  associated  with  a  specific  sensa- 
tion (prickings,  cold,  tickling,  etc.).  3.  Brief  stimulation  is  efficacious  for  their 
liberation,  just  as  it  is  for  the  spinal  reflexes  described  in  the  previous  paragraph. 
4.   A  light  "touch  has  often  a  more  vigorous  action  than  a  stronger  one;  individu- 

1  Gerhardt,  "  Uber  das  Yerhalten  der  Reflexe  bei  Querdnrcbtrennung  des  Ruck- 
enmarkes,"  Beutsch.  Zeits.  f.  Nervenheilkumie,  1895,  vol.  vi.,  p.  127,  and  Jendrassik, 
"  Uber  die  allgemeine  Localisation  der  Reflexe,"  Beutsch.  Arch.f.  kUn.  Med.,  1894,  vol.  hi. 

■i  ]}j[(i  '^  Quoted  by  Jendrassik. 

*  According  to  Bastian's  and  Jackson's  view,  especially  of  the  cerebellum. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  781 

ality  has  a  decided  influence.  5.  These  reflexes  can  scarcely  ever  be  liberated  by 
the  i^erson  himself,  and  then  only  very  slightly.  6.  The  latent  time  is  longer  and 
not  as  constant  as  with  the  spinal  reflexes.  It  is  quite  dependent  upon  the  sensa- 
tion time  and  corresponds  to  the  reaction  time — i.  e.,  the  time  which  the  voluntary 
reaction  demands  of  a  sensory  stimulation.  7.  The  resulting  movement  is  simple, 
and  its  principal  characteristic  is  that  it  shows  an  effort  to  escape  from  the  irrita- 
tion. 8.  Increased  activity  of  other  muscles  never  increases  the  reflex,  but  may 
even  diminish  it.  9.  These  reflexes  are  diminished  on  the  paralyzed  side  in 
cerebral  hemiplegia.  10.  They  are  delayed  in  cases  of  delayed  sensation. 
11.  Psychical  influences  can  either  diminish  or  even  increase  these  reflexes;  dis- 
traction of  the  attention  impairs  them. 

III.  Complex  Reflexes. — To  this  group  belong  reflexes  which  have  compli- 
cated ' '  centers, ' '  within  which  the  reflex  occurs,  not  as  a  single  movement,  but 
as  a  series  of  such — e.  g. ,  sneezing,  vomiting,  swallowing,  coughing,  urinating, 
defecating,  genital  reflex  (ejaculation).  The  characteristics  in  common  are  as 
follows  :  1.  They  are  liberated  from  sensitive  places.  2.  The  liberation  takes  place 
with  a  specific  sensation,  which  plays  even  a  greater  role  in  the  origin  of  the 
reflex  than  in  those  of  the  cerebral  group.  3.  The  liberation  requires  protracted 
stimulation.  4.  Individuality  has  a  great  influence  upon  the  occurrence  of  the 
reflexes.  5.  The  stimulation  which  produces  these  reflexes  is  a  specific  and  com- 
plicated one.  6.  The  latent  time  is  longer  than  for  any  of  the  other  reflexes. 
Their  liberation  seems  to  require  a  sort  of  summation  of  stimuli.  7.  The  result- 
ing movement  is  very  complicated  and  bilateral ;  several  muscle  groups  take  part, 
and  in  some  of  them  the  reflexes  act  antagonistically.  8.  Muscular  activity  pro- 
duces a  certain  enfeebling  in  their  action.  9.  Psychical  influences  produce  a 
great  effect.     10.   Reflexes  of  this  group  belong  to  the  vegetative  functions. 

The  distinction  between  Groups  III.  and  II.  is  essentially  this  :  in  the  latter 
the  sensation  is  transposed  directly  into  simple  reflex  movement ;  whereas  in  the 
former  the  sensation — i.  e.,  the  cortical  stimulation — first  of  all  excites  a  compli- 
cated reflex  center  to  activity.  This  center  is  composed  of  different  separate 
centers,  and  within  the  main  center  the  reflex  process  then  takes  an  independent 
course.  Should  this  subdivision  be  accepted,  the  writer  would  call  attention  to 
the  fact  that  the  peculiarities  stated  by  Jendrassik  as  characteristic  of  the  indi- 
vidual groups  do  not  always  materialize.  It  would  lead  us  too  far,  however,  to 
discuss  these  points  in  detail.  For  the  last  group  of  Jendrassik  the  Avriter  would 
suggest  the  name  of  corticonuclear  reflexes.  Those  which  also  involve  spinal 
areas  of  innervation  might  with  equal  propriety  be  designated  as  cerebrospinal 
reflexes.  In  the  individual  cerebronuclear  reflexes  the  cerebral  factor  plays  a 
varying  but  important  part,  as  is  shown  by  the  fact  that  completely  unconscious 
individuals  never  cough  nor  sneeze,  but,  on  the  other  hand,  they  can  under  some 
circumstances  still  swallow  and  normally  urinate  and  defecate,  even  if  unwit- 
tingly. Various  examples  might  be  added  to  show  how  dependent  the  reflexes 
of  Gi-roups  II.  and  III.  are  upon  the  cerebrum;  but  the  writer  will  allude  only  to 
the  following:  the  diminution  of  the  cutaneous  reflexes  over  the  anesthetic  area 
of  the  hysteric;  the  purely  cerebral  origin  of  the  plantar  reflex  in  ticklish  per- 
sons, in  whom  it  may  be  elicited  by  threatening  to  tickle  them,  even  without 
touching  them;  and  the  occurrence  of  vomiting  evoked  by  some  disgusting  con- 
ception. 

Recognizing  the  above  theories  of  the  origin  of  reflexes,  we  should  now 
attempt  to  explain  their  clinical  manifestations  under  pathologic  conditions,  espe- 
cially in  the  case  of  an  interrupting  focal  lesion  of  the  brain  and  spinal  cord. 

Cerebral  Hemiplegias. — The  tendon  reflexes  are  here,  as  a  rule,  preserved, 
because  they  come  under  Group  I.  (the  spinal).  In  the  beginning  they  may  be 
lost,  probably  on  account  of  the  inhibiting  action  of  the  lesion,  but  later  they  are 
usually  increased,  because  of  the  complete  abolition  of  cerebral  inhibition.  (See 
p.  74(3  et  seq.,  Active  Contractures.)  The  behavior  of  the  cutaneous  reflexes 
(Group  II.)  in  cerebral  hemiplegia  is  explained  by  the  supposition  that,  for  the 
most  part,  the  voluntary  tracts  (pyramidal  tracts)  are  either  identical  with,  or,  at 
least,  run  very  near,   the  motor  limb  of  the  cortical  reflex  arc.     We  therefore 


782  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

generally  find  upon  the  paralyzed  side  diminution  or  disappearance  of  the 
cutaneous  reflexes.  In  hemiplegia  of  indirect  origin — i.  e.,  when  the  lesion  is 
not  immediately  of  the  pyramidal  tract — the  cutaneous  reflexes  may  be  retained, 
although  they,  too,  are  in  the  beginning  usually  diminished.  This  is  explained 
by  the  supposition  that  the  lesion  here  does  not  permit  the  passage  of  the  vol- 
untary impulse,  while  it  offers  no  obstacle  to  the  reflex  impulse.  The  persists 
ence  of  the  cutaneous  reflexes  upon  the  hemiplegic  side  can  be  regarded  as  a 
favorable  prognostic  sign,  because  it  argues  for  an  incomplete  interruption  of 
the  motor  tract.  The  condition  of  the  combined  reflexes  (Group  III.)  in  cere- 
bral hemiplegia  depends  upon  the  varying  degree  of  influence  which  the  cere- 
bral factor  has  upon  their  origin.  As  a  general  rule  they  are  not  affected, 
because  bilaterally  innervated.  The  more  important  of  these  reflexes,  the  blad- 
der and  rectal,  will  be  discussed  later. 

Transverse  Lesions  of  the  Spinal  Cord. — If  Jendrassik's  conception  is 
correct,  the  tendon  reflexes  must  in  general  be  considered  pure  spinal  reflexes,  and 
the  cutaneous,  on  the  other  hand,  cerebral  reflexes.  Clinical  experience  does 
not  seem  to  coincide  perfectly  with  this  conception,  for  we  ordinarily  find  both 
the  cutaneous  and  the  tendon  reflexes  increased  in  transverse  spinal  cord  lesions, 
such  as  those  caused  by  myelitis.  How  is  this  to  be  explained  ?  The  persistence 
of  the  tendon  reflexes  is  clear  enough,  and  their  increase  is  easily  explained  by 
supposing  that  the  inhibitory  fibers  running  in  the  lateral  tracts  have  been  cut 
off";  but  how  can  we  explain  the  increase  of  the  cutaneous  reflexes,  if,  as  Jen- 
drassik  assumes,  they  really  have  their  reflex  arc  in  the  brain  ?  Jendrassik  con- 
siders that  these  reflexes,  which  in  transverse  cord  lesions  are  ordinarily  regarded 
merely  as  accentuated  cutaneous  reflexes,  are  in  reality  pathologic  cutaneous 
reflexes,  which  normally  do  not  occur  in  this  shape  at  all,  but  in  transverse 
lesions  take  the  place  of  the  normal  cutaneous  reflexes  which  have  been  destroyed. 
He  offers  the  following  arguments  in  support  of  this  theory;  The  normal  cuta- 
neous reflexes  of  the  lower  extremities  can  be  elicited  only  from  the  sole  of  the 
foot,  no  matter  how  vigorous  the  stimulation  may  be;  while  the  pathologic 
cutaneous  reflexes  in  cross-lesions  of  the  cord  can  be  elicited  by  irritating  any 
part  of  the  lower  extremities.  The  normal  plantar  reflex  is  associated  with  a 
sensation  of  pain  and  tickling,  and  the  time  of  its  appearance  depends  upon  the 
occurrence  of  such  sensations  (best  recognized  in  the  delayed  transmission  of 
pain  in  tabes  dorsalis);  the  pathologic  reflexes,  on  the  contrary,  are  not  depend- 
ent upon  this  sensation  nor  are  they  associated  with  it.  The  physiologic  reflex 
even  exhausts  after  repeated  testing  even  though  it  is  very  vigorous;  whereas 
the  pathologic  reflex  never  exhausts ;  it  can  be  elicited  again  and  again.  A  light 
touch  will  very  easily  stimulate  the  physiologic  cutaneous  reflex;  whereas  the 
pathologic  reflex  is  in  direct  ratio  to  the  intensity  of  the  irritation.  The  patho- 
logic cutaneous  reflex  always  consists  of  a  maximum  flexion  of  the  thigh,  out- 
ward rotation  of  the  knee,  and  dorsal  flexion  of  the  foot  (in  rare  instances  the 
reverse — i.  e.,  an  extension  of  the  thigh  and  plantar  flexion  of  the  foot).  Both 
of  these  types  are  very  different  from  the  physiologic  reflex,  which  is  essentially 
a  movement  of  escape,  and  consists  of  a  dorsal  flexion  of  the  foot,  accompanied 
by  a  very  slight  movement  of  the  muscles  of  the  thigh  and  pelvis.  Jendrassik 
explains  the  appearance  of  these  vigorous  abnormal  reflexes  of  transverse  cord 
lesions  in  the  place  of  the  normal  by  assuming  that  the  sensory  impulses  which 
are  cut  off"  at  the  point  of  the  lesion  make  for  themselves  a  sort  of  lateral  path 
which  is  not  normally  in  use.  There  are  cases  of  acute  transverse  lesions  of  the 
cord  in  which  the  cutaneous  reflexes  are  diminished  instead  of  increased.  In 
them  he  assumes  that  the  lower  part  of  the  spinal  cord  is  also  affected,  so  that 
these  pathologic  reflexes  cannot  take  place  perhaps  because  of  an  anatomic  lesion 
(deficient  blood-supply),  or  perhaps  on  account  of  an  inhibitory  influence  by 
the  lesion.  A  similar  explanation  will  account  for  the  loss  of  the  tendon  reflexes 
which  we  see  so  often'  in  acute  traumatic  transverse  division  of  the  cord.  The 
increase  of  the  tendon  reflexes,  and  the  appearance  of  the  pathologic  cutaneous 
reflexes  which  is  observed  later  in  the  course  of  these  cases,  are  sufficient  evidence 
to  support  such  an  explanation. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  783 

Jendrassik's  theory  of  the  genesis  of  the  reflexes  has  many  argu- 
ments in  its  favor,  but  in  the  writer's  opinion  is  very  weak  in  one 
point — the  supposition  that  in  cross-lesions  of  the  cord  the  reflexes 
which  belong  to  parts  supplied  by  the  lower  portion  of  the  cord  are 
not  the  ordinary  retained  reflexes,  but  newly  formed  pathologic 
reflexes.  This  assumption  seems  permissible  in  the  case  of  the  vigor- 
ous and  altered  reflexes  of  the  lower  extremities,  as  they  were  described 
above.  But  it  compels  us  to  assume,  should  the  cremaster  and  abdomi- 
nal reflexes,  etc.,  be  preserved  in  a  myelitis  of  the  upper  dorsal  cord  with 
complete  motor  and  sensory  paralysis,  that  such  circumscribed  reflexes 
must  arise  by  another  path  than  the  physiologic,  and  that  in  such  com- 
plete paralysis  the  physiologic  cerebral  reflex  is  injured.  The  persistence 
of  these  reflexes,  whether  weakened,  normal,  or  increased  (any  one  of 
these  conditions  is  possible  in  transverse  lesions),  is  most  readily 
explained  by  assuming  that  their  center  or,  better  expressed,  their 
reflex  area  lies  below  the  transverse  lesion,  and  is  thus  preserved.  On 
the  other  hand,  the  absence  of  these  reflexes  in  cerebral  hemiplegias 
seems  difficult  to  reconcile  with  such  a  supposition.  The  following 
theory  will,  the  writer  believes,  clear  up  the  difficulty  :  The  cutaneous 
reflexes  which  Jendrassik  considers  to  be  purely  cerebral  are  in  reality 
like  his  third  group  (p.  781),  corticonuclear — i.  e.,  cerebrospinal  in  so 
far  as  they  belong  to  spinal  areas.  They  have  a  reflex  center  or,  better,^ 
a  lower  short  reflex  arc  in  the  cord,  and  in  addition  a  more  highly 
differentiated  "  upper  "  reflex  arc  in  the  brain  (see  Fig.  368).  Under 
ordinary  circumstances  an  accompanying  excitation  of  the  cerebral  arc 
is  essential  to  the  operation  of  the  reflexes.  This  arc  when  so  stimu- 
lated transmits  a  centrifugal  impulse  to  the  spinal  reflexes.  In  a  motor 
hemiplegia  of  cerebral  origin,  the  lesion  {ah,  Fig.  368)  interrupts  the 
centrifugal  tract  from  the  brain  to  the  spinal  reflex  center  (this  tract  is 
either  identical  with  or  situated  very  near  to  the  pyramidal  tract). 
Hence  the  cutaneous  reflexes  upon  the  paralyzed  side  disappear.  In  a 
transverse  lesion  of  the  cord  {cd,  Fig.  368)  the  cerebral  reflex  arc  is 
also  interrupted,  and  one  would  naturally  expect  a  similar  disappear- 
ance of  the  cutaneous  reflexes ;  but  this  does  not  occur,  because  the 
lesion,  by  interrupting  the  sensory  condition  in  the  cord,  in  a  measure 
dams  the  sensory  stimulation.  Therefore  the  peripheral  impulse  must 
find  a  path  in  the  region  of  the  lower  cord  segments.  It  usually  selects 
the  usual  path — i.  e.,  the  formed  spinal  reflex  arc  of  the  corresponding 
cerebrospinal  reflex — and  so  the  cutaneous  reflexes  become  purely  spinal. 

This  explains  how  many  of  the  preserved  reflexes — /.  c,  the  abdomi- 
nal and  cremaster — retain  their  complete  physiologic  distribution.  It 
also  explains  how  other  reflexes,  by  means  of  the  damming  up  of  exciting 
pulses  at  the  lesion,  attain  both  abnormal  intensity  and  distribution  by 
transmission  of  the  impulse  to  neighboring  paths. 

The  stasis  of  the  excitation  at  the  level  of  the  lesion  is  sufficient  to 

^Compare  p.  927  e<  .se^.,  Segmental  Localization.  The  expression  "reflex  center," 
employed  merely  for  the  sake  of  brevity,  is  inaccurate  and  incorrect,  and  the  conception 
according  to  which  it  was  first  used  is  no  longer  tenable. 


784  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

account  for  the  abnormal  intensity  of  the  reflexes  in  transverse  lesions, 
even  without  the  assumption  of  abolition  of  the  reflex  inhibitory  tracts 
(although  the  latter  shall  not  be  contested). 

On  the  other  hand,  in  cerebral  hemiplegia  since  extensive  by-paths 
in  the  whole  cord  and  a  great  part  of  the  brain  are  open  to  centripetal 
excitation  (Fig.  368,  lesion  ab),  there  is  no  reason  for  an  actual  stasis, 
and  likewise  no  ground  for  assuming  a  pure  spinal  stasis  of  reflexes 
which  otherwise  come  from  the  brain.  These,  therefore,  from  lack  of 
cerebral  excitation,  disappear,  or  through  insufficient  exertion  appear 
weak.  Perhaps  we  can  assume  that  the  centripetal  impulses  here  are 
dispersed  so  completely  through  the  wide-open  tracts  of  the  nervous 
system  that  they  become  inert  and  run,  like  a  lightning-rod,  into  the 
ground.  The  writer  can  claim  more  than  a  mere  diagrammatic  repre- 
sentation for  this  theory  of  damming  back  and  jumping  over  of  sensory 
irritation  in  the  cord,  because  Golgi  has  demonstrated  the  existence  of 
branched  sensory  collaterals  (Fig.  368)  and  has  shown  that  paths  for 
discharge  are  open  upon  all  sides,  and  that  it  depends  only  upon  the 
intensity  of  the  resistance  which  of  these  pathways  will  be  selected  by 
the  stimulation — i.  e.,  the  reflex.  The  diminution  of  the  reflexes  some- 
times observed  in  very  acute,  especially  traumatic,  cord  affections  is, 
according  to  this  theory,  to  be  attributed  to  inhibition  or  to  injury  of 
the  lower  cord  segments  from  circulatory  disturbances,  etc. 

The  author's  theory,  contrasted  with  Jendrassik's,  simplifies  the 
scheme  of  the  reflexes.  We  should  differentiate  physiologically  between 
only  two  groups  of  reflexes.  The  first  group  would  comprise  purely 
spinal  or,  better,  purely  nuclear  reflexes  because  some  of  them  occupy 
the  region  of  the  cranial  nerves,  and  would  include  the  tendon,  peri- 
osteal, and  joint  reflexes.  The  second  group,  the  cerebrospinal — i.  e., 
cerebronuclear — reflexes,  would  include  both  the  normal,  simple,  cuta- 
neous, and  mucous  membrane  reflexes  and  the  combined  reflexes  of 
Jendrassik's  third  group — bladder,  rectal  functions,  etc.  In  the  second 
group  the  brain  and  spinal  cord  (or  the  cerebral  cortex  and  cranial 
nerve  nuclei)  act  normally  together — i.  e.,  the  activity  in  a  lower 
(nuclear)  reflex  arc  is,  under  physiologic  conditions,  discharged  by  the 
cortex.  In  transverse  lesions  of  the  cord,  reflexes  of  this  second  group 
may  proceed  merely  by  the  spinal  path,  and  so  be  increased  or  even 
deformed  by  reflex  damming.  This  conception  seems  to  the  writer  the 
only  one  which  corresponds  to  our  clinical  experience.  That  of  Jen- 
drassik  is  essentially  opposed  to  the  facts  in  so  much  as  it  does  not 
recognize  the  short  spinal  path  for  cutaneous  reflexes  which  has  been 
localized  by  pathologic  and  experimental  findings  (see  Table  upon  p. 
930  et  seq.),  and  which  is  made  use  of  for  the  purposes  of  local 
diagnosis. 

DIAGNOSTIC  AND  PROGNOSTIC  SIGNIFICANCE  OF  QUANTITATIVE 
ALTERATIONS  OF  THE  REFLEXES. 

The  demonstration  of  the  presence  of  a  reflex  is  of  greater  diagnostic 
significance  than  the  demonstration  of  its  absence,  because  its  presence  is 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  785 

conclusive  evidence  of  an  intact  reflex  arc ;  whereas,  although  its  ab- 
sence may  mean  that  the  arc  is  interrupted,  it  may  also  mean  that  the 
reflex  is  affected  by  a  mere  inhibition  or  by  remote  influence  from  some 
circulatory  disturbance.  Similarly,  an  increase  of  a  reflex  is  ambiguous. 
The  latter  may  be  caused  by  lesions  which  directly  stimulate  the  reflex 
centers  or  tracts,  or  by  those  which  remove  inhibition  or  injure  inhi- 
bitory fibers.  The  pathologic  relations  of  the  reflexes  are  therefore 
evidently  complicated.  Only  a  comparatively  few  types  will  be  men- 
tioned. 

The  relation  of  altered  reflex  to  lesions  which  are  situated  in  the 
lower  (nuclear)  reflex  arcs  is  perhaps  the  most  distinct  (see  p.  782  eb 
seq.,  and  Fig.  368).  Any  such  lesion,  whether  of  the  sensory  limb, 
nucleus  or  motor  limb,  is  capable  of  diminishing  or  destroying  the 
reflexes.  Such  reflexes  as  the  cutaneous,  which  are  purely  cortical,  and 
which  pass  through  the  lower  and  upper  reflex  arcs,  require  intactness 
of  the  lower  reflex  arc  for  the  proper  display  of  the  reflex,  because, 
according  to  the  author's  idea,  the  upper  reflex  arc  has  no  functional 
independence,  but  merely  incites  the  lower  reflex  arc  to  activity.  So 
anatomic  lesions  of  its  nuclear  arc  cause  a  diminution  or  disappearance 
of  that  reflex  tendon.  The  disappearance  of  the  tendon  reflexes  in 
tabes,  and  the  disappearance  of  all  the  reflexes  in  peripheral  neuritis 
and  other  peripheral  paralysis,  are  examples  in  point.  On  the  other 
hand,  an  accentuation  of  the  reflexes  results  from  an  increase  of  irrita- 
tion in  the  lower  reflex  arc — e.  g.,  in  tetanus,  in  hysteric  and  neuras- 
thenic conditions,  and  occasionally  in  the  beginning  stages  of  neuritis, 
especially  while  associated  with  hyperalgesia.  The  last  may  sometimes 
occasion  difficulty  in  diagnosis. 

The  reflexes  in  cerebral  hemiplegias  and  in  transverse  lesions  of  the 
cord  have  been  so  fully  discussed  in  the  preceding  section  (p.  781  et 
seq.)  that  only  a  few  diagnostic  points  need  be  added.  Cerebral  hemi- 
plegias can  sometimes  be  diagnosed  by  the  diminution  of  the  cutaneous 
reflexes,  and  the  alterations  of  the  tendon  reflexes  (increase  or  decrease) 
upon  the  paralyzed  side,  even  during  the  "  stroke,"  when  the  patient  is 
still  unconscious,  and  while,  therefore,  the  motility  cannot  be  directly 
tested.  The  abdominal  reflexes,  particularly  the  cremaster  in  men  and 
the  crural  in  women,  are  especially  significant,  unless  these  reflexes  are 
absent  upon  both  sides  on  account  of  inhibitory  influences.  In  the 
latter  event  the  criterion  fails,  and  the  condition  is  evidently  more  seri- 
ous. Preservation  of  the  cutaneous  reflexes  upon  the  paralyzed  side 
should  always  be  considered  a  relatively  favorable  prognostic  sign, 
because  it  shox^s  that  the  upper  reflex  arc  through  the  cerebrum,  whose 
motor  limb  is  practically  identical  with  the  voluntary  motor  tract,  has 
not  been  entirely  destroyed  (see  p.  781). 

In  transverse  lesions  of  the  cord  we  generally  find  an  accentuation 
of  the  reflexes  whose  nuclear  arc  lies  below  the  injury.  A  decided 
increase  of  the  cutaneous  reflexes — /.  e.,  the  appearance  of  pathologic 
skin  reflexes — implies  a  serious  lesion.  On  the  other  hand,  a  decided 
diminution  of  the  reflexes  originating  beneath  the  lesion  shows  either 

50 


786  ■     EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

that  an  inhibitory  influence  proceeds  from  the  injury  or  that  there  exists 
a  coincident  involvement  of  the  spinal  segment  situated  below  the 
lesion.  Such  an  involvement  may  be  the  result  of  circulatory  disturb- 
ance or  of  a  distinct  longitudinal  lesion  of  the  cord.  If  traumatic 
transverse  lesions  cause  a  disappearance  of  the  tendon  reflexes  of  the 
lower  part  of  the  body,  Bastian,  Kocher,  and  others  consider  that  this 
lesion  is  then  probably  complete.  The  author's  theory  would  attribute 
this  to  a  decided  inhibitory  action  in  the  lower  segment,  and  perhaps 
also  to  a  circulatory  impairment  from  lesion  of  the  spinal  arteries.  At 
all  events,  later  in  the  course  of  these  cases,  although  the  continuity  of 
the  cord  is  not  re-established,  the  tendon  reflexes  sometimes  reappear. 
Our  discussion  upon  the  causes  of  the  accentuation  and  variation  of  the 
cutaneous  reflexes  depending  upon  transverse  lesions  presents  an  import- 
ant consideration  for  the  operative  treatment  of  spinal  cord  compression 
(spondylitis,  etc.) — viz.,  the  nearer  the  reflex  approaches  to  the  normal, 
the  more  liable  the  cord  is  to  be  merely  compressed  and  otherwise 
intact.  Again,  the  more  profound  and  extensive  the  cross-lesion,  the 
more  pronounced  will  be  the  signs  of  what  we  have  called  reflex  dam- 
ming. In  other  words,  decided  accentuation  or  variation  or  loss  of  the 
reflexes  argues  in  favor  of  serious  lesion  and  against  simple  compres- 
sion. The  preservation  of  certain  reflexes  is  very  important  in  cross- 
lesions,  because  it  enables  us  to  localize  the  level  and  the  extent  of  the 
lesion  (p.  928  et  seq.).  The  loss  of  them  is,  as  we  have  seen,  less  ser- 
viceable for  localizing  diagnosis,  because  of  so  many  indirect  influences 
which  can  affect  them. 

In  spastic  paralyses  it  is  very  difficult  to  make  any  diagnostic  use 
of  certain  reflexes.  If  the  paralyzed  muscles  are  strongly  contracted, 
neither  cutaneous  nor  tendon  reflexes  can  be  elicited  from  the  very 
tense  muscles.  Sometimes  this  is  especially  noticeable  in  tetanus,  where 
the  permanent  tension  of  the  muscles  prevents  the  ordinary  reflexes, 
and  yet  the  appearance  of  jerks  at  any  irritation  leads  us  to  conclude 
that  there  is  an  accentuation  of  the  reflexes. 

The  behavior  of  the  vesical  and  rectal  reflexes  will  be  specially  con- 
sidered on  p.  939  et  seq. 

QUALITATIVE  ALTERATIONS  OF  THE  REFLEXES  ;  PATHOLOGIC  REFLEXES. 
Many  so-called  pathologic  reflexes  should  be  regarded  from  what  was  said 
upon  p.  783  as  deformations  of  the  normal  reflex,  depending  upon  an  encroach- 
ment of  the  reflex  impulses  upon  pathways  which  become  accessible  to  the  im- 
pulse only  because  an  obstruction  is  intercalated  in  the  ordinary  reflex  tract  in 
consequence  of  reflex  damming.  Frequently  by  this  procedure  the  original 
reflex  is  only  modified,  so  that,  although  disfigured,  we  can  still  recognize  it.  In 
other  cases,  however,  reflexes  occur,  in  quite  an  analogous  way,  entirely  as  path- 
ologic phenomena.  It  is  impossible  to  enumerate  here  all  those  which  are 
observed  in  transverse  lesions  of  the  spinal  cord ;  but  there  is  a  pathologic 
plantar  reflex  which  is  so  frequently  observed  in  such  lesions  that  it  deserves  a 
brief  notice.  Irritation  of  the  sole  of  the  foot  without  stimulating  the  plantar 
reflex  of  the  toes  or  even  dorsal  flexion  of  the  ankle-joint  often  causes  extensive 
contraction  of  the  external  rotators  of  the  thigh.  Not  infrequently  such  move- 
ments are  combined  with  reflex  movements  of  quite  distant  muscle  territories — 
e.  g.,  of  the  abdomen,  of  the  leg,  or  of  the  arm.     This  pathologic  reflex  can 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


787 


frequently  be  excited  by  irritating  otber  parts  of  tbe  extremity,   such  as  the 
thigh. 

Babinski's  phenomenon  or  the  Babinski  reflex  (phenomen  des  orteils) 
consists  of  a  dorsal  flexion  of  the  toes,  but  more  especially  of  the  great  toe  [and  a 
simultaneous  flexion  of  the  other  toes. — Ed.],  when  the  sole  of  the  foot  is  irri- 
tated by  pricking  or  stroking  with  a  moderately  sharp  instrument.  This  reflex 
comes  under  the  head  of  the  pathologic  plantar  reflexes,  and  is  sharply  contrasted 
with  the  normal  plantar  flexion  of  all  the  toes  to  irritation  of  the  sole  of  the  foot. 
Babinski  found  that  this  reflex  depended  nearly  always  upon  a  lesion  of  the  py- 
ramidal  tract.      H.  Schneider,!   [and   especially  Walton  and  Paul,  Journal  of 


*^.,, 


Fig.  299.— Plantar  reflex :  1,  Foot  at  rest ;  2,  plantar  flexion  fnormal) ;  3,  foot  at  rest ;  4,  dorsal 
flexion  of  great  toe  (Babinski's  reflex). 


Nervous  and  Mental  Diseases,  1903. — Ed.J  and  many  other  authors  since,  have 
confirmed  Babinski's  original  observation.  Schneider  explains  this  reflex  as 
follows  :  In  the  ordinary  reflex  of  the  sole  of  the  foot  the  plantar  flexion  of  all 
the  toes  depends  upon  a  cortical  component  of  the  reflex;  whereas  the  dorsal 
flexion  (especially  of  the  great  toe)  in  Babinski's  reflex  depends  upon  a  spinal 
component  of  the  reflex.  With  a  lesion  of  the  pyramidal  tract  the  reflex  for  the 
plantar  flexion  is  interrupted,  but  not  that  for  the  dorsal  flexion.  Babinski's 
reflex  may  also  be  produced  by  an  increase  of  the  spinal  component  of  the  reflex 

1  Berlin,  klin.  WocL,  1901,  No.  37. 


788  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

just  as  well  as  by  a  lesion  of  the  pyramidal  tract;  therefore,  its  demonstration 
does  not  prove  absolutely  a  lesion  of  the  pyramidal  tract.  It  seems  to  the  author, 
however,  that  the  hypothesis  of  deformations  of  the  normal  reflex  which  he  has 
advanced  will  explain  the  transformation  of  the  original  plantar  reflex  into 
Babinski's  reflex  quite  as  well  as  Schneider's  hypothesis. 

.In  transverse  lesions  of  the  spinal  cord,  the  frequent  occurrence  of  ejaculation 
and  erection  reflexes,  excited  by  light  stroking  of  the  genital  or  anal  region,  of 
the  perineum  or  of  the  thigh,  should  be  mentioned,  as  well  as  bladder  and  rectal 
emptying  from  stroking  a  bed-sore,  etc.  The  testicle  reflex  described  by  Kocher 
in  spinal-cord  aflfections  consists  in  a  lateral  bending  of  the  spinal  cord  toward 
the  irritated  side  when  the  testicle  is  firmly  pinched.  The  author  can  confirm 
the  appearance  of  this  reflex  in  transverse  lesions  of  the  spinal  cord.  Whether  it 
should  be  considered  as  pathologic  is  not  easy  to  determine,  because  the  attempt 
in  healthy  individuals — /.  e.,  those  with  normal  sensibility — is  very  painful  and 
possibly  injurious. 

Other  abnormal  reflexes  may  occur  both  from  cutaneous  and  from  tendon 
reflexes  without  assuming  congestion,  but  simply  increase  of  reflex  irritability. 
In  this  way  the  impulse  can  no  longer  be  limited  within  the  stimulated  territory, 
but  difl[uses  itself  according  to  Pfliiger's  laws  in  horizontal  and  then  in  longi- 
tudinal directions  (p.  777).  These  phenomena  really  belong  to  the  section  upon 
Quantitative  Alterations. 

V.  EXAMINATION  FOR  TROPHIC  DISTURBANCES. 

J.  TROPHIC  DISTURBANCES  OF  THE  MUSCLES. 

(a)  Increase  in  Volume  of  the  Muscles;  Hypertrophy  and  Pseudohypertrophy, 

True  hypertrophy  of  the  muscles — i.  e.,  an  enlargement  with  in- 
creased strength — is  a  very  rare  pathologic  condition.  It  occurs,  how- 
ever, in  Thomson's  disease  and  in  true  congenital  muscular  hypertrophies. 
The  latter  are  rarely  observed,  and  still  very  imperfectly  understood. 
In  most  cases  the  pathologic  increase  in  volume  of  the  muscles  is  not 
an  actual  hypertrophy,  but  a  pseudohypertrophy,  since  it  depends  not 
upon  an  increase  of  the  contracting  muscular  fiber,  but  upon  a  growth 
of  interstitial  connective  tissue  and  of  fat.  The  variety  of  muscular 
atrophy  known  as  pseudohypertrophic  progressive  muscular  atrophy 
furnishes  the  best  example  of  this  pseudohypertrophy.  Now  and  then 
other  myopathic  forms  of  chronic  progressive  muscular  atrophy  show 
pseudohypertrophy  in  certain  of  the  affected  muscles. 

(6)  Decrease  in  Volume  of  the  Muscles;   Muscular  Atrophy. 

Inactivity  Atrophy ;  Simple  Non-degenerative  Atro- 
phy.— This  means  a  diminution  of  the  contractile  substance  which 
goes  on  in  every  muscle  that  is  not  used.  An  absolute  increase  of 
interstitial  connective  tissue  does  not  accompany  it,  and  for  this  reason 
this  type  is  designated  as  a  non-degenerative  atrophy.  Paralysis, 
mechanical  fixation  of  an  extremity,  or  a  restrained  position  of  the 
latter  from  some  painful  affection  may  gradually  produce  inactivity 
atrophy.  This  atrophy  becomes  profound  only  when  the  immobility  is 
quite  absolute.  The  differentiation  of  inactivity  atrophy  from  degener- 
ative atrophy  is  easy  Avithout  the  aid  of  electrical  examination,  because 
the  volume  of  that  part  of  the  body  which  shows  the  atrophy  and 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  789 

which  is  no  longer  moved  is  diminished  in  toto  ;  while  in  degeneration 
atrophy  frequently  individual  muscles  or  groups  of  muscles  are  spared 
or  are  predominantly  involved  in  the  atrophy. 

The  above  rule,  that  an  inactivity  atrophy  which  depends  upon 
partial  inaction  of  the  muscles  never  attains  a  very  high  degree,  does 
not  hold  good  in  the  case  of  paralysis  appearing  in  a  growing  individual. 
The  physiologic  growth  then  seems  to  be  decidedly  inhibited  by  limited 
inaction — e.  g.,  we  frequently  observe  very  marked  atrophies  in  the 
cerebral  paralysis  of  children,  and  we  can  definitely  determine  that  these 
are  not  degenerate  by  means  of  the  anatomic  localization  of  the  primary- 
lesion  and  by  electric  and  anatomic  examination  of  the  muscles.  It 
should  nevertheless  be  remembered  that  some  of  the  marked  atrophy 
consequent  upon  cerebral  paralysis  in  children  is  possibly  also  of  a 
degenerative  nature,  and  is  brought  about  in  the  manner  indicated  in 
the  footnote  on  p.  790. 

Degenerative  Atrophy. — Degenerative  muscular  atrophies  are 
distinguished  from  inactivity  atrophies  by  the  presence  in  the  affected 
muscles  of  a  pathologic  proliferation  of  interstitial  connective  tissue, 
which  develops  as  well  in  those  idiopathic  muscular  atrophies  called 
progressive  as  in  the  so-called  atrophic  paralyses. 

Progressive  Muscular  Atrophies. — These  include  myopatkio,  neu- 
ritic,  and  spinal  (better  nuclear)  forms,  depending  upon  whether  the 
muscles  are  primarily  diseased  or  whether  they  atrophy  secondarily  to  a 
chronic  neuritis  or  to  a  chronic  degeneration  of  the  large  ganglion  cells 
or  nuclei  of  the  spinal  cord  (or  the  nuclei  of  the  cranial  nerves).  In 
all  three  forms  certain  muscles  and  muscle  groups  gradually  disappear. 
The  atrophy  affects  the  muscles  individually  and  increases  gradually, 
but  an  entire  extremity  does  not  show  diffuse  atrophy  until  an  advanced 
stage  of  the  process  has  been  reached.  The  muscular  power  diminishes 
in  proportion  to  the  disappearance  of  the  muscles.  This  is  in  contrast 
with  atrophic  paralysis,  in  which  the  paralysis  appears  first,  and  then 
the  atrophy.  The  question  whether  a  muscular  atrophy  is  myopathic^ 
neuritic,  or  nuclear  is  made  easier  to  answer  by  knowing  that  each  of 
these  forms  has  a  characteristic  way  of  spreading. 

(A)  Under  the  myopathic  form,  lately  designated  by  the  term 
dystrophic,  several  types  have  been  described.  Three  of  the  most 
Important  are  : 

1.  Erb's  juvenile  muscular  atrophy  (progressive  muscular  dys- 
trophy), which  begins  in  the  shoulder  girdle.  There  are  different  types 
of  this  group. 

2.  Ley den-Moebius's  juvenile  form  ;  this  begins  in  the  lowxr  extrem- 
ities.    Pseudohypertrophy  is  closely  related  to  this  form. 

3.  Duchenne's  infantile  variety  ;  this  begins  in  the  face. 

(B)  Nuclear  (spinal)  muscular  atrophy  begins  in  the  small  muscles 
of  the  hand  and  involves  early  the  bulbar  muscles — i.  e.,  pi'oduces  the 
picture  of  bulbar  paralysis  (better,  bulbar  atrophy). 

(C)  The  neuritic  or  neural  type  of  pirogressive  muscular  atrophy  is 
still  the  least    understood.     It    begins    most  frequently  in  the  lower 


790  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

extremities,  in  the  domain  of  the  peroneal  nerve  (peroneal  type),  and 
causes  a  pes  varus  or  equinovarus.  Ordinarily,  disturbances  of  sensi- 
bility are  associated  with  this  form. 

Other  methods  of  differentiating  these  three  groups  are  as  follows  : 
Fibrillary  hvitching  (p.  748)  and  reaction  of  degeneration  (p.  812)  are 
demonstrable  in  the  spinal  and  neuritic  forms,  but  rarely  in  the  myo- 
pathic. Disturbance  of  sensibility,  even  though  very  slight,  points  to 
the  neuritic  type.  Myopathic  muscular  atrophy  ii,  as  a  rule,  hereditary, 
and  affects  almost  exclusively  young  individuals.  The  same  is  true  for 
some  of  the  neuritic  cases ;  but  the  spinal  form  is  almost  entirely  con- 
hned  to  older  people  without  neuropathic  heritage. 

The  examination  of  the  nervous  system  by  means  of  the  newer 
methods  based  upon  more  minute  histology  of  the  ganglion  cells  will 
probably  determine  that  the  boundaries  of  the  individual  forms  are  in 
no  way  so  sharply  defined  as  we  have  thus  far  assumed.  In  this  regard 
the  entire  subject  of  muscular  atrophies,  especially  its  neuropathology, 
needs  anatomic  revision. 

Secondary  Degenerative  Muscular  Atrophies  After  So=called 
Atrophic  Paralyses. — Paralyses  are  described  as  atrophic  when  the 
cause  of  the  paralysis  deprives  the  muscles  not  only  of  the  impulse  of 
the  will,  but  also  of  the  trophic  influence  of  the  cells  of  the  nerve 
nuclei — i.  e.,  the  cells  of  the  cord  situated  in  the  gray  anterior  horns. ^ 

To  avoid  confusion  with  the  simple  inactivity  atrophies  (p.  788  et  seq.^, 
we  should  remember  that  the  secondary  degeneixdive  atrophies  depend 
entirely  upon  a  lesion  of  the  peripheral  nerves — i.  e.,  the  paralysis  is 
located  either  in  the  nucleus  or  peripherally  to  it  (nuclear  and  peripheral 
paralyses).^ 

These  atrophies  ordinarily  follow  the  onset  of  the  paralysis  quite 
rapidly — i.  e.,  within  a  few  weeks.  They  affect  individual  muscles  very 
differently,  depending  upon  the  degree  of  the  paralysis,  and  ordinarily 
attain  a  very  high  grade,  even  to  complete  disappearance  of  individual 
muscles.  They  present  the  reaction  of  degeneration  often  even  before 
the  diminution  of  volume  has  become  evident  (see  p.  812).  They  are 
also  frequently  associated  with  fibrillary  twitchings  (p.  748).  Such 
atrophies  are  always  an  indication  of  severe  paralysis  and  require  a  long 
time  for  recovery — many  months — even  in  favorable  cases.  The  prog- 
nosis is  not  always  absolutely  unfavorable  in  lesions  located  peripherally 
to  the  nuclei,  since  the  regenerative  power  of  peripheral  nerves  is 
exceedingly  good.  The  prognosis  of  the  degenerative  atrophies  which 
arise  from  a  paralysis  of  the  nuclei  themselves  is,  on  the  other  hand, 
absolutely  hopeless,  because  in  such  cases  regeneration  does  not  occur 

'  The  ordinary  assumption  that  these  nuclear  cells  preside  over  this  trophic  influence 
is  scarcely  correct.  However,  as  centers  of  spinal  reflexes — i.  e.,  of  the  tendon  reflexes — 
they  probably  preserve  the  muscle  tonus  and  prevent  a  complete  muscular  inactivity  if 
the  muscles  are  paralyzed  above  the  nuclei. 

'^  In  reference  to  the  rare  cases  of  degenerative  muscular  atrophy  following  upon 
lesions  of  the  central  motor  neuron,  and  its  possible  explanation  in  the  extension  of  the 
descending  degeneration  to  the  peripheral  neuron,  the  reader  is  referred  to  the  article  of 
Steinert  ("Cerebrale  Muskelatrophie,"  D.  Zeits.  f.  Nervenheilk.,  1903,  vol.  xxiv.,  parts 
1  and  2). 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  791 

(acute,  subacute,  and  chronic  poliomyelitis).  If  a  degenerative  paralysis 
does  recover,  the  volume  of  the  muscle  gradually  returns,  following  the 
reappearance  of   motility  and  improvement  in  the  electric  irritability. 

2.    TROPHIC  DISTURBANCES  OF  THE  SKIN. 

Ordinary  Decubitus. — This  occurs  in  all  sorts  of  severe  diseases, 
and  especially  in  transverse  lesions  of  the  spinal  cord.  It  consists  of 
necrotic  processes  in  the  skin  and  subcutaneous  tissues  of  those  parts 
which  endure  the  principal  weight  of  the  body  while  lying  in  bed — viz., 
the  sacrum,  the  trocanters,  and  the  heels.  In  mild  cases  there  is  simply 
an  exposure  of  the  corinm  from  destruction  of  the  epidermis  ;  in  more 
severe  cases,  a  deep  necrotic  destruction  of  the  tissues  even  down  to  the 


Fig.  300. — Perforating  ulcer  in  tabes,    .r-ray  plate  showed  involveinent  of  the  bone  (Dr.  J.  J. 
Putnam,  Massachusetts  General  Hospital;. 

bone.  The  phenomenon  is  practically  a  pressure  necrosis.  Since  decu- 
bitus is  never  found  in  health,  we  are  naturally  inclined  to  consider  it  due, 
in  a  certain  sense,  to  some  trophic  disturbance,  not  ito  an  actual  affection 
of  trophic  centers  or  trophic  nerves,  as  it  is  so  common  in  diseases  which 
have  no  nervous  involvement,  but  rather  to  the  generally  depressed  nutri- 
tion, in  which  the  skin  shares.  Decubitus  is  frequent  in  transverse  lesions 
of  the  spinal  cord  because  the  enforced  quiet  is  often  responsible  for 
impoverished  nutrition,  the  difficulty  in  moving  the  patient  favors  more 
constant  pressure  upon  the  dependent  places,  and,  even  if  movement  is 
possible,  the  impaired  sensibility  prevents  recognition  of  inequalities, 
such  as  folds  in  the  bedclothes,  which  a  healthy  person  would  instantly 
avoid.  Disturbance  in  the  functions  of  the  bladder  and  rectum,  so 
frequent  in  these  conditions,  often  keeps  the  sacral  region  unclean,  and 
so  gives  rise  to  infection. 


792  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

Acute  Unilateral  Decubitus. — The  trophic  influence  of  the 
nervous  system  seems  to  be  more  striking  in  the  case  of  the  acute 
unilateral  decubitus.  This  consists  of  a  rapidly  increasing  necrosis  of 
the  skin  over  the  sacrum,  which  is  observed  upon  the  side  of  motor 
involvement  in  severe  cerebral  hemiplegias,  and  upon  the  side  of  the 
sensory  paralysis  in  spinal  hemiplegias.  The  unilateral  character  of 
the  phenomenon  shows  the  influence  of  the  nervous  system,  but  at  the 
same  time  the  actual  trophic  elements  of  the  nervous  system  are  not 
apparently  responsible.  It  is  quite  possible  that  in  cerebral  hemiplegias 
the  essential  fault  is  disturbance  of  sensation,  which  robs  the  patient 
of  the  instinctive    protection   against   considerable  pressure   upon   the 


Fig.  301.— Saber  shin  (Dr.  Joseph  Collins,  New  York  City  Hospital). 

anesthetic  side.  Acute  unilateral  decubitus  is  almost  always  an  unfavor- 
able prognostic  sign,  apparently  because  it  arises  only  in  very  marked 
paralysis  ;  but  recovery  sometimes  occurs. 

Changes  in  the  Skin  Over  Paralysed  Parts. — The  skin 
over  peripherally  paralyzed  parts,  more  noticeably  the  hands,  frequently 
presents  a  characteristic  thin,  atrophied,  shining  appearance,  the  so-called 
glossy  skin.  Conversely,  an  increase  in  the  subcutaneous  fat  frequently 
masks  the  muscular  atrophy,  especially  in  the  cerebral,  but  also  in  the 
spinal  paralyses  of  children. 

Other  Trophic  Changes  of  the  Skin. — It  is  impossible  to 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


793 


discuss  here  all  the  changes  of  the  skin  which  we  meet  with  in  diseases 
of  the  nervous  system.  We  shall  merely  mention  the  presence  of  pig- 
mentation, of  abnormalities  in  the  formation  of  the  epidermis  and  in 
the  growth  of  the  hair,  of  deformities  of  the  nails  (ouychogryphosis), 
of  the  loss  of  the  nails  (alopecia  unguium),  of  herpes  zoster,  of  sym- 
metric gangrene  (maladie  de  Raynaud,  syringomyelia),  of  panaritium 
(Morvan's  disease ;  syringomyelia),  of  Dupuytren's  contracture,  and  of 
perforating  ulcer  of  the  foot  (see  Fig.  300).  All  these  occur  predomi- 
nantly with  diseases  of  the  peripheral  neurons,  and  for  their  descrip- 
tion we  must  refer  to  special  pathology. 

3.    TROPHIC  DISTURBANCES  OF  THE  BONES  AND  JOINTS. 

In  all  paralyses  occurring  in  early  youth,  whether  peripheral  or  cen- 
tral (cerebral  and  spinal  paralyses  of  children),  the  growth  of  the  bone 


Fig.  31)2.— Tabetic  arthropathy  of  left  ankle  (New  York  City  Hospital). 

is  impeded  ;  on  account  of  such  an  inhibition  of  growth  and  the  asso- 
ciated degenerative  or  inactivity  atrophy,  the  paralyzed  extremity  is 
much  smaller. 

An  aljnormal  fragility  of  the  bones,  which  is  responsible  for  the  so- 
called  spontaneous  fractures,  occurs  in  tabes  dorsalis  and  syringomyelia. 

Joint  affections  are  observed  in  the  most  diverse  diseases  of  the 
nervous    system.     They    depend    frequently   upon    purely    mechanical 


794 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


causes  (destruction  of  a  joint  on  account  of  the  suspended  paralyzed 
extremity,  or  of  contractures),  yet  sometimes  they  are  attributed  to 
actual  trophic  disturbances.  Even  here  this  expression  does  not  mean 
that  the  disturbances  depend  wholly  upon  a  lesion  of  the  nervous 
system,  nor  can  we  consider  that  a  nervous  apparatus  exists  whose 
only  function  is  trophic.  The  joint  affections  which  occur  in  tabes,  and 
which  we  designate  as  tabetic  arthropathy,  should  be  included  under 
such  trophic  disturbances.  They  are  ordinarily  characterized  by  their 
onset,  which  is  abrupt  and  painless,  by  the  presence  of  a  considerable 


Fig.  303.— Tabetic  arthropathy  of  the  knee  (Dr.  Joseph  Collins,  New  York  City  Hospital). 

fluid  effusion,  by  loosening  of  the  joint,  and  by  a  growth  of  bone  and 
cartilage,  leading  to  deformity  of  the  joint.  Tlie  knee-joint  is  most 
commonly  affected,  and  soon  becomes  an  actual  tottering  joint. 

These  specific  peculiarities  of  tabetic  arthropathies  argue  against  the  purely 
mechanical  explanation  which  has  been  so  frequently  assumed — viz.,  that  the 
joint  suffers  repeated  injuries  merely  on  account  of  the  ataxia.  Other  reasons 
for  assuming  a  trophic  influence  are  the  characteristic  wearing  away  of  the  bones 
(eburnation  fracture  of  the  bones  in  the  direct  neighborhood  of  the  diseased 
joint)  and  their  insensibility  to  tuning-fork  vibrations  (p.  765).  Even  here  the 
author  does  not  consider  it  necessary  to  assume  the  existence  of  special  trophic 
nerves  to  explain  the  joint  affections  and  the  bone  brittleness  of  tabes,  because 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  795 

a  sufficient  reason  for  disturbance  in  growth  seems  to  him  to  be  furnished  by  the 
anesthesia  of  the  bones  and  joint  ends,  as  well  as  by  the  occasional  involvement 
of  the  vasomotor  nerves. 

Acromegaly,  a  peculiar  disease  characterized  by  hypertrophy  of 

the  bones  of  the  hands,  of  the  feet,  of  the  nose,  and  of  the  lower  jaw, 
probably  depends  upon  some  trophic  disorder  of  the  nervous  system. 


Fig.  304.— Myxedema  (Dr.  Townsend,  Massachusetts  General  Hospital). 

The  hypertrophy  is  often  very  marked.  The  reader  is  referred  to 
works  upon  special  pathology  for  a  discussion  of  its  orio;in  and  its 
dependence  upon  disease  or  disorder  of  the  hypophysis  cerebri. 

VI.  EXAMINATION  OF  VASOMOTOR  DISTURBANCES. 
We  know  so  little  about  the  va.somotor  relations  in  nervous  diseases 
that  it  is  scarcely  worth  while  to  enter  upon  a  general  discussion.  The 
author  will  limit  himself  to  a  few  remarks,  at  the  same  time  referring 
to  the  section  upon  the  Examination  of  the  Skin  (p.  40  et  seq.),  and  to 
what  was  said  there  of  local  cyanosis. 

Vasomotor  differences  between  the  paralyzed  and  the  normal  half  of  the  body 
are  sometimes  found  in  cerebral  hemiplegias,  especially  if  the  lesion  causing  the 


796  EXAMINATION  OF  TEE  NERVOUS  SYSTEM. 

hemiplegia  be  situated  in  tlie  pons,  peduncles  of  the  brain,  or  the  internal  cap- 
sule. In  the  beginning  the  paralyzed  extremities  ordinarily  appear  warmer  and 
redder  ;  later,  colder  and  more  cyanotic  than  normal.  What  causes  these- pecu- 
liarities is  not  yet  fully  understood.  Since  the  cerebrum,  as  shown  by  the  action 
of  psychic  irritation,  possesses  an  influence  upon  the  vasomotors,  the  initial  heat 
and  redness  can  be  explained  by  assuming  a  paralysis  of  the  vasomotor  tracts  of 
the  brain.  The  vicarious  action  of  the  vasomotor  centers  of  the  spinal  cord,  how- 
ever, quickly  transforms  the  condition.  The  coolness  and  cyanosis  of  the  skin  of 
the  paralyzed  side,  which  appear  later  and  which  ordinarily  continue  as  long  as 
the  paralysis  lasts,  have  nothing  to  do  with  the  vasomotor  action  (though  this  is 
opposed  to  the  ordinary  supposition),  but  depend  upon  a  stagnation  of  the 
venous  blood,  caused  by  the  immobility  of  the  extremities.  Muscular  action 
in  movement  of  an  extremity,  as  is  well  known,  has  great  influence  in  pro- 
pelling the  venous  blood  forward. 

In  transverse  lesions  of  the  spinal  cord,  the  higher  the  lesion  the  more  pro- 
found is  the  vasomotor  paralysis  of  the  lower  half  of  the  body.  In  lesions  of 
the  oblongata,  the  paralysis  of  the  cutaneous  vasomotor  center  from  dilatation 
of  the  vessels  may  lead  to  a  fatal  sinking  of  the  blood-pressure,  accompanied  by 
marked  cyanosis  and  coolness  of  the  peripheral  parts.  In  transverse  lesions 
situated  below  the  oblongata,  the  paralysis  of  the  vasomotors  (vasoconstrictors) 
aflFects  the  territory  innervated  by  that  part  of  the  spinal  cord  situated  below  the 
lesion,  because  the  vasoconstrictor  impulses  of  the  oblongata,  except  those  sup- 
plying the  head,  run  downward  through  the  spinal  cord  and  leave  the  cord  along 
with  the  motor  nerves  for  the  same  territory  to  merge  into  the  sympathetic  system. 
The  territory  showing  motor  paralysis  then  also  shows  vasomotor  paralysis.  This 
is  made  evident  by  increased  temperature  and  redness  of  the  paralyzed  limb.  Yet 
this  paralysis  is  ordinarily  slight  and  often  transitory,  because  the  vasomotor 
apparatus  situated  beneath  the  lesion,  as  well  as  the  sympathetic  fibers  of  the 
spinal  cord  arising  above  the  lesion,  are  able  to  functionate  vicariously  for  the  nerves 
which  have  been  cut  off.  Later,  the  paralyzed  parts  frequently  become  cool  and 
cyanotic  on  account  of  the  immobility,  as  in  cerebral  hemiplegia.  Priapism,  so 
frequently  observed  in  transverse  lesions  of  the  spinal  cord,  probably  depends  upon 
a  vasomotor  paralysis.  The  vasoconstrictor  fibers  of  the  face  probably  first  issue 
from  the  spinal  cord  in  the  region  of  the  upper  dorsal  cord  (according  to  animal 
experiments  on  the  spinal  cord,  see  p.  934).  Therefore  they  may  be  aflTected  in 
all  lesions  of  the  spinal  cord  situated  above  the  sixth  dorsal  nerves.  As  yet  we 
know  nothing  definite  about  the  behavior  of  vasodilator  nerves  in  lesions  of 
the  brain  and  spinal  cord. 

Tache  cerebrale,  Trousseau's  spots,  dermographism,  are  the  diflerent 
names  applied  to  a  cutaneous  vasomotor  phenomenon  of  unexplained  origin. 
It  probably  depends,  however,  upon  changes  in  irritability  of  the  vasomotor 
nerves.  It  consists  of  a  deep-red  color  of  the  skin,  often  accompanied  by  the 
formation  of  a  wheal  wherever  the  skin  is  irritated — e.  g. ,  by  light  scratching 
of  the  finger  or  the  head  of  a  pin.  It  occurs  in  purely  functional  diseases, 
sometimes  in  brain  diseases  (especially  meningitis),  and  not  rarely  in  spinal  cord 
diseases. 

We  must  refer  to  special  pathology  for  the  description  of  the  characteristic 
redness  of  the  skin  observed  in  erythromelalgia. 

Vn.  EXAMINATION  OF  DISTURBANCES  OF  SECRETION. 

Abnormalities  of  sweat  secretion  are  common,  but  as  yet  we  cannot 
accord  them  much  diagnostic  significance.  Hemihyperhidrosis  and 
hemianhidrosis — i.  e.,  unilateral  increase  or  absence  of  sweat  produc- 
tion— often  occur  physiologically  in  otherwise  healthy  persons.  In 
such  a  case  a  suspicion  of  a  disease  of  the  sympathetic  system  is  natural. 
We  also  observe  hemihyperhidrosis  in  syringomyelia.     In  hemiplegias 


EXAMINATION  OF  THE  NEBVOUS  SYSTEM.  797 

of  cerebral  origin,  sweating  of  the  affected  side  is  sometimes  more, 
sometimes  less,  marked  than  upon  the  healthy  side ;  frequently,  how- 
ever, it  is  entirely  normal.  A  decided  tendency  to  increased  perspira- 
tion'is  often  noted  in  extremities  which  are  affected  with  an  acute  poly- 
neuritis, even  when  there  is  no  fever.  This  is  peculiar  and  of  some 
diagnostic  importance. 

We  know  so  little  about  the  alteration  of  urinary  secretion  in  diseases 
of  the  nervous  system  that  it  is  impossible  to  draw  diagnostic  conclu- 
sions. A  pale,  abundant  urine  of  low  specific  gravity  (urina  spastica) 
generally  follows  attacks  of  epilepsy  and  hysteria.  Transitory  glyco- 
suria, or  even  diabetes  mellitus  ending  in  death,  often  accompanies  dis- 
eases of  the  brain,  particularly  when  situated  in  the  posterior  cerebral 
fossa.  Diabetes  insipidus  has  a  predilection  for  neuropathic  individ- 
uals, especially  neurasthenics.  _       i  •      i 

Pathologic  variations  of  the  salivary  secretion  are  mentioned  in  the 
section  upon  Examination  of  the  Facial  Nerve. 

Vm.  EDEMA  IN  NERVOUS  DISEASES. 

It  is  not  certain  that  the  acute  idiopathic  edemata  really  depend  upon  the 
nervous  system,  but  certainly  the  name  "angioneurotic"  edema  (see  p.  52), 
rather  prejudices  one  in  favor  of  such  an  origin.  The  edemata  which  compli- 
cate actual  nervous  diseases  are:  (a)  The  so-called  ''blue  edema"  of  hysteria. 
This  is  discussed  under  the  heading  of  Angioneurotic  Edema  (p.  52),  and  its 
occurrence  was  utilized  as  an  argument  for  assuming  that  hysteric  symptoms  are 
frequently  to  be  attributed  to  vasomotor  disturbances.  (6)  Whether  the  edenia 
of  the  paralyzed  members  in  all  kinds  of  paralysis  is  due  to  vasomotor  paresis 
must  be  determined  in  each  case  ;  but  the  immobility  and  lack  of  muscular 
activity,  leading  to  venous  stasis  (as  explained  upon  p.  796),  is  generally  a  sufh- 
cient  explanation,  (c)  The  edema  of  the  paralyzed  members  m  polyneuritis  A 
vasomotor  origin  in  such  cases  is  especially  plausible,  because  if  the  peripheral 
vasomotor  fibers  are  involved,  the  vasomotor  disturbance  would  be  exceptionally 
pronounced,  since,  as  contrasted  with  cerebral  and  spinal  paralysis,  the  vicarious 
action  of  the  auxiliary  vasomotor  centers,  with  the  exception  of  those  situated  on 
the  vessels  themselves,  is  cut  off.  Still,  with  the  edema  of  neuritis,  we  should  also 
consider  the  possibility  of  an  inflammatory  origin. 

IX.   METHOD  OF  TESTING   THE  MECHANICAL  IRRITABILITY  OF 
NERVES  AND  MUSCLES. 

I.  MECHANICAL  IRRITABILITY  OF  MOTOR  NERVES. 

Contraction  of  muscle  may  sometimes  be  produced  by  striking 
with  a  percussion  hammer  the  nerve  supplying  it.  This  occurs  in 
health  under  the  appropriate  conditions — i.  e.,  when  the  nerve  runs 
superficially  upon  some  firm  underlying  tissue.  This  mechanical  irri- 
tability is  increased  in  tetany,  especially  in  the  facial  nerve  (facial  phe- 
nomenon, Chvostek's  phenomenon),  and  more  rarely  in  writer's  cramp. 

2.  MECHANICAL    IRRITABILITY  OF    MUSCLES  ;  IDIOMUSCULAR 
MECHANICAL  IRRITABILITY. 

Only  vigorous  percussion  will  stimulate  muscles  in  health.  Such 
a   stimulation  causes  a  sudden,  quick  contraction  of  the  bundles  of 


798  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

fibers  which  lie  in  the  long  axis  of  the  muscles  near  the  point  struck. 
At  the  same  time  a  smooth  local  swelling  is  produced  at  the  spot 
tapped,  or  in  the  long  axis  of  the  muscle  at  a  greater  or  less  distance. 
After  the  lapse  of  some  seconds  this  swelling  very  gradually  disappears, 
or  first  merges  into  a  series  of  waves  running  along  in  the  direction  of 
the  fibers. 

In  all  cachectic  conditions  (tuberculosis,  carcinoma,  etc.)  the  idio- 
muscular  irritability  is  apt  to  be  increased  and  the  muscle  swelling 
quite  pronounced. 

The  mechanical  irritability  is  also  increased  wherever  muscle  exhibits 
reaction  of  degeneration  with  increased  galvanic  irritability  (see  p.  814). 
The  longitudinal  wave-like  contractions  are  here  exceptionally  slight, 
and  much  slower  than  the  normal.  This  phenomenon  is  called  mechan- 
ical reaction  of  degeneration. 

X.  METHOD  OF  TESTING  THE  ELECTRIC  IRRITABILITY  OF 

NERVES  AND  MUSCLES. 

I.   GENERAL  DISCUSSION. 

Electrical  examination  of  sensory  nerves,  including  the  nerves  of 
special  sense,  has  not  yet  developed  anything  of  practical  value.  The 
following  description  will  therefore  be  limited  to  the  electrical  exami- 
nation of  motor  nerves  and  muscles. 

For  this  purpose  a  faradic  (induced,  interrupted)  or  a  galvanic  (con- 
stant) current  is  employed  almost  exclusively.  One  of  the  many  modi- 
fications of  the  Du  Bois-Raymond  sliding  apparatus  w'ith  one  or  two 
zinc-carbon  cells  will  furnish  the  faradic,  while  for  the  constant  current 
the  stationary  L6clanche  batteries  are  most  useful.  These  latter  are 
expensive  and  cannot  be  transported,  so  that  a  portable  dry  battery  with 
sulphuric-acid-zinc-carbon  elements  is  better  adapted  for  the  practi- 
tioner's needs.  Chardin,  of  Paris,  makes  one  of  the  best  of  the  latter 
type,  and  also  supplies  a  satisfactory  induction  apparatus.  [Satisfactory 
and  adequate  batteries  are  to  be  had  from  dealers  in  electrical  apparatus 
in  nearly  all  the  larger  cities  of  this  country. — Ed.] 

For  stimulation  we  employ  flat  electrodes  or  those  w'ith  a  bulb  on 
the  end.  They  are  covered  with  chamois  leather,  and  before  being  used 
should  be  moistened  with  warm  water.  If  salt  is  added  to  the  water 
the  current  strength  is  increased,  but  the  electrodes  soon  become  tar- 
nished and  spoiled.  Different  sizes  of  button-shape  and  flat  electrodes 
are  required,  and  some  of  the  former  should  be  made  with  a  contact 
contrivance  for  opening  and  closing  the  current. 

For  an  accurate  electrical  examination  we  need  an  appliance  to 
measure  the  strength  of  the  galvanic  current.  Until  recently  this  pur- 
pose has  been  served  by  a  galvanometer  divided,  according  to  the  abso- 
lute strength  of  current,  into  milliamperes.  The  apparatus  of  Gaiffe 
(Paris),  Edelman  (Munich),  or  Edison  (New  York),  can  be  recommended. 
The  galvanometer  is  an  essential  for  electrotherapeutic  purposes ;  but 
the  volt  meter  offers  many  advantages  for  electrodiagnosis  (see  later,  p. 
806  et  seq.). 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  799 

Medical  batteries  are  supplied  with  a  commutator,  or  current 
changer,  for  quickly  changing  the  poles,  and  with  a  contrivance  for 
connecting  or  disconnecting  the  individual  cells  in  order  to  increase 
or  decrease  c|uickly  the  strength  of  the  current.  Finer  gradations  are 
obtained  by  inserting  a  fluid  rheostat  into  the  main  circuit.  Although 
quite  practical  with  the  ordinary  galvanometer,  a  rheostat  in  the  main 
circuit  cannot  be  used  with  the  volt  meter — i.  e.,  a  galvanometer  with 
a  very  strong  resistance  in  the  lateral  circuit — and  so  is  not  practicable 
for  diagnostic  purposes.  If  we  use  the  volt  meter  we  must  employ 
either  a  rheostat  in  lateral  circuit  or,  still  better,  the  "  GaiflPe  reducteur 
de  potentiel." 

The  polar  method  of  electrical  stimulation  is  nowadays  ordinarily 
employed  for  electrical  examination.  One  pole  is  placed  upon  the  spot 
to  be  stimulated,  the  other  upon  an  indifferent  spot,  as  far  distant  as  pos- 
sible— e.  g.,  upon  the  abdomen  or  the  breast.  The  examination  is  thus 
essentially  simplified  by  disregarding  the  direction  of  the  stream.  For 
all  practical  purposes  both  poles  of  the  faradic  current  may  be  said  to 
act  alike,  although  not  with  equal  strength.  With  the  galvanic  current, 
on  the  other  hand,  there  is  a  fundamental  diiference  between  the  two 
poles.  This  diiference  is  apparent  in  the  so-called  laws  of  contraction 
of  motor  nerves  and  muscles.  The  cathode  of  the  opening  induction 
current  acts  most  powerfully ;  therefore  it  is  agreed  to  employ  this  for 
faradic  stimulation.  On  the  other  hand,  in  every  case  where  we  use  the 
galvanic  stream,  we  must  test  cathode  and  anode  stimulation  separately 
and  compare  the  results. 

The  electrode  should  not  be  too  large  if  the  object  is  to  stimulate 
isolated  nerves  or  muscles.  Too  small  electrodes  are  impracticable, 
because  with  them  the  intensity  of  the  current  is  so  great  that  the  pain 
of  the  examination  is  materially  increased.  For  most  purposes  a  button- 
shaped  electrode  of  1  to  2  cm.  diameter  answers  the  purpose.  If  we 
wish  to  compare  the  results  of  different  electrodiagnostic  examinations 
uniform  electrodes  should  be  used,  since  the  stimulation  effect  depends 
not  only  upon  the  strength,  but  also  upon  the  intensity  of  the  current 
(see  p.  807).  Erb  and  Stintzing  recommend  so-called  normal  electrodes 
for  all  electrical  examinations.  Erb's  normal  electrode  is  10  sq.  cm. 
in  size  (a  circular  surface  of  3.6  cm.  diameter).  Stintzing's  electrode, 
which  is  serviceable  for  stimulating  small  muscles— e.  g.,  of  the  hand — 
has  a  circular  surface  of  3  sq.  cm.  (1.8-2  cm.  diameter).  The  indiffer- 
ent electrode  should  be  as'  large  as  possible,  in  order  to  decrease  the 
intensity  of  the  current  through  it,  even  when  a  strong  current  is  em- 
ployed, and  so  to  lessen  the  pain  caused  by  the  passage  of  the  current. 
The  pain  is  due  essentially  to  electrolizing  the  skin. 

There  are  some  exceptions  to  the  rule  given  above,  that  the  indiffer- 
ent, large  electrode  should  be  applied  as  far  as  possible  from  the  point 
to  be  stimulated.  These  exceptions  occur  frequently  enough  to  merit 
mention — e.  g.^  when  employing  strong  currents  in  diminished  irrita- 
bility, if  we  should  apply  the  indifferent  electrode  to  the  abdomen  and 
then  attempt  to  stimulate  the  small  muscles  of  the  hand,  the  effect  would 


800  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

be  very  confusing.  The  current  passing  through  the  nerves  and  mus- 
cles of  the  arm  would  produce  contraction  of  the  muscles  not  only  of 
the  hand,  but  also  of  the  arm  ;  the  entire  arm  would  naturally  be  jerked 
about,  and  so  confuse  us.  In  such  a  case  it  would  be  better  to  apply 
the  indifferent  electrode  to  the  other  surface  of  the  same  hand.  The 
employment  of  the  largest  possible  indifferent  electrode  establishes  a 
great  difference  in  current  intensity  between  the  two  electrodes,  so  that 
an  almost  exclusive,  and  practically  a  polar,  action  results  at  the  differ- 
entiating electrode.  Such  devices  should  be  made  use  of  upon  other 
parts  of  the  body. 

A  complete  electrical  examination,  evidently,  must  include  testing 
each  muscle  and  nerve.  It  consumes  a  great  deal  of  time,  because  con- 
trol tests  must  be  made  in  order  to  verify  results.  In  fact,  the  electri- 
cal examination  of  an  extensive  paralysis  requires  more  time,  skill,  and 
patience  than  any  other  kind  of  examination,  if  it  is  to  be  accurate  and 
thorough,  and  leads  to  many  serious  errors  if  it  is  carried  out  hastily  or 
carelessly.  An  accurate  testing  of  one  muscle  is  of  more  service  than 
the  careless  examination  of  all  the  paralyzed  muscles.  Multum  is 
better  than  multa  ;  quality  than  quantity.  A  complete  examination  of 
all  the  muscles  implicated  in  a  paralysis  is  impracticable  for  a  busy 
practitioner,  especially  if,  in  the  interest  of  prognosis,  continued  changes 
in  the  reaction  during  the  course  of  the  disease  are  to  be  followed. 
Testing  some  few  muscles  and  nerves  is,  fortunately,  sufficient  for  diag- 
nostic purposes. 

A  complete  electrical  examination  of  a  nerve  muscle  should  include 
testing  of  both  muscle  and  nerve  by  the  galvanic  as  well  as  by  the 
faradic  current.  A  nerve  generally  reacts  the  same  to  galvanism  as  to 
faradism,  so  that,  if  anything  has  to  be  slighted,  it  is  advisable  to  omit 
the  galvanic  test.  Still,  the  latter  has  here,  as  elsewhere,  a  distinct  advan- 
tage over  faradism,  because  with  it  the  amount  of  stimulation  can  be 
measured. 

The  term  faradic  stimulation,  as  employed  here  and  in  what  follows, 
implies  the  use  of  a  rapid  induction  current  (tetanic  contraction)  from  a 
rapidly  vibrating  sliding  apparatus.  Single  induction  shocks  can  also 
be  obtained  from  this  instrument  by  fastening  the  hammer,  and  then 
opening  and  closing  the  primary  current  by  hand.  The  latter  method 
is  particularly  useful  and  practical  in  peripheral  palsies  with  a  decided 
diminution  of  irritability,  because  it  is  much  less  painful,  and  because 
degenerated  muscles  retain  a  reaction  much  longer  to  individual  inter- 
ruptions than  to  an  interrupted  tetanic  current.  This  is  a  point  worth 
remembering  in  treating  such  paralyses. 

There  are  certain  places  scattered  over  the  surface  of  the  body  which, 
when  stimulated  by  a  small  electrode,  evoke  the  best  response  from  one 
definite  nerve  or  muscle.  These  are  the  so-called  "motor  points" 
determined  by  Duchenne,  Erb,  v.  Ziemssen,  and  others,  and  make 
possible  the  individual  stimulation  of  single  motor  nerves  and  muscles. 
They  are  represented  in  the  accompanying  figures  (305  to  309).  Their 
location  has  been  confirmed  by  the  writer's  own  examinations.     Most 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

11  12  13  14 


801 


Fig.  305.— Motor  points  on  the  head  and  neck  : 


Occipitali.s. 

Retrahens  aurem. 

Posterior  auricular  nerve. 

Splenius. 

Spinal  accessory  nerve. 

Sternocleidomastoid. 

Trapezius. 

Circumflex  nerve  (deltoid). 

Long  thoracic  nerve  (serratus  magnus). 

Brachial  plexus. 

Lower  branch. 

Facial  nerve  (trunk) 

Upper  branch. 

Middle  branch. 

Temporalis. 

Frontalis. 

Corrugator  supercilii. 

Orbicularis  palpebrarum. 


19.  Nasal  muscles. 

20.  Levator  labii  superioris. 

21.  Zygomaticus  major. 

22.  Orbicularis  oris. 

23.  Masseter. 

24.  Levator  labii  inferioris. 

25.  Depressor  labii  inferioris. 

26.  Depressor  anguli  oris. 

27.  Hypoglossal  nerve  (in  the  depths). 
27  a.  Platy.sma. 

28.  Sternohyoid. 

29.  Omohyoid. 

30.  Phrenic  nerve. 

31.  Sternothyroid. 

32.  Erb's  point '  (deltoid,  biceps,  brachi- 

alis  anticus,  supinator  longus). 

33.  Anterior   thoracic   nerve    (pecloralis 

major). 


motor  points  for  nerves  are  situated  where  the  nerve  lies  superficially 
and  at  some  little  distance  from  other  nerves.  The  motor  point  of  a 
muscle  is  usually  at  the  point,  where  the  motor  branch  of  the  nerve 

^  Erb'.s  point  i.s  situated  2  to  3  cm.  above  the  clavicle,  somewhat  to  the  outer  side  of 
the  posterior  border  of  the  sternocleidomastoid,  immediately  in  front  of  the  transverae 
process  of  the  sixth  cervical  vertebra. 

51 


802 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


Musculospiral  nerve 


Deltoid. 


yti> Musculocutaneous 

nerve. 

■-•Biceps. 
^5*^^  Brachialis  anticus. 


^gf-- Ulnar  nerve. 

■  Median  nerve. 

Supinator  longus •/-•  '      "'"^"^ 

•  --J- Pronator  radii  teres. 

, — . -  Palmaris  longus. 

Flexor  carpi  radialis X —  •  d —  Flexor  carpi  ulnaris. 

^  »     _    __/_        _  __  Flexor  digitorum  pro- 

m/y  "    /  fundus. 

Flexor  digitorum  suhlimis  .— ^'.«        ^£^ ^^^^^^  digitorum  sublimis. 

Flexor  longus  pollicis., 

• — T-;;^^ Pronator  quadratus. 

Median  nerve. ^-f V?-'  y^ Tlnar  nerve. 

Abductor  pollicis 

Opponens  pollicis i^-'-k  "'     14— Palmaris  brevis. 

Flexor  brevis  pollicis.^       /  _,    t,  j  .  ,.  .  . 

Adductor  pollicis. „   JZZ^.  ^ .\bductor  minimi  digiti.      _ 

•'   •  "  •") Flexor  brevis  minimi  digiti. 

^'  ->:r^=::.-/l~  Oppoucns  minimi  digiti. 

■•'-    'n  *.^/         ^^3s»»_ — Palmar  interossei. 
-"^^^.^ 

^^'**"*«—  Lumbricales. 


Fig.  306.— Motor  points  on  the  anterior  aspect  of  the  arm. 


enters  the  muscle  belly.  In  point  of  fact,  it  is  here  that  the  nerve  is 
generally  stimulated.  Therefore,  when  endeavoring  to  obtain  a  pure 
muscular  reaction,  it  is  a  good  plan  to  keep  as  far  as  possible  from  the 

1  This  point  should  be  sought  for  in  the  external  bicipital  groove,  at  the  junction  of 
the  middle  and  lower  thirds  of  the  arm.  According  to  Erb,  it  is  midway  between  the 
external  condyle  and  the  insertion  of  the  deltoid.  It  is  frequently  difficult  to  locate, 
because  the  nerve  easily  rolls  from  beneath  the  electrode,  and  possibly  also  because  the 
electrode  is  lifted  away  from  the  nerve  by  the  contraction  of  the  biceps  and  triceps.  A 
very  fine  electrode  should  be  employed  for  this  examination.  It  should  be  noted_  that 
the'  trunk  of  the  musculospiral  nerve  may  also  be  irritated  in  the  axilla  at  the  inner 
border  of  the  upper  extremity  of  the  coracobrachialis.  Erb's  point  (see  Fig.  305)  may 
also  be  employed  for  the  supinator  longus.  These  points  possess  a  special  clinical  interest, 
as  will  be  shown  on  p.  819. 


EXAMINATION  OF  THE  NERVOUS  SYSTE3I. 


803 


motor  points,  unless  the  nerve  irritability  is  lost.  In  this  way  stimula- 
tion will  produce  local  contractions  only  in  the  individual  bundles  which 
are  stimulated. 

In  all  electrical  tests  it  is  essential  to  determine  three  factors  :  First, 


Triceps  (long  head)  XM 


Deltoid  (posterior  half). 


Extensor  carpi  ulnaris... 


Extensor  longus  pollicis. 


Abductor  minimi  digiti 


Triceps  (external  head). 

Musculospiral  nerve.* 

»^. —  Supinator  longus. 

'^/      \  Extensor  carpi  radialis 

%•  1 — longior. 

'   \  Extensor  carpi  radialis 

(#- brevior. 

*    -"'~!"i -___  Extensor  communis  digi- 

"^jltjmm  ''.'.y- ~        torum. 

'''■■""'■  '\  "■■      Supinator  brevis.i 

•  ^ 

\  ~  Extensor  indicis. 

'"*  ^  Abductor  longus  pollicis 

and  extensor  brevis 
pollicis. 

%Jj1 

^M^l  ~""^*<  Dorsal  inter- 

ossei. 


Fig.  307.— Motor  points  on  the  posterior  aspect  of  the  arm. 


whether  both  the  motor  nerve  and  the  muscle  react  to  the  faradic  and  to 
the  galvanic  current ;  secondly,  whether  the  reaction  to  either  current  is 
quantitatively  altered — /.  e.,  whether  it  is  increased  or,  as  most  frequently 
happens,  diminished ;  and  finally,  whetiier  any  qualitative  alteration  in 

'  It  is  possible  to  irritate  the  supinator  brevis  by  itself  only  when  the  extensor  com- 
munis digitorum  is  atrophic  and  fails  to  respond  to  the  electric  current  (as  in  lead  palsy, 
for  example).  ^  See  note  to  preceding  figure. 


804 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


irritability  can  be  demonstrated — i.  e.,  any  deviation  from  the  ordinary 
type  of  contraction.  With  the  galvanic  current  the  effect  of  each  pole 
must  be  noted. 

The  "  dosage  " — i.  e.,  the  strength  of  current  employed — must  always 
be  estimated  in  examining  for  quantitative  changes. 

This  has  been  done  heretofore  in  using  the  galvanic  current  by  read- 


Tensor  fasciae  latse. 

Quadriceps  (common  point). 
Rectus  femoris. 


Vastus  externus.  «. 


External  popliteal  nerve. 

Peroneus  longus. 
Extensor  longus  digitorum. 


Peroneus  brevis. 


Extensor  brevis  digitorum 


Anterior  crural  nerve. 


Sartorius. 

Obturator  nerve. 
Pectineus. 

Adductor  longus. 
Adductor  magnus. 
Gracilis. 


Crureus. 
Vastus  internus. 


ibA. .  Tibialis  anticus. 


Extensor  hallucis  longus. 
Dorsal  interossei. 


Fig.  308. — Motor  points  on  the  anterior  aspect  of  the  leg 


ing  the  strength  of  the  current.  The  latter  changes  so  very  rapidly 
that  in  closure  contracture  it  must  be  read  immediately.  In  examina- 
tion of  the  opening  contraction,  it  is  read  directly  before  the  contraction 
begins.  Before  taking  the  reading,  the  current  should  be  allowed  to 
flow  through  the  body  and  the  galvanometer  until  the  needle  of  the 
latter  becomes  quiet.  In  a  well-made  instrument  adapted  for  medical 
purposes,  with  a  good  rheostat,  this  will  occur  in  a  few  seconds. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


805 


Dubois  (Bern)  ^  has  recently  shown,  however,  that  in  estimating  the 
galvanic  irritability  of  a  nerve  or  muscle  it  is  more  accurate  to  make 
the  calculation  in  volts  than  in  amperes,  for  the  same  movement  of  the 
muscle  always  takes  almost  the  same  voltage,  while  the  current  rises  with 
the  resistance  interposed. 


Adductor  magnus.  -__^_^ 


Semitendinosus.  - 

Gracilis.  ■ 

Semimeinbranosus.  - 


Internal  popliteal  nerve. 

Gastrocnemius  (inner  head). 
Soleus. 

Flexor  longus  digitorum. 


Posterior  tibial  nerve.  —  — 


Gluteus  maximus. 


Sciatic  nerve. 


-  Biceps  (long  head). 


--  Biceps  (short  head). 


External  popliteal  nerve. 


Gastrocnemius  (outer  head). 


Soleus. 


— .-»  Flexor  longus  ballucis. 


Fig.  309.— Motor  points  on  the  posterior  aspect  of  the  leg. 

This  coincides  with  the  experience  of  Cornaz,^  pupil  of  Dubois. 
He  found  that  measurements  made  in  volts  conformed  much  more 
nearly  than  when  made  in  amperes  when  he  tested  the  same  nerve  of 
the  same  individual  at  different  times,  or  similar  nerves  of  different 
people,  or  similar  nerves  of  the  two  sides  of  the  body.    Dubois  explains 

1  Arch,  de  physiol.,  Oct.,  1897.  '  J.  A.  Diss.,  Bera,  1898. 


806  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

this  phenomenon  by  the  following  fact,  which  he  established  experi- 
mentally (for  the  details  his  monograph  must  be  consulted) :  The 
resistance  of  the  human  body,  in  consequence  of  its  great  "capacity," 
has  practically  no  influence  on  the  amount  of  stimulation,  which  depends 
upon  potential.  So  that  if  the  metallic  resistance  of  the  current  cir- 
cuit does  not  change,  and  if  the  current  strength  varies  only  with  alter- 
ations in  the  electromotive  force,  the  stimulation  can  be  determined 
with  considerable  accuracy  by  the  volt  tension.  To  be  sure,  this  is  no 
longer  the  case  if  rheostat  resistance  is  interpolated  into  the  main  circuit 
and  the  action  of  the  current  is  thus  graded,  as  was  formerly  the  custom 
in  electrodiagnosis.  Dubois  has  shown  that  such  resistance,  whether 
fluid  or  metallic,  produces  strong  auto-induction.  Therefore  it  must 
cause  a  change  not  only  in  the  current  strength,  but  also  in  the  increase 
of  the  current.  Under  these  conditions  neither  the  volt  tension  nor  the 
current  strength  can  be  considered  a  measure  of  the  irritative  effect,  so 
that  this  old  procedure  loses  its  value.  Examining  the  same  muscle 
repeatedly  with  the  same  strength  of  current  but  with  varying  rheostat 
resistance  would  therefore  explain  many  previously  inexplicable  con- 
tradictions in  electrodiagnosis. 

Hence,  in  employing  the  volt  meter  it  is  advisable  to  regulate  the 
galvanic  apparatus  so  that  the  resistance  in  the  main  current  will  not 
vary  with  a  gradation  of  current  activity.  In  other  words,  in  addition 
to  the  employment  of  the  element  transformer,  the  current  activity 
should  be  graded  only  by  altering  the  volt  tension.  The  latter  effect 
can  be  accomplished  by  inserting  a  rheostat  into  the  lateral  circuit,  or, 
still  better,  by  Gaiffe's  "  reducteur  de  potential,"  constructed  according 
to  the  principle  of  the  rheochord. 

Instead  of  the  galvanometer,  Dubois  recommends  substituting  the 
volt  meter,  combined  with  the  "  reducteur  de  potential,"  for  electro- 
diagnosis (though  not  for  electrotherapy).  The  volt  meter  is  prac- 
tically a  galvanometer  situated  in  the  lateral  circuit,  but  of  so  great  a 
resistance  that  the  resistance  of  the  battery  does  not  enter  into  consider- 
ation. Gaiffe's  instrument  is  especially  serviceable  for  electrodiagnostic 
purposes,  because  a  simple  alteration  will  in  a  few  seconds  change  it  to 
a  galvanometer  with  accurate  divisions.  The  volt  meter  possesses 
another  great  advantage.  Its  needle  does  not  oscillate  with  the  opening 
and  closing  of  the  current,  so  that  the  reading  may  be  made  during  the 
examination.  This  is  much  more  trustworthy  than  the  estimation  of 
the  current  strength,  which  can  be  read  only  after  the  stimulation  is 
finished  or  with  opening  stimulation  before  it  begins. 

This  combination  of  volt  meter  with  "  reducteur  de  potential "  has 
been  used  at  the  author's  clinic,  and  has  been  entirely  satisfactory. 

It  should  be  noted  that  the  accuracy  of  the  measurement  of  galvanic  reaction 
by  means  of  the  volt  meter  has  recently  been  questioned  by  Mann,i  who  recom- 
mends, as  the  method  most  free  from  objection,  the  employment  of  condenser 
discharges.  Since  this  method  has  not  yet  been  extensively  employed,  the  author 
will  simply  refer  the  reader  to  the  article  by  the  above-mentioned  author, 

1  Berlin.  kUii.  Woch,  1904,  No.  33. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  807 

The  induction  current,  as  Dubois  has  shown,  has  faults,  even  with 
the  modern  simplified  gradations  of  the  apparatus.  Unfortunately,  it 
must  be  confessed  that  thus  far  no  method  has  been  devised  to  estimate 
the  physiologic  action  of  the  induction  current  in  a  universally  efficient 
way — i.  e.,  in  figures  independent  of  the  apparatus  employed.  The 
physiologic  action  of  one  induction  apparatus  cannot  be  compared  with 
the  action  of  another,  so  that  for  quantitative  examination  or  for  com- 
parison of  results  we  should  always  employ  the  same  apparatus.  The 
distance  that  the  secondary  coil  is  moved  will  measure  the  current 
strength ;  provided,  of  course,  that  the  elements  or  cells  are  freshly 
prepared.  Since  the  individual  centimeters  of  the  scale  usually  placed 
upon  the  induction  apparatus  correspond  to  entirely  different  variations 
in  the  effect  of  the  current,  it  would  be  much  better  to  graduate  the 
scale  also  in  absolute  units,  according  to  the  method  of  Krouecker.^ 
It  must  not  be  supposed,  however,  that  such  a  graduation  will  enable 
us  to  compare  different  induction  apparatuses,  since  the  rapidity  of 
increase  in  the  individual  induction  currents,  and  their  consequent  irri- 
tating effects,  are  quite  different,  being  dependent  upon  the  quality  of 
the  coils  as  well  as  upon  the  electromotive  force  of  the  elements  which 
run  the  apparatus.  The  absolute  graduation  simply  possesses  the 
advantage  that,  if  we  always  use  the  same  machine  with  freshly  pre- 
pared elements,  we  obtain  a  better  idea  of  the  effect  of  the  current. 

Even  with  a  faradic  current  the  bodily  resistance  varies  physio- 
logically, because  the  stimulation  takes  place  under  variable  conditions 
in  a  circuit  of  great  capacity ;  but  such  variation  does  not  produce  any 
decided  difference  in  the  effect  of  the  stimulation  any  more  than  with 
galvanism  (see  above).  Therefore  it  seems  unnecessary  to  follow  many 
authors'  advice  and  measure  the  skin  resistance  galvanically,  as  well  as 
the  distance  of  the  secondary  coil,  when  applying  the  faradic  current. 
But  in  any  event  the  electrodes  must  be  well  moistened,  in  order  that 
the  contact  may  be  as  complete  as  possible. 

It  is  quite  as  important,  in  determining  the  dosage  of  the  faradic  as 
in  determining  that  of  the  galvanic  currents,  to  employ  electrodes  of  defi- 
nite size ;  because,  naturally,  the  intensity  with  which  the  current  impinges 
upon  a  given  spot  is  quite  as  important  as  the  current  strength  and  the 
volt  tension.  The  current  intensity  is  equal  to  the  current  strength  divided 
by  the  square  surface  of  the  electrode.  Therefore,  under  otherwise  equal 
conditions,  an  electrode  of  2  sq.  cm.  surface  provides  only  half  as  great 
a  stimulation  effect  as  one  of  1  sq.  cm.  surface.  Such  an  estimation  is 
accurate  only  for  the  skin  surface  directly  in  contact  with  the  electrode. 
In  penetrating  the  skin  the  current  is,  of  course,  diffiised  over  a  much 
greater  area,  and  since  most  of  the  muscles  and  nerves  to  be  stimulated 
lie  at  a  certain  depth,  the  size  of  the  electrode  is  in  reality  not  so 
important  as  this  discussion  would  lead  one  to  think.  At  all  events,  in 
order  that  the  conditions  may  be  kept  as  constant  as  possible,  electrodes 
of  the  same  size  should  be  employed  in  comparative  examination,  and 
^  Zeits.  f.  Instrumentenkunde,  1889. 


EXA3nXATI0N  OF  THE  NERVOUS  SYSTEM. 

their  dimensions  should  be  mentioned  in  the  description.     The  so-called 
"normal"  electrodes  (p.  799)  are  the  most  satisfactory. 

The  teclinic  of  applying  tlie  electrode  is  naturally  important,  for  a  larger 
electrode  set  against  the  body  surface  at  an  angle  naturally  acts  like  a  smaller 
one.  Again,  one-sided  pressure  should  be  avoided,  the  pressure  should  not  crowd 
the  soft  parts  too  much,  and  the  well-moistened  surface  of  the  electrode  should  be 
in  intimate  contact  with  the  body. 

If,  as  is  sometimes  the  case,  especially  in  employing  a  portable  gal- 
vanic battery,  we  wish  to  differentiate  the  poles  quickly,  it  can  be  done 
very  easily  by  grasping  the  electrodes  one  in  each  hand,  and  then  esti- 
mating which  electrode  causes  more  intense  burning  on  closing  the  cur- 
rent. The  one  that  does  will  be  the  cathode.  Of  course,  the  electrodes 
should  be  of  the  same  size  and  equally  well  moistened.  Again,  the 
cathode  turns  moistened  violet  litmus  paper  blue ;  the  anode  turns  it 
red.  With  the  faradic  current  a  stronger  irritation  is  produced  bv  a 
cathodal  opening,  and  after  the  passage  of  some  current  a  blue  S}x»t  will 
appear  upon  the  litmus  paper.  The  opening  of  the  induced  current,  on 
account  of  its  greater  strength,  is  of  chief  importance  for  the  collective 
action  of  the  alternating  stream. 

The  electrode  to  be  employed  in  such  tests  should  be  of  polished  metal ; 
for  this  will  give  sufficient  current  strength  for  the  slight  electrolytic  action  of 
the  induction  current ;  and  we  need  not  fear  any  discoloration  of  the  litmus  paper 
by  the  acid  metallic  salts  which  always  collect  upon  old  electrodes. 

The  following  abbreviations  are  employed  to  tabulate  the  results  of 
an  electrical  examination  : 

X  mm.  D  =  distance  in  millimeters  that  the  secondary  has  been  withdrawn  from 

the  primary  coil. 
M.  A.  =  milliamperes. 
V.  =  volt. 
Ca.   C.  C.  =  Cathodal  closing  contraction. 
An.  C.  C.  =  Anodal  closing  contraction. 
An.  0.  C.  =  Anodal  opening  contraction. 
Ca.  0.  C.  =  Cathodal  opening  contraction. 
Ca.  C.  T.  =  Cathodal  closure  tetanus. 
Ca.  C.  C.  =^  2  M.  A.  signifies  that  a  minimal  cathodal  closure  contraction  will 

be  produced  by  2  milliamj^eres  of  current. 
Far.  C.  90  mm.  D.    signifies  that  a  minimal  faradic   contraction  will  be  excited 

when  the  secondary  coil  is  withdrawn  90  millimeters. 
Ca.  C.  C.  >  An.   C.   C.  signifies  that  the  cathodal  closure  contraction  is  greater 

than  the  anodal  closure  contraction,  etc. 

2.  METHOD  OF    TESTING    THE    QUANTITATIVE    ELECTRICAL  IRRITABILITY 
OF    THE  NERVE  MUSCLE. 

We  test  the  quantitative  electrical  irritability  of  a  nerve  or  of  a 
muscle  by  estimating  how  strong  a  galvanic,  and  then  how  strong  a 
faradic  current  is  required  to  produce  a  minimal  contraction  (see  p. 
803  et  seq.').  With  a  galvanic  current  the  cathodal  closure  contraction 
is  normally  the  easier  to  obtain  ;    hence,   it  is  ordinarily  employed  for 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  809 

this  estimation.  When  a  maximum  current  produces  no  further  con- 
traction, the  condition  is  called  exhausted  irritability.  Since  this  con- 
dition holds  good  only  for  that  particular  maximum  current  strength  or 
volt  tension  employed,  it  is  advisable  to  determine  both  of  these. 

Physiologically,  the  irritability  of  different  nerves  and  muscles,  as 
well  as  that  of  the  same  muscle  or  nerve,  varies  considerably  in  differ- 
ent individuals.  It  is  not  by  any  means  easy,  therefore,  in  any  given 
case  to  determine  whether  the  results  of  the  examination  overstep  the 
normal  limits,  and,  if  so,  how  much.  The  following  method  seems 
the  most  practical :  We  estimate  the  irritability  and  then  compare  it 
with  that  of  a  healthy  person,  or,  if  the  disturbance  is  unilateral,  with 
that  of  the  healthy  side.  The  latter  is,  of  course,  always  more  accurate. 
Symmetric  points  and  an  identical  position  must,  of  course,  be  selected. 
Erb  and  Stintzing  have  shown  that  the  normal  differences  in  irritability 
upon  the  two  sides  are  very  slight.  In  comparing  the  results  with 
those  found  in  a  healthy  person,  decided  differences  only  should  be 
regarded  as  significant. 

Galvanic  Current. 

Normal  Estimations  to  be  Used  in  Comparing  the  Galvanic  Irritability 
of  the  Two  Sides. — The  following  figures  reisresent  the  luaximal  differences  of  the 
galvanic  current  strength  which  is  needed  to  stimulate  actively  the  normal  nerve  of 
both  sides  of  the  body.  They  are  copied  from  Stintzing,  and  were  estimated  with 
his  normal  electrode  of  3  sq.  cm.  : 

Maximal  Physiologic  Differences  betiveen  the  Galvanic  Irritability  of  the 
Two  Salves  of  the  Body  Expressed  in  Current  Streyigth  (after  Stintzing). 

Ramus  frontalis  of  the  facial  nerve 0.7  M.  A. 

Nervus  accessorius 0.15  " 

Nervus  median  us 0.6  '' 

Nervus  ulnaris  2^^  (above  the  olecranon)  ...    .    .    . 0.6  " 

Musculospiral  nerve 1.1  " 

Nervus  peroneus 0.5  " 

Nervus  tibialis 1.1  " 

Rates  of  the  Volt  Tensions  which  are  Required  for  a  Minimal  Stimulation 
of  the  Corresponding  Normal  Nerves  of  the  Tivo  Sides  of  Body  (after 
Dubois  and  Cornaz). 

These  figures  are  important: 
Faciales  (maxim.)  100: 122  (corresponding  ratio  of  current  strength  =100  :  129) 
Medianus         "       100:117  (  "  "  =100:503) 

Musculospiral"       100:112  (  "  "  =100:145) 

Ulnaris         ,   "       100:116  (  "  "  =100:253) 

Peroneus  "       100:  130  (  "  "  =100:175) 

Normal  Estimations  to  be  Used  in  Comparing  the  Galvanic  Excita- 
bility of  Different  Individuals. — The  following  figures  represent  the  averages 
which  Stintzing  computed  from  an  examination  of  58  healthy  individuals.  They 
are  usefiil  when  we  cannot  compare  the  two  sides  of  the  body. 


810  EXJJIINATION  OF  THE  NERVOUS  SYSTE3I. 

Limits  of  the  Normal  Irritability  Expressed  in  Current  Strength  (after 

Stintzing). 

Ramus  frontalis  of  the  facial  nerve,   irritated  by  0.9  —  2.0  M.  A, 

Ramus  zygomaticus  of  the  facial  nerve,  "  0.8  —  2.0  " 

Ramus  mentalis,  "  0.5 —  1.4  " 

Ner^^.ls  accessorius,  "  0.1  —  0.4  " 

Nervus  ulnaris  2^^  above  the  olecranon,  "  0.2  —  0. 9     " 

Musculospiral  nerve,  "  0.9 — 2.7  " 

Nervus  jjeroneus,  "  0.2  —  2. 0  " 

Nervus  tibialis,  "  0. 4  —  2. 5  " 

Limits  of  the  Physiologic  Irritability  of  Corresjyonding  Nerves  of  Different 
Individuals  and  of  the  Same  Individual  at  Different  Times,  Expressed 
in  Volt  Tension  and  in  Current  Strength  (after  Dubois  and  Cornaz): 

MAXIMAL  DIFFERENCES. 

VOLTS.  MILLIAMPERES. 

Facialis.  Ratio.  Ratio. 

1.  In  different  individuals,  3.8—    9.4(100:247)  0.8—3.0(100:    375). 

2.  In  the  same  individual  at  different  times,   100  :  126  100  :    190 
Medianus. 

1.  In  different  individuals,  4.4  —  14.2  (100  :  323)  0.2—2.7  (100  :  1350). 

2.  In  the  same  individual  at  different  times,   100  :  212  100  :  1000 
Musculospiral  Nerve. 

1.  In  different  individuals,  5.2  —  12.8  (100  :  246)  0.8—2.5  (100  :    246). 

2.  In  the  same  individual  at  different  times,     100  :  152  100  :    225 

Ulnaris. 

1.  In  different  individuals,  1.6  —   7.8  (100  :  487)      0.1  —  1.9  (100  :  1900). 

2.  In  the  same  individual  at  different  times,     100  :  260  100  :    575 

Peroneus. 

1.  In  different  individuals,  4. 0  —  10. 5  (1 00  :  265)     0. 6  —  1. 8  (100  :    300). 

2.  In  the  same  individual  at  different  times,     100  :  225  100  :    225 

When  a  weaker  current  strength  or  volt  tension  excites  a  minimal 
contraction,  the  stimulability  is  increased ;  when  a  stronger  one  is 
required,  the  stimulability  is  diminished. 

As  mentioned  above,  the  measurement  by  volt  tension  is  the  more 
accurate  method — e.g.,  a  minimal  volt  tension  which  will  produce  the 
necessary  stimulation  will  correspond  to  a  much  greater  current  strength 
if  the  resistance  is  slight  than  if  the  resistance  is  high  (according  to 
p.  805  et  seq.).  The  milliampere  value  will,  in  the  former  case,  conceal 
a  diminished,  and,  in  the  latter  case,  an  increased,  stimulability. 

Faradic  Current. 
Every  examiner  will  gradually  become  accustomed  to  his  own  appa- 
ratus, so  that  he  knows  what  differences  come  within  physiologic  limits. 
Stintzing  found  that  with  his  own  apparatus  the  maximal  physiologic 
difference  for  all  nerves  examined  was  15  mm.  D.  This  is  a  rather 
indefinite  statement,  since  this  15  mm.,  even  with  Stintzing's  apparatus, 
corresponds  to  entirely  different  amounts  of  irritation,  dependent  upon 
the  position  of  the  secondary  coil,  and  these  values,  moreover,  do  not 
obtain  when  another  apparatus  is  employed.     Differences  which  exceed 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  811 

a  physiologic  maximum  should  be  regarded  as  pathologic.  If  a  shorter 
distance  is  necessary  to  excite  a  minimal  contraction,  it  shows  a  diminu- 
tion of  irritability ;  if  a  greater  distance  is  required,  an  increase  of 
irritability. 

3.    METHOD    OF  TESTING    THE  QUALITATIVE  ELECTRICAL    STIMULABILITY 
OF  THE  NERVE  MUSCLE. 

The  irritability  of  motor  nerves  is  subject  only  to  quantitative  altera- 
tion. But  with  the  muscles,  quantitative  changes  are  often  accom- 
panied by  qualitative  alterations,  which  require  a  special  description. 

(a)   Normal  Conditions. 

The  qualitative  normal  reaction  of  motor  nerves  and  muscles  to  a 
galvanic  stimulation  is  expressed  in  the  following  so-called  law  of  con- 
traction : 

The  Normal  Law  of  Contraction  for  the  Motor  Nerves  with  a  Galvanic  Current. 

WEAK  CURRENT. 

Ca.C.C. An.  C.  :  no  effect. 

Ca.  0.  :  no  eflfect An.  0. :  no  effect. 

MODERATE    CURRENT. 

Ca.  C.  C.  :  vigorous An.  C.  C.  :  weak. 

Ca.  0.  :  no  effect An.  0.  C.  :  weak. 

VERY  STRONG  CURRENT. 

Ca.C.T. An.C.G.  :  vigorous. 

Ca.  0.  (7.  .•  variable ^n.  0.  C..- vigorous. 

The  normal  lavj  of  contraction  for  the  muscles  with  a  galvanic  current 
differs  from  the  above  only  by  the  fact  that  the  opening  contraction  is 
either  obtained  with  great  difficulty  or,  more  commonly,  cannot  be  pro- 
duced. The  contraction  of  a  muscle  to  galvanism,  whether  the  muscle  is 
stimulated  directly  or  indirectly  through  the  nerve,  normally  appears  very 
suddenly,  like  lightning.  Yet  some  differences  occur,  depending  upon 
whether  the  differential  electrode  is  applied  to  the  motor  point  of  the 
muscle  or  at  some  distance  from  it.  The  latter  (avoiding  the  motor 
point  as  far  as  possible)  is  the  only  way  in  which  we  can  excite  a  pure 
muscular  contraction.  Although  sudden,  the  contractions  are  some- 
what less  lightning-like,  and  the  distinction  between  Ca.  C.  C.  and 
An.  C.  C.  is  less  pronounced.  A  stimulation  from  the  motor  point 
itself  should  be  regarded  really  as  the  stimulation  of  a  nerve. 

Normal  Laios  of  Contraction  for  Motor  Nerves  and  Muscles  with 
the  Ordinary  Faradic  Current  (the  rapidly  interrupted  and  alternating 
induced  current). — Faradic  stimulation  of  both  muscle  and  nerv^e  is 
tetanic — i.  e.,  soon  as  D.  (the  distance)  is  diminished  enough  to  pro- 
duce any  contraction  at  all,  the  muscle  remains  contracted  so  long  as 
the  alternating  current  flows  through  it  or  through  its  motor  nerve. 
The  onset  and  the  cessation  of  the  tetanic  muscular  contraction  corre- 
spond to  the  closure  and  the  opening  of  the  current,  and  are  sudden  and 


812 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


lightning-like.  The  two  poles  of  the  faradic  current  differ  only  in 
their  quantitative  effect — i.  e.,  the  pole  at  which  the  opening  induction 
current  has  its  cathode  is  somewhat  stronger.  The  faradic  current 
produces  a  much  weaker  contraction  when  applied  near  a  motor  point 
than  when  applied  directly  to  it.  Qualitatively,  on  the  contrary,  the 
effect  is  identical. 

{h)  Pathologic   Conditions. 

Reaction  of  Degeneration  (D.  R.) — The  essential  factor  in 
the  reaction  of  degeneration  which  occurs  in  peripheral  and  muscular 
paralyses  is  the  condition  of  the  muscles  (see  p.  817  et  seq.  in  regard  to 
its  significance).  This  reaction,  in  the  broadest  sense  of  the  term, 
presents  very  different  modifications.  The  two  cardinal  symptoms 
common   to   all   forms   are   the   following : 

1.  The  essentially  different  reaction  of  the  muscle  to  prolonged  and 
to  transitory  stimulation — that  is,  to  galvanic  and  faradic.     The  muscle 


^ffa     j4n       ICcc     An     Ka,     An      Ka     An    ICu    Att     /Ca     An 


(a)  Healthy  g^rl.    Ca.  C.  C.  decidedly  greater  than  An.  C.  C.    Contraction  lightning-like. 


(6)  Poliomyelitis  reaction  of  degeneration.  An.  C.  C.much  greater  than  Ca.  C.  C.   Contraction  slow. 

Fig.  310.— Myographic  curves  of  galvanic  closure  contraction  from  a  direct  muscular  stimulation 
in  the  peroneal  region  :  (a).  Normal ;  (b),  reaction  of  degeneration  (taken  from  Kast). 

either  does  not  react  at  all  to  the  faradic  current,  or  its  reaction  is  very 
much  weaker  than  to  the  galvanic  current.  Dubois's  experiments,  how- 
ever, show  that  single  shocks  of  a  very  strong  current  will  produce  a 
contraction  even  where  the  reaction  of  degeneration  is  complete.  He 
believes  that  rapidly  succeeding  shocks — i.  e.,  with  a  freely  vibrating 
hammer — so  fatigue  the  muscle  that  it  cannot  contract. 

2.  The  contraction  no  longer  exhibits  a  lightning-like  character,  but 
is  slow  and  vermiform.  An  after-contraction  may  sometimes  be  noticed 
to  persist  after  the  original  effect  has  ceased  ;  and  in  a  pronounced 
example  a  tetanic  contraction  will  be  excited  which  will  persist  most  of 
the  time  while  the  current  is  applied. 

The  other  characteristics  of  the  reaction  are  very  variable  ;  they  will 
be  mentioned  below. 

The  two  peculiarities  just  outlined  are  common  to  all  forms  of  reac- 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


813 


tion  of  degeneration,  and  are  to  be  regarded  as  the  clinical  expression 
of  a  degenerative  atrophy  of  the  muscle  due  to  some  peripheral  lesion 
(see  p.  789  et  seq.). 

The  complete  reaction  of  degeneration  may  be  schematically  described 
as  follows  : 


Motility 

,     f  Galvanic 
Muscle  J 

(    Faradic 

(     Galvanic 

Nerve ^  and  faradic 

(  irritability 


Degenera-  r- 


Atrophy  and  nuclear  prolifera- 
tionof  the  muscle  fibers. 


Cirrhosis. 


tion  of  the  nerves. 
1.        2. 


Regeneration. 


Motility 

(  Galvanic 
Muscle  < 

(    Faradic 

[     Galvanic 

Nerves  aud  faradic 

(.  irritability 


(oj  Paralysis  with  a  relatively  early  recovery  of  the  motility. 

Cirrhosis. 


Degeneration  of        Atrophy,  etc.,  of 
the  nerves.  the  muscles. 


Regeneration. 


40.     -!.5.      .:.0.      55.  Week. 


Motility 

f  Galvanic 
Muscle  < 

(    Faradic 

C      Galvanic 

Nerve<  and  faradic 

(,  irritabilit\ 


(6)  Paralysis  with  a  later  recovery  of  the  motility. 

Atrophy.    Nuclear  proliferation.    Cirrhosis. 


Degeneration  of 
the  nerves. 


■   Complete 
disappearance. 


1. 


10.      20.       30.       -10.      .50.      60. 


SO.      90.     100.    Week. 


(c)  Irreparable  paralysis.    Disappearance  of  motility  persists. 

Fig.  311.— Diagram  of  the  course  of  irritability  in  peripheral  paralysis  with  complete  reac- 
tion of  degeneration  :  The  wavy  character  of  the  line  which  represents  the  galvanic  irritability 
signifies  that  the  irritability  is  qualitatively  modified— ;'.  e.,  there  is  a  I).  R.  Where  the  line  is 
even  the  condition  is  qualitatively  normal.  The  asterisk  marks  the  return  of  voluntary  motility. 
The  histologic  changes  in  the  nerve  and  muscle  arc  printed  at  each  .stage  above  the  curves. 
The  figures  above  the  curves  correspond  to  the  number  of  weeks  which  have  elapsed  since  the 
onset  (if  the  paralysis.  The  abscissae  of  the  later  course  of  the  paralysis  had  to  be  shortened  in 
different  degrees  for  the  three  curves  on  account  of  the  space,  so  that  the  curves  cannot  be  exactly 
compared  as  to  their  length  (Erb^ 


814  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

Faradic  test :  Excitability  of  the  nerves  lost. 

Faradic  test :  Excitability  of  the  muscles  lost. 

Galvanic  test :  Excitability  of  the  nerves  lost. 

Galvanic  test :  Excitability  of  the  muscles  immediately  after  the 
onset  of  the  paralysis  quantitatively  normal,  later  increased,  and  finally 
often  decidedly  diminished.  The  contraction  is  slow.  An.  C.  C.  is 
excited  more  rapidly  than  Ca.  C.  C.  An.  C.  C.  >  Ca.  C.  C.  for  the 
same  current  strength  or  volt  tension. 

The  myographic  curves  (Fig.  310)  illustrate  these  quantitative 
changes  of  the   muscle  reaction. 

The  duration  of  complete  reaction  of  degeneration  in  peripheral 
paralysis  is  very  typical.  It  has  been  studied  thoroughly  in  severe 
facial  paralysis  of  rheumatic  origin,  and  has  been  graphically  represented 
by  Erb  (Fig.  311). 

Mechanical  reaction  of  degeneration,  mentioned  upon  p.  798,  occurs 
principally  where  there  is  complete  electrical  reaction  of  degeneration 
with  increased  irritability. 

Partial  (^Incomplete)  Reaction  of  Degeneration. — In  this  form  the 
faradic  and  galvanic  irritability  of  the  nerves  and  the  faradic  irrita- 
bility of  the  muscles  are  not  lost,  but  merely  diminished.  A  slow  con- 
traction is  ordinarily  caused  only  by  galvanic  excitation  of  the  muscles, 
although  sometimes  faradic  excitation  with  isolated  shocks  at  some  dis- 
tance from  the  motor  point  will  produce  the  same  eflPect.  A  scheme  of 
the  incomplete  reaction  of  degeneration  follows  : 

Faradic  :  "|  f  Irritability  merely  diminished.     Contractions  not  slower, 

Nerve.       J-   ....  ^  except  sometimes  in  the  case  of  the  faradic  muscle 

Muscle.     J  (         contractions  when  the  motor  point  is  avoided. 

Oalvanic:)  f 

Nerve.       >  ....  J  Like  the  complete  reaction  of  degeneration. 

Muscle,    j  (_ 

The  course  of  an  incomplete  reaction  of  degeneration  in  peripheral  paralyses 
is  represented  in  Fig.  312. 

Incomplete  Reaction  of  Degeneration  with  Forced  Indirect  Slower  Contractions. 
— In  this  form,  as  distinguished  from  the  simple  incomplete  reaction  of  degen- 
eration, all  the  contractions  are  slowed,  not  only  those  excited  by  galvanic  mus- 
cular stimulation,  but  also  those  excited  by  faradic  stimulation  of  the  muscles 
and  by  faradic  or  galvanic  stimulation  of  the  nerves. 

Mixed  Reaction  of  Degeneration. — When  some  of  the  fibers  of  a  muscle  pre- 
serve a  normal  reaction,  while  others  present  a  reaction  of  degeneration,  the 
result  is  called  a  mixed  reaction  of  degeneration.  In  such  cases  we  cannot  examine 
each  type  of  fiber  separately,  so  that  the  resulting  mixed  reaction  is  frequently 
difficult  to  understand,  and  it  is  quite  impossible  to  pick  out  which  of  the  fibers 
show  a  normal  and  which  a  degenerate  reaction.  Many  instances  of  incomplete 
reaction  of  degeneration  really  belong  to  this  variety. 

Peculiar  Electric  Reactions  of  Certain  Old  Peripheral  Palsies  as 
Described  by  Placzek. — Placzek,^  and  subsequently  Bernhardt,'^  have  described  a 
peculiar  phenomenon  which  is  in  rare  cases  observed  as  a  termination  of  severe 
peripheral  facial  palsies.  In  contrast  to  the  usual  findings,  the  electrical  reac- 
tions of  the  nerve  muscle  in  some  of  these  old  facial  palsies  reappear,  although  the 
paralysis  of  voluntary  motion  remains  permanent.  This  phenomenon  is  highly  inter- 
esting from  a  theoretic  standpoint,  and  the  author  would  regard  it  as  analogous  to 

1  Berlin,  klin.  Woch.,  1893.  '  Ibid.,  1903. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


815 


the  behavior  of  the  so-called  mild  peripheral  palsies,  in  which  the  paralysis  of 
voluntary  motion  exists  together  with  maintained  electrical  excitability  of  the 
peripheral  parts.  Both  conditions  may  be  explained  by  the  supposition  that 
changes  exist  in  the  peripheral  nerves  which  block  voluntary  impulses,  but  do 
not  disturb  the  peripheral  excitability  of  the  nerve  or  muscle.  In  the  old  palsies 
exhibiting  this  phenomenon  there  can  be  no  doubt  that  peripheral  regeneration 
has  taken  place,  but  that  the  blockading  of  voluntary  impulses  nevertheless  per- 
manently remains.  This  is  difficult  to  understand  if  we  cling  to  the  old  theory 
of  the  necessity  of  efferent  irritations  for  the  trophic  integrity  of  the  nerve  muscle. 
This  old  theory,  however,  does  not  seem  to  obtain  in  all  cases,  since  Bethe  has 
shown  that,  when  the  union  of  divided  nerve  fibers  is  prevented  in  young  animals, 


Motility 

f  Galvanic 
Muscles 

(    E'aradic 

(     Galvanic 

Nerve  <  and  farad ic 

(.  irritability 


Degenerative  atrophy 
of  the  muscle  fibers. 


Regeneration. 


9.     Week. 


Fig.  312. — Diagram  of  the  course  of  irritability  in  partial  reaction  of  degeneration.  See  the 
explanation  of  Fig.  310.  The  faradic  and  galvanic  irritability  of  the  nerves  and  the  faradic  irri- 
tability of  the  muscles  are  only  slightly  diminished.  Motility  returns  early.  Compensation  early 
and  complete.    Nerve  degeneration  probably  absent. 

a  peripheral  regeneration  may  nevertheless  occur,  so  that  the  nerve  fibers  regain 
their  electrical  irritability. 

Myotonic  Reaction  (Erb). — This  occurs  only  in  Thomsen's  disease  (myo- 
tonia congenita).  It  is  characterized  by  a  peculiar  persistence  of  the  contraction 
after  the  cessation  of  the  stimulation.  The  contractions  are  slow  and  frequent, 
and,  when  the  galvanic  current  is  steadily  applied  to  the  muscles,  are  often  char- 
acteristically rhythmic  and  wave-like.  Even  very  weak  currents  will  excite  these 
phenomena  (muscle  hyperirritability).  The  anodal  closing  contraction  (An. 
C.  C.)  of  the  muscle  is  frequently  more  vigorous  than  the  cathodal  closure 
(Ca.C.  C,). 

Neurotonic  Reaction. — A  few  years  ago  Marina '  and  Remak  ^  independently 
described  a  rare  form  of  reaction  which  they  called  neurotonic  reaction.  Marina 
found  it  in  hysteria,  and  Remak  in  a  case,  in  all  probability,  of  progressive  mus- 
cular atrophy. 

In  this  reaction  without  any  increase  of  the  quantitative  minimum  irrita- 
bility, anodal  opening  contraction  appears  very  early  from  stimulation  of  the  nerve 
but  not  of  the  muscle.  There  is  also  a  special  tendency  of  the  nerve  to  cathodal 
closure  and  anodal  opening  tetanus.  The  closure  tetanus  can  be  prolonged  beyond 
the  opening  of  the  current,  and  even  the  faradic  tetanus  of  the  nerve  may  per- 
sist after  stopping  the  stimulation.  These  characteristic  phenomena  depend 
essentially  upon  nerve  irritation,  and  they  cannot  be  excited  by  stimulation  of 
the  muscle. 

Reaction  in  Tetany. — A  quantitative  increase  of  the  electrical  irritability 
of  the  nerve  trunks  is  found  in  this  disease,  although  it  does  not  affect  the  mus- 


'  See  Neural  CentralhL,  1896,  No.  17. 
ject  by  Marina  are  mentioned  here. 


The  older  Italian  publications  upon  this  sub- 
'  Neurol.  Centralbl.,  1896,  No.  13. 


816  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

cle,  or,  at  least,  not  nearly  to  so  great  an  extent.  The  quality  of  the  reaction 
of  the  nerve  is  frequently,  though  not  constantly,  altered — e.  g.,  a  neurotonic 
reaction  appears  with  a  tendency  to  anodal  opening  and  cathodal  closure  contrac- 
tion and  a  prolongation  of  the  contraction.  The  essential  difference  is  that  in 
tetany,  as  contrasted  with  neurotonic  reaction  proper,  a  quantitative  increase  of 
irritability  accompanies  the  qualitative  changes. 

Characteristic  Reaction  in  Certain  Traumatic  Neuroses. — Eumpf  ^  has 
applied  the  unfortunate  term  "  traumatic  reaction  "  to  this  peculiar  phenomenon. 
For  some  time  after  the  cessation  of  a  vigorous  faradic  stimulation  the  muscle 
will  exhibit  a  characteristic  fluctuating  movement,  made  up  of  alternating  fibrillary 
and  clonic  contractions.  In  many  cases  these  complex  results  occur  even  during 
the  stimulation.  Each  contraction  may  spread  from  the  muscle  which  is  directly 
stimulated  and  become  generalized.  In  these  patients  similar  appearances  are 
observed  to  follow  vigorous  efforts  and  the  action  of  cold.  (See  p.  748,  Fibrillary 
Contractions  in  the  Healthy.) 

Myasthenic  Reaction. — A  peculiar  electrical  condition  of  the  affected  parts 
accompanies  myasthenia  gravis  pseudoparalytica  or  asthenic  bulbar  paralysis,  as  the 
disease  is  usually  called.  It  was  first  described  by  Jolly.  ^  When  a  tetanic  in- 
duction current  is  permitted  to  act  upon  a  muscle,  whether  directly  or  through 
the  nerve,  the  contraction  gradually  diminishes  and  finally  disappears.  This 
electrical  phenomenon  is  entirely  analogous  to  the  pathologic  fatigue  of  the  mus- 
cle after  voluntary  impulses,  which  is  so  characteristic  of  this  disease.  A  similar 
phenomenon  can  be  elicited  experimentally  in  muscles  poisoned  with  protover- 
atrin. 

4.  DIAGNOSTIC  SIGNIFICANCE  OF  THE  DIFFERENT  ELECTRICAL  REACTIONS. 

The  myotonic,  neurotonic,  "  traumatic,"  and  tetany  reactions  have 
been  sufficiently  described  above,  and,  so  far  as  our  present  knowledge 
goes,  each  is  limited  to  its  corresponding  disease. 

In  psychic  or  hysteric  paralysis  the  electrical  irritability  remains  nor- 
mal. This  is  also  a  general  rule  for  all  paralyses  which  depend  upon 
a  lesion  of  the  voluntary  tracts  above  the  nucleus — i.  e.,  above  the  gray 
anterior  horn  (cereh^al  hemiplegias,  transverse  lesions  of  the.  spinal  cord). 
Sometimes,  however,  in  these  cases,  especially  if  the  paralysis  has  per- 
sisted for  some  time,  the  electrical  irritability  is  considerably  dimin- 
ished. 

The  condition  during  the  first  few  days  following  a  peripheral  par- 
alysis (see  Figs.  311  and  312),  and  that  during  the  entire  course  of 
the  milder  forms,  will  illustrate  very  typically  a  simple  diminution  in 
the  electrical  irritability.  When  the  peripheral  interruption  of  conduc- 
tion is  complete — i.  e.,  when  the  paralysis  is  severe — reaction  of  degen- 
eration will  generally  take  the  place  of  simple  diminution  of  irrita- 
bility. 

Some  cases  of  polyneuritis  and  of  lead-poisoning  furnish  striking 
exceptions  to  the  above  statements.  In  some  cases,  instead  of  the 
expected  reaction  of  degeneration,  not  only  is  the  irritability  diminished, 
but  the  diminution  is  so  pronounced  that  even  direct  contract  of  the 
galvanic  current  excites  no  response.  This  proves  that  in  these  cases 
the  muscles  are  affected  by  the  toxins  directly,  and  not  alone  through 

1  Deutseh.  med.  WocL,  1890,  No.  9,  p.  165. 

^  Berlin,  klin.  Woch.,  1895,  vol.  i.,  p.  2,  et  seq. 

^  Prognosis  will  be  discussed  separately  upon  p.  819  et  seq. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  817 

involvement  of  the  nerve.  In  fact,  there  are  many  other  reasons  for  such 
an  hypothesis.  This  supposition  is  at  least  probable  in  those  cases 
which  recover,  despite  a  marked  diminution  of  the  direct  galvanic 
muscular  irritability.  At  all  events,  in  incurable  cases  of  polyneuritis 
and  lead-poisoning,  the  disappearance  of  the  galvanic  irritability,  and 
the  rapidly  appearing  terminal  stage  of  the  reaction  of  degeneration, 
must  be  considered  to  be  the  expression  of  definite  secondary  degenera- 
tion of  the  muscle  (see  Fig.  311). 

In  the  myopathic  forms  of  progressive  muscular  atrophy  simple  dimi- 
nution of  electrical  irritability  is  the  rule. 

A  simple  increase  of  electrical  irritability  is  a  comparatively  rare 
phenomenon.  It  does  occur  in  quite  recent  paralyses  of  neural  origin, 
and  in  tetany.  It  then  depends  chiefly  upon  nerve  excitability.  In- 
creased excitability  of  the  nerve  or  muscle,  with  coincident  qualitative 
change,  should  not  be  confused  with  such  a  condition.  (Reaction  of 
Degeneration,  Myotonic  Reaction,  Tetanic  Reaction,  see  above.) 

The  various  alterations  in  reaction  of  degeneration  (in  the  widest 
sense  of  the  term)  occur  only  in  cases  in  which  the  muscle  is  aifected 
by  a  break  in  conduction  between  it  and  its  so-called  trophic  center  ^ 
(situated  in  the  nucleus — i.  e.,  in  the  anterior  horns),  or  where  a 
lesion  of  the  center  itself  occurs,  or  where  the  muscle  is  primarily 
degenerated.  The  degeneration  of  the  muscle,  and  with  it  the  reaction 
of  degeneration,  may  be  absent,  even  when  the  lesion  is  so  situated, 
provided  it  be  slight  and  transitory.  Degenerative  changes  in  the 
muscle  are  found  in  all  instances  of  reaction  of  degeneration  and,  in 
fact,  seem  to  be  physiologically  expressive  of  such  a  reaction.  If  com- 
plete, the  degeneration  also  spreads  to  the  nerve.  A  partial  reaction 
of  degeneration,  on  the  contrary,  which  depends  upon  a  moderately 
severe  disturbance  of  conduction,  accompanies  a  degeneration  of  the 
muscle  with  normal  or,  at  most,  only  slightly  degenerated  nerves.  The 
retention  of  nerve  irritability  in  partial  reactions  of  degeneration  seems 
to  depend  upon  the  preservation  of  the  medullary  sheaths. 

In  accordance  with  the  above,  the  most  frequent  lesions  which  pro- 
duce the  various  types  of  the  reaction  of  degeneration  are  nuclear  or 
jp&'ipheral  paralyses.  The  spinal  and  the  neuritic  muscular  atrophies 
also  often  lead  to  partial  reactions  of  degeneration.  Yet  numerous 
divergences  in  the  electrical  results  occur  iu  individual  cases  of  these 
muscular  atrophies,  because  in  them,  as  contrasted  with  actual  paralyses, 
each  fiber  is  saccessively  and,  iu  a  certain  measure,  individually  dis- 
eased. Therefore  each  muscle  we  examine  contains  a  series  of  fibers  in 
diflPereut  conditions  of  irritability,  and  the  resulting  reaction  will 
depend  upon  whether  seriously  injured,  slightly  affected,  or  intact  fibers 
predominate.  In  spinal  and  neuritic  muscular  atrophies  a  mixed  reac- 
tion is  the  rule,  whereas  a  partial  or  complete  reaction  of  degeneration 
is  much  commoner  in  peripheral  palsies. 

Many  cases,  however,  of  spinal  or  neuritic  muscular  atrophies  show 

^  See  p.  790,  note,  for  the  significance  of  tliis  center — i.  e.,  how  its  trophic  character 
is  regarded. 
52 


818  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

absolutely  no  signs  of  reaction  of  degeneration  as — e.  g.,  if  the  fibers 
which  are  seriously  affected  are  very  rapidly  and  quite  completely 
destroyed,  so  that  the  reaction  to  stimulation  actually  comes  from 
intact  fibers  or  from  those  only  slightly  affected,  and  is  merely  quanti- 
tatively diminished.  We  might  call  this  result,  which  is  by  no  means 
uncommon  in  spinal  neuritic  muscular  atrophies,  a  sort  of  latent  reac- 
tion of  degeneration.  The  same  peculiarity  is  presented  in  bulbar 
paralysis  which  in  its  origin  is  identical  with  the  spinal  form  of  muscu- 
lar atrophy,  and  with  the  closely  related  amyotrophic  lateral  sclerosis. 
Reaction  of  degeneration  may  or  may  not  be  present.  The  myopathic 
forms  of  muscular  atrophy  exhibit  similar  variations.  Here  and  there 
a  suspicion  of  reaction  of  degeneration  does  occur,  although  from  the 
nature  of  the  cause  we  should  suppose  that  it  was  impossible.  This 
apparent  inconsistency  may  depend  upon  the  presence  of  many  seriously 
affected  fibers  which  still  react  to  stimulation  at  the  time  of  the  exam- 
ination. If  many  such  fibers  are  present,  reaction  of  degeneration  will 
result ;  if  few,  the  reaction  will  depend  upon  the  normal  fibers,  and 
simply  be  normal  or  but  slightly  diminished.  The  occurrence  of  such 
variations — i.  e.,  reaction  of  degeneration  in  purely  myopathic  forms, 
and,  conversely,  its  absence  in  spinal  and  neuritic  forms  of  muscular 
atrophies — makes  it  plain  that  we  must  not  rely  upon  the  electrical 
examination  to  decide  the  form  of  the  muscular  atrophy,  but  turn  to 
other  clinical  evidence,  such  as  heredity,  age,  mode  of  extension  of  the 
disease,  etc. 

From  what  has  been  said,  it  is  plain  that  it  is  much  more  important 
for  diagnosis  to  demonstrate  that  the  reaction  of  degeneration  is  present 
than  that  it  is  absent.  A  positive  reaction  of  degenera- 
tion (this  is  perhaps  the  most  important  law  in  electro- 
diagnosis)  completely  excludes  a  central  or  supranuclear 
origin  for  the  disease).  The  absence  of  reaction  of  de- 
generation, however,  even  if  we  except  the  cases  where 
the  lesion  is  too  slight  to  produce  it,  does  not  always 
permit  the  exclusion  of  a  nuclear  or  subnuclear  cause 
of  disease. 

There  is  another  difficulty  which  makes  it  some- 
times impossible  to  recognize  reaction  of  degeneration, 
even  when  the  muscles  are  paralyzed  from  peripheral 
lesion.  This  is  the  exceptionally  diminished  muscular 
excitability,  even  to  the  galvanic  current,  in  the  late 
stages  of  the  reaction  of  degeneration.  Frequently  the 
batteries  are  either  too  weak  to  excite  contractions,  or 
so  strong  a  current  is  required  that  either  the  pain  or 
the  electrolytic  action  of  the  current  upon  the  skin 
prevents  the  examination.  Such  an  exceptionally  diminished  irritability 
should  be  considered  for  clinical  purposes  as  equivalent  practically  to 
the  reaction  of  degeneration.  (See  p.  816,  Direct  Injury  to  the  Mus- 
cles by  the  Toxins.) 

We  can  sometimes  utilize  an  electrical  examination  to  locate  some 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  819 

obstruction  to  conduction  in  a  peripheral  nerve  with  its  muscle  (Fig. 
313).  If  some  obstruction  to  the  conduction — i.  e.,  some  injury- 
occurs  at  c,  no  contraction  will  result  from  a  stimulation  between  a  and 
G,  but  will  from  one  between  c  and  b.  In  this  way  the  lesion  can  be 
localized  at  c,  provided  the  nerve  is  accessible  to  examination  through- 
out its  course.  The  test  will  fail,  of  course,  if  c  6  is  no  longer  capable 
of  being  stimulated — e.  g.,  in  a  more  degenerative  lesion  where  the 
nerve  below  c  soon  loses  it  irritability.  In  a  comparatively  fresh  or 
mild  paralysis  there  will  be  at  least  a  partial  reaction  of  degeneration. 
This  condition  is  well  illustrated  by  the  so-called  "drunkard's  par- 
alysis "  or  "  sleep  paralysis  "  of  the  musculospinal  nerve,  in  which  we 
can  sometimes  locate  the  injury  at  the  point  of  origin  of  the  radial 
nerve,  because  ordinarily  the  radial  nerve  can  be  stimulated  directly 
above  this  point — i.  e.,  in  the  axilla,  or,  for  the  supinator  longus,  at 
Erb's  point  (see  note  to  Fig.  306). 

5.  PROGNOSTIC  SIGNIFICANCE  OF  THE  ELECTRICAL  REACTION. 

Nothing  could  be  more  misleading  than  to  base  the  prognosis  upon 
the  alteration  in  the  electrical  reaction  without  at  the  same  time  heeding 
other  facts,  especially  the  spinal  anatomic  diagnosis — e.  g.,  a  rheumatic 
facial  paralysis  even  with  a  typical  reaction  of  degeneration  frequently 
recovers ;  whereas  a  cerebral  hemiplegia  with  perfectly  normal  elec- 
trical reaction  is  often  incurable.  Again,  a  myopathic  muscular  atrophy 
with  normal  electrical  reaction  is  no  less  incurable  than  a  spinal  mus- 
cular atrophy  with  reaction  of  degeneration.  Many  similar  instances 
could  be  mentioned. 

At  the  same  time  electrodiagnosis  is  often  of  incalculable  value  in 
determining  the  prognosis,  provided  that  we  compare  only  the  elec- 
trical examinations  of  cases  limited  to  the  same  type,  and  draw  onr 
conclusions  only  after  several  careful  examinations  repeated  at  some 
little  interval  of  time  from  each  other.  A  few  examples  will  make  this 
evident. 

Rheumatic  facial  paralysis,  which  Erb  has  studied  so  carefully  in 
regard  to  the  sequence  of  its  electrical  conditions,  supplies  us  with  an 
excellent  example  of  the  prognostic  value  of  the  electrical  examination. 
If  in  this  disease  reaction  of  degeneration  can  still  be  demonstrated 
after  about  fourteen  days,  it  is  evident  from  the  diagram  upon  p.  813 
that  at  least  some  months,  or  under  some  conditions  even  as  much  as  a 
year,  will  elapse  before  perfect  recovery  will  ensue,  or  the  case  may  be 
incurable.  If  after  the  lapse  of  fourteen  days  no  more  pronounced 
alterations  of  the  electrical  excitability  occur,  the  paralysis  is  slight, 
and  may  recover  in  a  few  weeks.  If  after  the  lapse  of  fourteen  days 
only  a  partial  reaction  of  degeneration  occurs,  we  can  count  upon  recov- 
ery in  eight  to  nine  weeks  (according  to  the  scheme.  Fig.  312).  If 
the  affection  is  severe  and  associated  with  reaction  of  degeneration,  a 
single  electrical  examination  is  not  sufficient  to  determine  whetlier  it  is 
curable  or  not.     We  must  follow   the  entire  course  of  the  electrical 


820  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

changes.  If  after  the  lapse  of  about  thirty  weeks  we  can  determine  no 
return  of  the  motility,  and  no  improvement  in  the  electrical  irritability, 
or  perhaps  a  still  further  impairment,  the  prognosis  would  be  very 
grave  indeed  (Fig.  311  c).  Conversely,  the  slightest  improvement  in 
the  electrical  reaction — viz.,  an  increase  of  the  galvanic  irritability  in 
the  nerve  or  the  muscle  supplied  by  it,  or  even  cessation  of  its  further 
depression — is  of  favorable  significance. 

The  above-mentioned  prognostic  laws  apply  only  to  those  peripheral 
paralyses  which,  like  a  rheumatic  facial  paralysis,  owe  their  existence  to 
a  single  injury — i.  e.,  whose  anatomic  causes  neither  persist  nor  progress. 
It  would  be  obviously  illogical  to  apply  this  law  to  other  types  of  facial 
paralysis,  such  as  a  paralysis  caused  by  a  tumor  or  by  an  osteitis  of  the 
petrous  bone,  or  even  to  the  facial  paralysis  of  a  bulbar  palsy.  The 
distinction  is  that  the  rheumatic  facial  paralysis  tends  to  recover, 
whereas  these  others  tend  to  persist  and  progress. 

The  prognosis  of  a  case  of  infantile  spinal  jM^-alysis  (poliomyelitis 
acuta)  is  also  very  materially  assisted  by  the  results  of  an  electrical 
examination.  For,  just  as  in  rheumatic  facial  paralysis,  the  cause  is  in 
operation  but  a  short  time ;  even  in  the  very  severe  cases  of  polio- 
myelitis the  cause  persists  and  progresses  for  only  a  few  weeks,  and 
after  that  the  disease  itself  is  stationary.  If  after  fourteen  days  to 
three  weeks  no  reaction  of  degeneration  can  be  detected  in  certain  of 
the  affected  muscles,  we  can  safely  apply  the  same  prognostic  law  to 
them  that  we  have  just  mentioned  for  a  rheumatic  facial  palsy.  Reaction 
of  degeneration  is,  however,  much  more  serious  a  sign  in  poliomyelitis 
than  it  is  in  a  rheumatic  facial  palsy,  for  experience  has  taught  us  that 
in  infantile  paralysis  those  muscles  which  show  reaction  of  degeneration 
never  recover.  The  reason  is  probably  that  the  lesion  is  located  in 
central  organs,  which  have  little  or  no  recuperative  power. 

With  lead  jicdsy  reaction  of  degeneration  almost  always  appears 
promptly,  or,  if  this  is  not  so  marked,  at  least  a  pronounced  diminution 
of  the  muscular  irritability  to  the  galvanic  current  (see  pp.  816  and  818) 
promptly  results ;  either  effect  is  equally  significant  from  the  prognostic 
standpoint.  If  no  pronounced  changes  in  the  electrical  stimulability 
occur  some  time  after  the  onset  of  a  lead  palsy,  the  prognosis  will  be 
favorable,  just  as  in  the  rheumatic  facial  palsies.  In  lead  paralysis, 
however,  there  is  nothing  absolutely  unfavorable  in  the  appearance  of 
reaction  of  degeneration  or  in  the  pronounced  diminution  of  electrical 
irritability  mentioned  above.  Only  examinations  repeated  at  consider- 
able intervals  suffice  to  determine  the  prognosis  in  cases  of  lead  paralysis 
with  reaction  of  degeneration.  If  the  reaction  constantly  progresses  the 
prognosis  will  be  grave ;  if,  on  the  contrary,  it  remains  the  same  the 
prognosis  will  be  less  serious ;  and  if  it  evidently  improves  the  prog- 
nosis will  be  favorable.  For  experience  has  taught  us  that  when  once 
an  improvement  commences  in  a  lead  paralysis,  it  almost  always  pro- 
ceeds to  complete  recovery,  and  that  partial  recoveries  are  much  less 
common.     The  same  is  found  in  polyneuritic  and  diphtheric  paralyses. 

We  scarcely  need  mention  that  in  polyneuritis    there  is  always  a 


EXAMINATION  OF  THE  NEBVOUS  SYSTEM.  821 

very  decided  tendency  to  recover  just  as  soon  as  the  determining  causes 
stop ;  and,  of  course,  this  fact,  as  well  as  the  result  of  electrical  exami- 
nation, must  be  kept  in  mind  in  making  the  prognosis,  which  must  be 
sharply  determined  for  each  individual  muscle,  and  not  for  all  those 
affected. 

In  central  paralyses  due  to  lesions  in  the  supranuclear  neurons,  the 
results  of  electrical  examination  are  of  much  less  prognostic  importance 
than  in  disturbances  due  to  lesions  of  the  peripheral  neurons.  For  the 
electrical  irritability  is  not,  as  a  rule,  very  much  altered  in  these  cases 
even  when  the  prognosis  has  from  the  onset  been  grave.  However,  an 
unfavorable  prognosis  should  be  given  in  disease  dependent  upon  cen- 
tral lesions  (cerebral  hemiplegias,  transverse  lesions  of  the  cord)  which 
lead  to  a  pronounced  depression  of  the  electrical  irritability,  because 
they  point  to  a  decided  secondary  involvement  of  the  peripheral  motor 
neurons.  This  involvement  may  be  corrected  up  to  a  certain  point  by 
appropriate  electrical  treatment. 

B.  SPECIAL  PART. 

I.  EXAMINATION  OF  THE  DIFFERENT  CRANIAL  NERVES. 

In  examining  the  cranial  nerves,  the  most  convenient  and  logical 
plan  is  to  take  them  up  one  after  the  other  in  their  anatomic  sequence. 
In  the  case  of  the  nerves  to  the  eye  muscles,  it  is,  however,  more  prac- 
tical to  discuss  them  all  together,  beginning  with  the  third  pair,  the 
oculomotor. 

I.  CRANIAL  NERVE  I  OLFACTORY. 

To  test  this  nerve  Ave  employ  substances  with  different  odors,  such 
as  cologne,  asafetida,  oil  of  anise,  etc.  We  request  the  patient  to  smell 
each  of  them,  closing  first  one  nostril  and  then  the  other.  It  is  rather 
convenient  at  the  same  to  test  the  trigeminus,  employing  for  this  pur- 
pose acetic  acid  and  ammonia.  The  two  sides  should  be  tested  sepa- 
rately. If  any  differences  are  made  out,  we  must  not  attribute  them 
to  the  olfactory  or  the  trigeminus  until  we  have  convinced  ourselves 
by  a  careful  rhinoscopic  examination  that  they  do  not  depend  upon  a 
local  alteration  of  the  mucous  membrane. 

Among  other  conditions,  cerebral  pressure  will  generally  produce  a 
paralysis  of  the  olfactory.  Huguenin,  judging  from  his  own  expei'i- 
ments,  considers  that  this  condition  possesses  "diagnostic  significance 
similar  to  that  of  the  choked  disk."  A  unilateral  diminution  of  smell, 
provided  no  local  cause  exists  in  the  nasal  mucous  membrane,  appears 
most  frequently  as  an  accompaniment  of  the  hemianedhesias  of  hysteria, 
and  of  the  traumatic  neuroses.  It  is  ]nirely  functional.  The  so-called 
capsular  hemianesthesia,  which  depends  upon  lesions  of  the  posterior 
part  of  the  internal  capsule,  is  not  ordinarily  associated  with  any  dis- 
turbance of  smell.  The  olfactometer  constructed  for  physiologic  exami- 
nations has  very  little  clinical  utility,  because  gross  changes,  those 
easily  demonstrated  without  any  instrument,  are  the  only  ones  of  any 
diagnostic  importance. 


822 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 
II.  GRANIAL  NERVE  :   OPTIC. 


1.  Determination  of  Acuteness  of  Central  Vision. — Snellen's 
or  Pfliiger's  well-known  test  types  are  the  most  convenient  and  suitable 
for  testing  the  acuteness  of  central  vision.  Landolt's  new  vision  tests 
are  more  conveniently  carried  about,  and  therefore  better  adapted  for 
examining  patients  in  bed.  Errors  of  refraction  must  first  be  corrected. 
Ophthalmologic  text-books  must  be  consulted  for  more  exact  directions. 
We  should  remember,  however,  that  even  if  the  acuteness  of  vision  is 


Fig.  314.— Perimeter :  The  examination  may  be  made  with  the  carrier  which  moves  along 
the  semi-circle,  or  the  test  objects  may  be  carried  along  this  by  means  of  dark  disks  attached  to 
a  long  handle,  each  disk  containing  in  its  center  the  test  object.  The  patient's  chin  is  placed  in 
the  curved  chin  rest ;  the  notched  end  of  the  upright  bar  is  brought  in  contact  with  the  face, 
directly  beneath  the  eye  to  be  examined,  which  attentively  fixes  upon  the  center  of  the  semi- 
circle. The  other  eye  should  be  covered,  preferably  with  a  neatly  adjusted  bandage.  The  record 
chart  is  inserted  at  the  back  of  the  instrument,  and,  by  means  of  an  ivory  vernier,  the  exam- 
iner is  enabled  to  mark  exactly  with  a  pencil  the  point  on  the  chart  corresponding  to  the  position 
on  the  semi-circle,  at  which  the  patient  sees  the  lest  object.  The  various  marks  are  then  joined 
by  a  continuous  line. 

normal,  we  cannot  absolutely  exclude  the  existence  of  pronounced 
changes  of  the  retina  or  of  the  optic  nerve,  so  that  an  opthalmo- 
scopic  examination  is  essential  (retinal  hemorrhages,  retinitis,  choked 
disk,  optic  atrophy). 

2.  Testing  the  Field  of  Vision — We  employ  the  perim.eter  (Fig. 
314)  to  determine  accurately  the  field  of  vision ;  to  demonstrate  hemi- 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  823 

opia  and  other  visual  defects  (as  central  scotomata,  quadrant  defects  and 
quadrant  anopsia)  ;  to  establish  the  existence  of  unilateral  or  bilateral 
limitations  of  the  visual  field,  such  as  accompany  hysteria  and  other 
neuroses,  especially  in  the  so-called  traumatic  neuroses ;  as  well  as  to 
show  the  frequently  associated  fatigue  of  the  retina.  Books  upon  oph- 
thalmology must  be  consulted  for  the  technical  application  of  this  instru- 
ment. 

We  can  determine  the  visual  field  quite  accurately  by  a  very  simple 
device.  The  patient,  with  his  left  eye  closed,  sits  opposite  the  examiner. 
The  latter  closes  his  right  eye.  The  patient's  right  eye  and  the 
examiner's  left  eye  are  now  fixed  upon  each  other ;  the  examiner  then 
moves  his  finger  in  a  frontal  plane  halfway  between  the  two  eyes,  from 
the  periphery  into  the  field  of  vision.  He  can  then  directly  compare 
the  patient's  field  of  vision  with  his  own.  Of  course,  the  distance  of 
the  finger  from  each  eye  should  be  exactly  alike.  With  but  one  eye  it 
is  difficult  to  be  accurate  about  this  distance,  so  that  it  is  advisable  for 
the  examiner  to  orient  himself  by  opening  the  closed  eye  from  time  to 
time.  Pronounced  defects  in  the  visual  field  are,  according  to  the 
author's  experience,  easily  recognized  by  this  method. 

Significance  of  Scotomata  or  Defects  in  the  Visual  Field. — Dufour  was 
the  first  to  call  attention  to  the  great  difference  between  "  not  seeing  " 
(vision  nulle)  and  "  seeing  indistinctly  "  (vision  obscure).  If  the  visual 
defect  consists  of  a  simple  lack  of  perception  of  sight  (not  seeing), 
without  obscuration  of  the  affected  areas  in  the  visual  field,  the  trouble 
must  be  attributed  to  a  functional  or  anatomic  lesion  of  the  visual  center 
in  the  cortex.  Very  likely  the  patient  appreciated  it  for  the  first  time 
during  the  examination.  Should  the  patient,  on  the  contrary,  complain 
that  the  defect  in  the  visual  field  does  not  appear  to  be  complete, 
but  merely  an  obscured  area  (in  which  case  the  patient  is  annoyed 
by  this  condition  and  is  conscious  of  it),  we  should  then  naturally  con- 
clude that  the  visual  center  is  intact,  and  that  the  visual  defect  depends 
upon  some  involvement  of  the  visual  conducting  apparatus,  either  of  the 
refracting  media,  the  retina,  the  optic  nerve,  the  optic  tract,  or  the  visual 
fibers.  "  Seeing  indistinctly  "  is  nothing  more  than  the  reaction  of  the 
intact  visual  centers  to  a  faulty  transmission  of  optical  impulses  ;  whereas 
"  not  seeing  "  is  a  consequence  of  the  lack  of  optical  appreciation  of  the 
object  in  question,  and  naturally  it  occurs  only  in  functional  or  ana- 
tomic lesions  of  the  visual  center.  This  distinction  between  "  not  see- 
ing" and  "seeing  indistinctly"  is  of  importance  in  the  differential 
diagnosis  between  central  and  peripheral  hemiopia.  Thus,  the  observa- 
tion that  the  hemiopic  scotoma  in  scintillating  scotoma  or  in  ophthal- 
mic migrain  is  an  absolute  defect  and  not  an  obscuration  of  the  visual 
field  entirely  agrees  with  the  supposition  (probable  from  other  reasons) 
that  the  process  is  central  and  located  in  tlie  meninges  or  iu  the  cortex. 
Visual  Color  Fields. — We  are  often  assisted  in  the  diagnosis  of 
hysteric  and  other  neurotic  conditions  by  determining  the  visual  color 
fields.  These  are  frequently  contracted  and  their  sequence  disturbed. 
The  visual   field   for   blue   is   normally  the  largest ;    but  iu   the  above 


824 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


affections  we  frequently  find  that  other  colors  encroach  upon  its  borders. 
The  text-books  upon  eye  diseases  show  how  to  determine  these  con- 
ditions by  means  of  the  perimeter. 

Compare  section   4  for  the  typographic  diagnostic  significance  of 
defects  in  the  field  of  vision. 

3.  Ophthalmoscopic  Bxamination  (see  p.  703  et  seq.). 

4.  Topographic  Diagnosis  of  l/csions  in  the  Course  of  the 
Optic  Fibers. — Fig.  315  represents  diagrammatically  the  course  of 
the  optic  fibers  from  the  retina  to  the  occipital  lobes.     The  fibers  ari- 


Right 


f/opi.  deoct 


^^v^  tract,  opt.  f/exi 


PHmary_optic  center^  V^'fe''''^'^ 


corp-genicukft  ecct. 


CorteX'  occipit. 

Fig.  315.— Diagram  of  the  course  of  the  optic  fibers. 

sing  from  homonymous  retinal  halves  form  the  optic  tract  by  a  semi- 
decussation at  the  chiasm.  Then  they  proceed,  in  part  direct,  but 
mostly  indirect,  through  the  so-called  primary  optic  centers  to  the 
occipital  cortex. 

Without  further  explanation,  the  diagram  (Fig.  315)  makes  it  plain 
that  a  focal  lesion  (o)  of  the  optic  nerve  will  cause  unilateral  blindness ; 
a  lesion  (6  or  c)  in  front  or  behind  the  chiasm  will  cut  off  the  nasal 
halves  of  the  retina  and  produce  a  temporal  hemiopia  ;  a  lesion  (cZ,  e,  or/) 
will  cut  off  both  left-sided  retinal  halves  and  produce  a  homonymous 
right-sided  hemiopia. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


825 


Grasset  has  modified  Fig.  315  hypothetically  in  Fig.  316  m  order  to  explain 
the  occurrence  of  unilateral  blindness  from  a  lesion  in  the  extreme  posterior 
(sensory)  portion  of  the  internal  capsule.  This  condition  is  sometimes  observed 
instead  of  a  hemiopia.  For  the  sake  of  simplicity  the  optic  fibers  are  represented 
in  this  diagram  as  uninterrupted— i  e.,  the  primary  optic  centers  are  omitted. 
The  diagram  assumes  that  the  fibers  which  have  not  already  crossed  at  the 
chiasm  finally  decussate  between  the  corpora  quadrigemina  and  then  directly  return 
to  their  original  side  ;  both  a  and  b  are  supposed  to  be  situated  m  the  posterior 
part  of  the  internal  capsule.  Hence  a  lesion  in  the  internal  capsule  will,  accord- 
ing to  its  position,  produce  either  a  crossed  blindness— i.  e.,  amblyopia  (lesion  a) 
or  a  homonymous  hemiopia  (lesion  b).  Eecent  observations,  however,  seem  to 
prove  that  lesions  of  the  internal  capsule  probably  do  not  produce  hemiopic 


Posterior 
;=  corpora 
\guadrigemina 

\ 


Cortex  oc4npitxtlis 


FIG.  316.-Grasset's  modification  of  the  preceding  diagram:  T^f.  optic  fibers  are  depi^te^^^^^ 
plicity  sake,  as  if  they  were  uninterrupted,  without  intercalation  of  the  primary  optic  centers. 

disturbances  of  sight.  Henschen  has  recently  examined  the  innervation  of  the 
different  retinal  quadrants— t.  e.,  the  course  of  the  visual  fibers  of  each  retinal 
quadrant  in  the  trunk  of  the  optic  nerve  and  in  the  optic  tracts.  By  dividing 
the  retina  into  four  quadrants  with  a  vertical  and  a  horizontal  meridian  he  found 
that  the  visual  fibers  of  each  of  these  quadrants  run  as  a  compact  bundle  in  the 
optic  fibers. '  This  circumstance  can  sometimes  be  utilized  in  establishing,  by  aid 
of  an  exact  representation  of  the  visual  field,  a  local  diagnosis  of  peripheral 
interruptions  of  the  visual  fibers. 

The  following  diagrams  from  Henschen  ^  illustrate  this  point: 

5.  Detection  of  Simulated   Unilateral   Blindness.— Uni- 
lateral  blindness   is  quite   frequently  simulated.       Ordinarily  we  can 
1  See  Salomonsohn,  BeuUch.  med.  Woch.,  1900,  No.  xlii.,  p.  677. 


826 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


discover  it  very  readily  by  using  the  stereoscope.  The  instrument  is 
placed  in  front  of  the  two  eyes  ;  diiFerent  letters  are  arranged  so  as  not 
to  coincide  in  stereoscopic  union.  The  patient  cannot  recognize  to 
which  eye  the  individual  pictures  belong.  If,  now,  he  simulates  a  one- 
sided blindness,  the  simulation  is  evident,  because  he  reads  the  characters 
which  could  be  seen  only  by  the  supposedly  blind  eye  quite  as  well  as 


med. 


II. 


III. 


lot    ned. 


Fig.  317.— I.  The  four  retinal  quadrants :  To  the  left  is  the  position  in  cross-section  of  the  fibers 
in  the  vascular  part  (anterior)  of  the  optic  nerve.  The  shaded  parts  correspond  to  the  macula 
lutea— 1  e.,  the  transmission  of  central  vision.  The  arrows  show  the  way  the  retinal  quadrants 
correspond  to  the  individual  parts  of  the  optic  nerve.  This  arrangement  of  the  fibers  can  be 
similarly  made  out  at  the  part  of  the  optic  nerve  which  is  visible  to  the  ophthalmoscopic  (optic 
disk)  examination.    Mtcr-retinal  quadrants  with  uncrossed  fibers. 

II.  Cross-section  of  the  optic  nerve  in  the  non- vascular  (posterior)  portion.  Here  the  macular 
bundles  (represented  by  shading)  lie  in  the  center  of  the  nerve,  and  the  fibers  corresponding  to 
the  individual  retinal  quadrants  are  arranged  like  quadrants  about  an  imaginary  axis  running 
in  the  center  of  the  nerve. 

Explanation  of  the  terms  in  the  figure  :  The  fasciculus  dorsalis  cruciatus  corresponds  to  the 
internal  superior  retinal  quadrant.  The  fasciculus  ventralis  cruciatus  corresponds  to  the  in- 
ternal inferior  retinal  quadrant.  The  fasciculus  dorsalis  incruciatus  corresponds  to  the  external 
superior  retinal  quadrant.  The  fasciculus  ventralis  incruciatus  corresponds  to  the  external 
inferior  retinal  quadrant. 

The  figure  also  shows  that  the  quadrant  arrangement  is  retained  in  the  non-vascular  part  of 
the  optic  nerve— i.  e.,  by  imagining  the  quadrant  picture  of  the  retina  seen  from  in  front  (1)  with 
the  upper  end  of  the  vertical  meridian  rotated  outward  about  45°. 

III.  Cross-section  of  the  posterior  part  of  the  optic  tract :  P.F.,  Fibers  of  the  pupillary  reflex 
(see  p.  812  et  seq.).  Other  abbreviations  have  the  same  meaning  as  in  II.  The  four  quadrant 
bundles  are  bound  together  again,  but  still  distinct.  They  surround  the  shaded  bundle  in  the 
center,  which  corresponds  to  the  tract  of  the  macular  fibers.  The  arrangement  of  the  quadrant 
bundles  in  III.  is  very  similar  to  that  in  the  cross-section  II.,  except  that  the  pupillary  fibers  do 
not  appear  in  the  latter. 

the  other.  There  are,  however,  some  cases  of  hysteric  unilateral  blind- 
ness with  monocular  vision  which  are  really  not  simulated.  In  such 
cases  the  above  would  not  show  anything.  Appropriate  stereoscopic 
pictures  for  such  an  examination  with  the  stereoscope  will  be  found  at 
the  end  of  Dr.  M.  Burchardt's  treatise,  "  Practical  Diagnosis  of  Simula- 
tion" (Berlin,  Enslin,  1891). 

III.  IV.  VI.    CRANIAL  NERVES ;  THE  OCULAR  MUSCLES'  NERVES,  INCLUDING 
THE  SYMPATHETIC  ;    MOTOR  INNERVATION  OF  THE  EYE  REGION. 

J.    Functions  of  the  External  Ocular  Muscles. 

The  III.  cranial  nerve  (oculomotor)  supplies  the  following  muscles : 
Levator  palpabrse  superior,  rectus  superior,  rectus  inferior,  rectus  internal, 
and  oblique  inferior,  the  pupillary  sphincter,  and  the  muscles  of  accom- 
modation (both  the  latter  from  the  short  branch  of  the  ciliary  ganglion). 

The  IV.  cranial  nerve  (trochlear)  supplies  the  superior  oblique 
(trochlearis)  muscle. 

The  VI.  cranial  nerve  (abducens)  supplies  the  external  rectus  muscle. 

The  muscles  which  move  the  eyeball  have  the  following  functions  : 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  827 

I.  Internal  rectus  :  movement  of  the  eyes  inward  without  any  wheel 
motion. 

II.  External  rectus  :    movement  outward  without  wheel  motion. 

III.  Superior  rectus  :  movement  upward  and  inward  with  rotation 
of  the  upper  extremity  of  the  vertical  meridian  inward. 

IV.  Inferior  oblique  :  movement  downward  and  outward  with  rota- 
tion of  the  upper  extremity  of  the  vertical  meridian  outward. 

V.  Inferior  rectus  :  movement  downward  and  inward  with  rotation 
of  the  upper  extremity  of  the  vertical  meridian  outward. 

VI.  Superior  oblique  :  movement  downward  and  outward  with 
rotation  of  the  upper  extremity  of  the  vertical  meridian  inward. 

The  external  and  internal  recti  suffice  for  directing  the  eyes  in  the 
horizontal  axis,  but  movement  in  the  vertical  axis  (upward  and  doM^n- 
ward)  requires  the  joint  action  of  one  rectus  and  one  oblique.  The 
principal  function  of  the  obliques  is,  therefore,  to  limit  the  tendency  to 
wheel  rotation  of  the  eye,  which  would  take  place  without  their  action. 
Any  vision  directed  obliquely  between  the  vertical  and  the  horizontal 
axes  necessitates  the  joint  action  of  three  different  muscles.  One  of 
them  acts  to  counteract  the  tendency  to  wheel  rotation. 

2.   Paralysis  of  the  Muscles  which  Move  the  Eyeball. 

The  disturbances  of  function  which  may  result  from  a  paralysis  of 
the  eye  muscles  can  be  essentially  determined  from  the  preceding 
description  of  their  function.  If  one  or  more  muscles  of  the  eye  are 
paralyzed,  the  eye  will  remain  immobile  when  attempting  to  follow  the 
direction  of  vision  ordinarily  accomplished  by  the  muscles  affected. 
To  demonstrate  readily  the  existence  of  a  paralysis  of  the  eye  muscles, 
the  patient  should  follow  with  his  eyes  (but  with  the  head  absolutely 
fixed)  the  movement  of  the  examiner's  finger  in  every  direction,  while 
the  examiner  compares  the  excursions  of  the  two  eyes.  This  is  easily 
accomplished  by  observing  the  position  of  the  corneal  margin  in  rela- 
tion to  the  angle  of  the  eye,  a  procedure  generally  sufficient  for  a  hasty 
test.  A  slight  paresis  may,  however,  be  hidden  by  the  tendency  such 
a  patient  has  to  fuse  the  double  images.  Therefore,  in  any  doubtful 
case,  it  is  well  to  test  each  eye  alone,  covering  the  other  eye.  A  slight 
weakness  will  sometimes  be  disclosed  by  having  the  patient  attempt  the 
extreme  positions,  and  then  observing  either  that  the  position  cannot 
be  retained  for  any  length  of  time  or  else  that  it  produces  an  accom- 
panying tremor  of  the  globe  (nystagmus),  although  the  weakness  is  not 
sufficient  to  diminish  the  size  of  the  excursions.  In  testing  the  internal 
recti  we  must  especially  note  their  behavior  in  attempted  convergence 
of  the  eye  (see  p.  836). 

In  complicated  muscular  paralyses  of  the  eyes  it  is  often  difficult  to 
forrii  a  judgment  as  to  the  function  of  the  oblique  muscles,  because  they 
are  in  such  intimate  association  with  the  recti.  In  such  a  case,  and 
especially  in  distinguishing  the  more  delicate  disturbances  of  the  eye 
movements,  testing  the  torsion  of  the  eyeball  is  es])ecially  significant. 
If  the  eyeball  moves  normally,  no  axial  deviations  occur,  because  the 


828  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

axial  deviating  components  common  to  all  the  eye  muscles,  excepting- 
the  external  and  internal  recti  (p.  827),  are  counteracted  by  the  asso- 
ciated action  of  the  other  muscles.  Just  as  soon  as  this  extremely 
finely  balanced  associated  action  of  the  eye  muscles  is  injured  by  the 
paralysis  of  such  muscles  as  possess  axial  deviating  components,  axial 
deviations  of  the  bulb  must  ensue.  The  determination  of  such  axial 
deviations  or  movements  of  rotation  in  a  definite  visual  direction,  and 
the  ascertaining  which  muscles  are  responsible,  permit  conclusions  in 
regard  to  the  finer  defects  of  movement.  These  cannot  be  made  out 
in  an  examination  of  the  gross  excursions  of  the  eyeballs,  for  in  com- 
plicated paralyses  it  is  especially  difficult  to  recognize  the  functions  of 
the  obliques  in  the  movements  of  the  eyeball,  because  the  direction  in 
which  these  muscles  pull  is  affected  by  the  action  of  the  two  recti 
muscles.  In  order  to  draw  diagnostic  conclusions  concerning  rotation 
it  is  only  necessary  to  keep  in  mind  that  rotation  with  a  tendency  of 
the  upper  extremity  of  the  vertical  meridian  inward,  depends  upon 
the  superior  rectus  and  the  superior  oblique,  while  the  reverse  rotation 
depends  upon  the  inferior  rectus  and  the  inferior  oblique.  If  a  rotation 
occurs  in  any  individual  movement  of  the  eye,  we  naturally  infer  that 
the  fault  depends  upon  the  muscle,  which  by  its  help  should  prevent 
such  rotation,  and  which,  unaided  and  unopposed,  would  accomplish 
the  opposite  rotation.  We  test  rotation  by  having  the  patient  look 
upward  and  outward,  and  then  downward  and  outward.  While  looking 
upward  and  outward,  rotation  of  the  right  eye  in  the  direction  of  the 
hands  of  a  clock  (as  seen  by  the  examiner)  signifies  paresis  of  the 
inferior  oblique  and  preservation  of  the  superior  rectus ;  while  looking 
downward  and  outward,  a  similar  rotation  signifies  paresis  of  the  inferior 
rectus  with  intact  superior  oblique. 

More  pronounced  paralyses  of  the  eye  muscles  are  also  evidenced  by 
strabismus  {paralytic  squinting,  paralytic  strabismus).  Paralytic  stra- 
bismus can  be  differentiated  from  concomitant  strabismus  by  the  fact 
that  in  the  former  a  deviation  of  the  eyeball  from  the  normal  reciprocal 
position  shifts  with  the  direction  of  vision,  whereas  in  concomitant  stra- 
bismus it  remains  the  same  in  every  direction  of  vision. 

Patients  with  paralyses  of  the  eye  muscles  ordinarily  complain  of  double 
vision;  hence  the  existence  of  diplopia  and  its  peculiarities  may  be  utilized  for 
diagnosis.  For  this  purpose  it  is  essential  to  know  to  which  eye  each  one  of  the 
double  pictures  belongs.  This  is  determined  most  readily  by  putting  before  the 
patient's  eyes  differently  colored  glasses,  which  may  be  conveniently  slipped  into 
the  spectacle  frame  used  by  ophthalmologists.  From  the  patient's  statements  as 
to  the  color  of  the  pictures,  it  is  easy  to  determine  the  eye  to  which  each  of  the 
double  pictures  belongs.  In  many  cases,  especially  in  old  paralyses,  double 
vision  is  first  discovered  by  making  use  of  these  colored  glasses,  whereas  -ndthout 
this  device  patients  disregard  one  of  the  pictures — i.  e.,  they  no  longer  see  it. 
It  is  quite  possible,  without  the  colored  glasses,  to  determine  to  which  eye  each 
of  the  double  pictures  belongs,  by  covering  one  of  the  patient's  eyes,  and  then 
having  him  say  which  of  the  pictures  disappears.  In  paralyses  of  the  eye  mus- 
cles which  act  horizontally,  the  double  pictures  will  stand  side  by  side.  These 
we  call  crossed  double  pictures  (crossed  double  vision),  if  the  picture  lying  to  the 
left  (from  the  patient)  belongs  to  the  right  eye.      On  the  contrary,  we  speak  of 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


829 


homonymous  or  non-crossed  double  pictures,  if  the  left  picture  belongs  to  the  left 
eye.  In  accordance  with  well-known  physiologic  laws  of  projection,  the  appre- 
ciated picture — that  is,  the  projection  of  the  retinal  picture  in  space — seems  to  be 
inverted.  Hence  homonymous  or  non-crossed  double  pictures  depend  upon  a  cross- 
ing of  the  visual  axes  in  front  of  the  object — i.  e.,  upon  convergence;  or,  in  other 
words,  upon  abducens  paralysis.  On  the  contrary,  non-homonymous  or  crossed 
double  pictures  depend  upon  divergence  of  the  visual  axes — i.  e.,  paralysis  of  one 
or  both  internal  recti.  The  following  laws  of  double  vision  are  applicable  for 
diagnostic  use.  They  depend  upon  the  fact  that  the  projection  of  the  retinal 
pictures  in  space  seems  to  be  inverted,  just  as  does  the  corresponding  eye  : 

(1)  That  eye  is  paralyzed  whose  image  appears  to  be  deviated  from  that  of 
the  other  in  any  one  direction  of  vision;  and  (2)  the  paralysis  involves  the  muscle 
or  muscles  in  whose  direction  of  pulling,  projected  into  space,  the  deviated 
picture  appears  to  move  when  the  direction  of  vision  is  altered. 

In  examining  for   double   vision,  it   is  useful   to  know  that  many  cases  see 
double  only  objects  which  are  at  a  considerable  distance  from  the  eye,  perhaps 
because  the  effort  of  accommodation  in  focusing  at  a  near  distance  simplifies  and 
disregards  the  second  indefinite 
picture.     It  is  also  important  ^  „nrt*' 

to  remember  that  double  pic- 
tures separated  but  little  from 
one  another  are  frequently  not 
recognized  as  such  by  the  pa- 
tient, but  are  described  by  him 
as  "ialurred" — i  e.,  obscure — 
vision.  Closing  one  eye  im- 
proves the  patient's  vision  in 
this  type  of  disturbance. 

Besides  double  vision,  pa- 
tients with  paralysis  of  the  eye 
muscles  very  frequently  com- 
plain of  vertigo  (ocular  ver- 
tigo), and  disturbances  of  equi- 
librium in  walking  and  stand- 
ing (see  p.  882).  This  is  psy- 
chical, and  depends  upon  dis- 
turbances of  orientation  in 
space.  According  to  the  au- 
thor's experience,  ocular  ver- 
tigo depends  principally  upon 
paralysis  of  the  ocular  mus- 
cles which  rotate  the  eyeballs; 
whereas  mere  paralysis  of  the 
abducens  and  internal  recti  or- 
dinarily causes  no  vertigo.  This 
is  comprehensible  without  fur- 
ther explanation;  for,  despite  the  diplopia,  the  patient  with  these  latter  paralyses 
sees  objects  at  least  in  normal  vertical  orientation;  whereas  in  paralysis  leading 
to  rotation,  objects  appear  upside  down.  Ocular  vertigo  differs  from  other  kinds 
of  vertigo,  inasmuch  as  it  disappears  upon  closing  the  eyes. 

If  the  paralysis  is  simple,  and  especially  if  it  is  unilateral,  the  diagnostic  laws 
concerning  the  significance  of  the  kind  of  double  pictures  mentioned  above  easily 
lead  to  a  diagnosis;  but  in  complicated  binocular  paralysis  the  recognition  of  the 
paralyzed  muscles  from  the  double  pictures  alone  is  often  very  difticult.  Here 
one  of  the  most  reliable  methods  is  to  determine  the  fields  of  vision  by  means  of 
the  perimeter.  It  is  merely  an  improved  method  of  testing  the  excursions  of  the 
eyebulb  in  various  directions,  and  is  accomplished  by  fixing  the  head  by  means 
of  the  perimeter,  and  estimating  those  points  in  the  instrument  which  can  be 
directly  (centrally)  seen — i.  e.,  at  which  fine  type  can  still  be  read. 


Decussation-  in  Ihs 
Teginefitum.- 


Ter^hend  fibers 


Fig.  318.— Diagram  of  the  bilateral  central  innerva- 
tion of  the  nerves  to  the  eye  muscles  and  most  of  the 
remaining  motor  cranial  nerves :  The  focus  x  causes  no 
evident  paralysis,  because  the  tracts  of  the  opposite  side 
remain  intact ;  the  lesion  v  would,  however,  and  so  would 
lesions  x  and  s  together.  Simultaneous  lesions  in  the  latter 
places  {x  and  z)  cause  so-called  bulbar  paralysis  (p.  878). 


830 


EXAMINATION   OF  THE  NERVOUS  SYSTEM. 


Monocular  double  vision,  whicti  is  not  uncommon  in  hysteric  conditions,  must 
not  be  confused  with  binocular  diplopia  occasioned  by  paralyses  of  the  muscles  of 
the  eye.  The  former  is  often  attributed  to  a  partial  spasm  of  the  ciliary  muscle, 
in  consequence  of  which  a  portion  of  the  lens  acts  as  a  prism  and  produces  a 
second  picture  upon  the  retina.  This  theory  is  probably  incorrect,  for  certainly 
it  will  not  apply  to  many  cases;  in  those  which  the  author  himself  has  observed 
the  monocular  diplopia  was  evidently  a  purely  psychical  phenomenon.  Monocular 
diplopia  is  therefore  a  stigma  of  hysteria,  and  it  is  important  to  bear  this  in  mind, 


Fig.  319.— Unilateral  ptosis  (New  York  City  Hospital). 

in  any  instance  of  double  vision,  before  making  a  diagnosis  of  ocular  muscle 
paralysis,  which  causes  only  binocular  diplopia. 

The  diagnostic  importance  of  ocular  muscle  paralysis  is  considerable, 
because  experience  has  shown  that  it  almost  always  depends  upon  a 
lesion  of  the  peripheral  motor  neurons — i.  e.,  the  subnuclear  fibers,  or 
the  nuclear  region  itself — and  practically  never  upon  a  supranuclear 
lesion,  or  a  lesion   of  the  central  fibers.     As  each  one  of  the  ocular 


EXAMINATION  OF  THE  NEEVOUS  SYSTEiM.  831 

nerve-muscles  must  possess  a  central  tract  running  to  the  cortex,  this 
peculiarity  demands  explanation.  This  may  be  given  by  the  supposi- 
tion that  the  nuclei  of  the  ocular  muscles  are  innervated  not  by  one, 
but  by  both  hemispheres.  Fig.  318  readily  explains  why  a  unilateral 
hemisphere  lesion,  even  if  it  destroys  the  central  libers,  causes  no  appar- 
ent paralysis  of  the  corresponding  eye  muscle ;  although  a  portion  of 
the  innervation  for  both  sides  is  aflPected,  the  intact  hemisphere  appar- 
ently furnishes  sufficient  innervation  for  both  sides.  Therefore,  since 
there  is  no  method  of  measuring  the  absolute  power  of  the  muscles,  the 
bilateral  defect  of  innervation  escapes  observation.  When  the  lesion, 
even  though  small,  occurs  at  y,  in  the  region  of  the  nucleus  or  below  it, 
all  the  fibers  are  interrupted.  Still  another  circumstance  may  aid  in 
preventing  the  occurrence  of  a  muscle  paralysis  in  unilateral  supra- 
nuclear lesions  of  the  hemisphere ;  it  is  possible  that  the  central  fibers 
do  not  run  as  compactly  as  is  represented  in  the  figure,  but  are  dis- 
tributed over  different  points  of  the  cortex,  so  that  a  circumscribed  lesion 
could  not  very  easily  destroy  many  of  them. 

On  the  contrary,  in  bilateral  hemispheric  lesions  or  in  excessive  superficial 
affections  of  the  two  sides  of  the  brain  (meningitis,  etc.),  bilateral  ocular  muscle 
paralyses  may   occur   as   "pseudobulbar"   paralyses   (p.    876  et  seq.).     A  few 


Fig  320.— Bilateral  ptosis,  normal  position  (Neurologic  Department,  Massachusetts  General 

Hospital). 

examples  in  which  with  unilateral  cortical  lesions,  contrary  to  ordinary  experi- 
ence, isolated  crossed  ocular  muscle  paralyses  have  been  discovered — /.  e.,  ptosis — 
are  explained  by  assuming  that  in  many  individuals  the  bilateral  hemispheric 
innervation  is  insufficiently  developed,  or  that  the  central  fibers  are  more  compact 
in  their  course  and  localized.  The  parietal  k>be  has  been  found  to  have  suffered 
in  these  few  cases  of  central  ocular  muscle  paralyses.  This  will  be  discussed  upon 
p.  834  along  with  the  localization  of  the  center  for  conjugate  ocular  movements 
(see  Fig.  339,  p.  884). 


832  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

In  paralyses  of  the  ocular  muscles  one  can  therefore  generally  exclude 
supranuclear  causes,  so  that  a  diagnosis  of  the  situation  of  the  lesion  is 


FiQ.  321. — Bilateral  ptosis,  showing  effort  to  open  eye,  using  muscle  of  forehead  (Neurologic 
Department,  Massachusetts  General  Hospital). 

for  the  most  part  limited  to  a  distinction  between  a  nuclear  and  a  sub- 
nuclear  type.     This  differentiation  in  the  case  of  the  oculomotor  is  fre- 


FlG.  322.— Bilateral  ptosis,  showing  effort  to  open  mouth  (Neurologic  Department,  Massachusetts 

General  Hospital. 

quently  simple,  because  in  subnuclear — i.  e.,  entirely  peripheral — paral- 
ysis the  nerve  is  affected  almost  always   as   an  entirety ;  whereas   in 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  833 

nuclear  paralyses  the  separate  functions  of  the  nerve  can  be  affected,  so 
to  speak,  individually,  since  the  oculomotor  nucleus  is  anatomically 
situated  in  functionally  different  areas.  Especially  characteristic  for 
most  nuclear  paralyses  is  the  non-involvement  of  the  pupillary  and 
accommodation  fibers  of  the  oculomotor.  The  following  plan,  copied 
from  Kahler  and  Pick,  presents  the  anatomic  arrangement  of  the  different 
parts  of  the  oculomotor  nucleus  and  their  relations  to  the  neighboring 
trochlear  nuclei.  Its  study  will  facilitate  a  more  exact  local  diagnosis 
in  nuclear  paralyses. 

Anatomic  Arrangement  of  the  Different  Components  of  the  Oculomotor  Nucleus. 
[Anterior  (proximal).] 

1.  Accommodation. 

2.  Sphincter  iridis. 

!3.  Rectus  intei-nus.  5.  Levator  palpebrse  superioris.  ^ 

6.  Rectus  superior.  >•  Lateral. 

4.  Rectus  inferior.  7.  Obliquus  inferior.  J 

Trochlearis. 
[Posterior  (distal).] 

3.  Ptosis,  Including  So-called  Sympathetic  Ptosis. 

By  ptosis  is  meant  a  paralytic  drooping  of  the  upper  eyelid  so  that 
the  lid  covers  the  eyeball  more  or  less  completely  and  thereby  narrows 
the  ocular  aperture.  Ptosis  ordinarily  results  from  paralysis  of  the 
levator  palpebrae  superioris,  supplied  by  the  oculomotor.  (See  below. 
Sympathetic  Ptosis.)  In  this  connection  it  is  necessary  to  differentiate 
paralytic  ptosis  from  a  spasmodic  condition  of  the  orbicularis  oculi  by 
which  the  upper  lid  is  drawn  down  over  the  eye  and  the  ocular  aperture 
narrowed.  The  distinction  is  usually  easy.  In  the  former,  paralytic 
or  true  ptosis,  the  excursion  of  the  upper  lid  upward  is  diminished  if 
not  entirely  prevented ;  whereas  in  a  spasm  of  the  orbicularis  this  need 
not  be  the  case.  In  a  spasm  of  the  orbicularis,  moreover,  the  w^'inkles 
about  the  eye  are  ordinarily  more  prominent,  and  the  eyebrow'  is  placed 
lower  than  upon  the  normal  side ;  whereas  in  paralytic  ptosis  the  eye- 
brow, by  means  of  its  innervation  by  the  facial,  seems  instinctively 
elevated  higher  than  normal  to  counterbalance  the  defect. 

The  so-called  sympathetic  ptosis,  which,  was  first  described  by  Homer  in  1869, 
must  not  be  confused  with  ptosis  due  to  paralysis  of  the  levator  palpebrse.  Here, 
although  the  lid  aperture  of  the  affected  side  is  narrower  than  upon  the  healthy 
side  and  its  upper  lid  hangs  lower,  it  can  be  demonstrated  that  the  excursions  of 
the  levator  palpebrse  are  in  no  way  diminished;  but  the  eyeball  often  seems 
sunken  into  the  orbital  cavity,  the  pupil  is  ordinarily  somewhat  narrowed,  and 
frequently  abnormalities  of  the  sweat  secretion  and  of  the  vascular  innervation 
appear  upon  the  affected  side  of  the  face.  This  symptom-complex  depends  upon 
a  paralysis  of  the  so-called  Miiller  muscle  (supplied  by  the  sympathetic),  com- 
prising the  smooth  muscle  fibers  of  the  superior  oblique,  inferior  oblique,  and 
orbitalis.  Stimulation  of  the  two  former  widens  the  lid  aperture;  stimulation  of 
the  latter  projects  the  eyeball  somewhat  forward  from  the  orbit.  A  paralysis  of 
these  fibers  causes  a  diametrically  opposite  api)earance  of  the  eyes  to  that  in 
Graves's  disease  (exophthalmos)  (Grafe's  symptom,  see  p.  838).  This  latter 
symptom  is  to  be  attributed  to  an  irritation  of  these  smooth  muscles. 

53 


834  EXAMI^^ATION  OF  THE  SERVO  US  SYSTEM. 

Congenital  ptosis,  which  is  not  very  rare,  is  partly  sympathetic  in  nature,  and 
partly  dependent  upon  a  congenital  (nuclear)  paralysis  of  the  levator  palpebrse 
superioris. 

4.  Conjugate  Paralyses  and  Conjugate  Deviation  of  the  Eyes, 

The  so-called  conjugate  eye  paralysis  will  be  discovered  in  a  binocular 
examination  for  the  mobility  of  the  eyes  (described  above)  by  means  of 
fixation  upon  a  finger  held  in  front.  It  occurs  in  cerebral  diseases,  and 
consists  of  weak,  deficient,  or  absent  mobility  of  the  two  eyes  to  the 
same  side.  These  conjugate  paralyses  are  usually  due  to  a  lesion  situ- 
ated in  a  tract  which  leads  possibly  from  the  middle  portion  of  the 
frontal  lobe,  adjacent  to  the  anterior  central  convolution,  to  the  nucleus 


jVuc/eeisoft/t£  _^//m  I  iS\\ 
irvl.redusmusele.'n    \ |/     \\ 

Nucleus  afthe  J  {    ^/iv      )\ 
Alducensm    ^~^    |    ^— ^  VT 

Fig.  323. — Diagram  of  the  tracts  for  the  associated  lateral  moTements  of  the  eyes  :  The  upper 
half  of  the  diagra'm,  as  far  as  the  decussation 'at  upper  edge  of  the  pons  i,  is  to  be  regarded  as  a 
frontal  section :  the  lower  half  of  the  diagram  (the  pons ),  as  a  horizontal  section  through  the 
brain.  The  heavier  of  the  two  pairs  of  lines  w-hich" intersect  each  other  represents  the  central 
tract  of  the  abducens  :  the  lighter,  the  central  tract  of  the  internal  rectus  of  the  opposite  side. 
In  conformity  with  an  incorrect  conception,  this  diagram  represents  the  infraparietal  lobe  not 
only  as  giving  passage  to  innervating  fibers,  but  also  as  the  center  for  innervation  of  ocular 
movements. 

of  the  abducens  of  the  opposite  side  and  to  the  nucleus  of  the  rectus 
internus  of  the  same  side.  They  may  probably  also  be  due  to  a  lesion 
in  a  fasciculus  which  is  situated  in  the  infraparietal  lobe  and  connects 
the  centers  for  ocular  movement  with  the  center  for  the  optic  nerve 
(Landouzy  and  Wernicke).  Fig.  323  is  a  schematic  representation  of 
the  course  of  this  tract  based  upon  pathologic  findings  (Leichtenstern- 
Hunnius),  and  conforms  to  the  old  view  now  proven  to  be  incorrect, 
that  the  infraparietal  lobe  not  only  gives  passage  to  innervating  fibers, 
but  is  also  the  center  for  the  innervation  necessary  for  ocular  move- 
ments. It  will  be  seen  that  the  fibers  for  the  rectus  internus,  instead 
of  passing  directly  to  this  nucleus,  take  a  circuitous  course  through  the 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


835 


region  of  the  opposite  abdacens  nucleus,  and  that  the  entire  tract 
decussates  in  the  anterior  half  of  the  pons. 

In  order  to  explain  the  way  in  which  this  tract  can  be  affected  by 
cerebral  lesions  at  different  locations,  it  is  best  to  simplify  the  diagram, 
as  in  Fig.  324.  The  arrows  mean  that  the  tract  proceeding  from  the 
left  hemispheric  cortex  supplies  the  lateral  movements  of  the  eyes  to  the 
right ;  the  tract  from  the  opposite  side,  those  to  the  left.  With  this 
explanation  it  is  easy  to  understand  that  a  lesion  (x)  above  the  pons 
will  prevent  the  movements  of  the  eyes  to  the  side  opposite  the  lesion, 
while,  on  the  contrary,  a  lesion  (^y)  below  the  upper  edge  of  the  pons 
will  paralyze  the  movements  of  the  eyes  to  the  same  side  as  the  lesion. 

Since  conjugate  paralyses  are  ordinarily  combined  with  a  conjugate 
deviation  of  both  eyes  to  the  side  of  the  non-paralyzed  antagonists, 


Fig.  324. — The  same  diagram  simplified, 


with  a  lesion  x  (Fig.  324)  an  ocular  deviation  to  the  right  will  be  noted, 
and  with  a  lesion  y  one  to  the  left.  Briefly,  in  lesions  above  the  pons 
the  patient  looks  toward  his  cerebral  lesion  ;  whereas  in  lesions  of  the 
pons  and  below  the  pons  he  looks  away  from  it. 

Conjugate  paralysis  with  deviation  of  the  eyes  occurs  in  cerebral 
lesions,  especially  hemiplegia  (hemorrhage,  softening).  Like  hemiplegic 
paralyses  of  the  extremities,  it  is  frequently  an  indirect  focal  symptom, 
depending  upon  lesions  located  at  various  points,  and  then  generally 
soon  disappearing  with  the  subsidence  of  the  remote  action.  In  some 
cases,  however,  the  persistence  of  the  hemi])legia  proves  that  the  entire 
unilateral  voluntary  tract  is  destroyed,  and  with  it  the  accompanying 
conjugate  ocular  tract  running  through  the  internal  capsule,  and  yet  the 
conjugate  ocular  paralysis  gradually  di.~appears.     We  are  compelled  to 


836 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


assume,  therefore,  that,  although  most  of  the  tract  decussates,  there 
must  exist  in  the  other  hemisphere  an  uncrossed  tract,  possessed  of  the 
same  function,  which  in  apoplexy  is  affected  more  or  less  strongly  by 
the  remote  action,  but  which,  after  the  subsidence  of  the  apoplexy,  can 
take  the  place  of  the  aifected  crossed  tract.  Fig.  324  must  therefore 
be  modified  in  accordance  with  this  theory,  as  in  Fig.  325.  Naturally  it 
may  also  be  inferred  that  the  vicarious  action  of  the  healthy  hemisphere 
can  be  improved  by  constant  use. 

Besides  being  due  to  paralysis,  conjugate  deviation  of  the  eyes  may 
result  from  spasmodic  action.     This  cause  may  be  assumed  when  we 


J^r  the  nwoement 
of  the  eyes  to  tke  tt'jfkt.. 

Fig.  325.— The  same  diagram  modified  to  include  the  uncrossed  vicarious  innervation. 

note  the  existence  of  similar  spasms  in  other  muscles  upon  the  side 
of  the  deviation.  The  local  diagnostic  conclusions  from  the  direction 
of  the  deviation  are  then  naturally  simply  reversed. 

5.  Paralysis  and  Weakness  of  Converging  Movements  of  the  Eyes. 

Convergence  of  the  eyeballs  requisite  for  binocular  vision  of  near  objects  is 
naturally  affected  or  rendered  impossible  by  paralysis  of  one  or  both  internal 
recti.  However,  characteristic  conditions  also  do  occur  in  which  the  internal 
recti  functionate  normally  for  all  conjugate  lateral  movements  of  the  eyes,  but 
not  for  converging  movements.  Such  observations  have  led  to  the  assumption 
of  a  separate  convergence  center  localized,  it  seems  probable,  in  the  pons.  Its 
existence  is  still,  however,  problematic,  because  isolated  convergence  paralysis 
could  quite  as  well  depend  upon  the  paralysis  of  a  special  tract  supplying  each 
internal  rectus  as  upon  the  lesion  of  a  center.  A  lesion  of  a  central  tract--/,  e., 
a  supranuclear  oculomotor  and,  naturally,  a  bilateral  convergence  tract — different 
from  the  tract  for  the  conjugated  movements  of  the  eyes  (Fig.  323)  would  explain 
the  peculiarity.     The  only  thing  which  seems  to  be  certain  (and  this  was  con- 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


837 


firmed  by  one  of  the  author's  autopsies  upon  a  tumor  of  the  pons)  is  that  conver- 
gence can  be  paralyzed  by  a  lesion  of  the  pons,  while  the  other  movements  (con- 
jugate, see  p.  834  ef  seq.)  of  the  internal  recti  remain  intact.  In  this  sense  the 
symptom  can  be  utilized  for  local  diagnosis. 

Without  characteristic  and  complete  paralysis,  a  mere  weakness  and  insulfi- 
ciency  of  convergence  may  be  of  considerable  diagnostic  importance  in  neuras- 
thenic conditions  and  in  exophthalmic  goiter.  In  the  latter  this  phenomenon  is 
called  Mobius's  symjitom.  Insufficiency  of  convergence,  which  occurs  also  in 
myopia,  is  experienced  subjectively  by  the  appearance  of  the  so-called  asthenopic 
difficulties,   by  a  sense  of  fatigue,  by  obscure  and  double  vision  when  steadily 


Fig.  326.— Exophthalmic  goiter,  showing  exophthalmos  anrl  goiter  (Dr.  .1.  J.  Putnam,  Massa- 
chu.setLs  General  Mus[)ital). 

looking  at  near  objects,  and,  on  the  other  hand,  objectively  confirmed  by  the 
exhibition  of  latent  external  stral)ismus  for  near  vision.  This  latent  external 
strabismus  appears  when  the  binocular  focusing  power  fails,  and  can  be  demon- 
strated by  fixing  the  glance  ujxm  a  near  ol)ject — e.  f/.,  25  cm. — and  then  sud- 
denly covering  one  eye  with  the  hand.  With  insufficient  convergence  the  covered 
eye  will  noticeably  deflect  outward,  since  the  cff'ort  for  convergence  has  become 
unnecessary.  In  spite  of  such  subjective  and  objective  confirmation  of  insuffi- 
ciency of  convergence,  the  degree  of  convergence  which  is  transitorily  accom- 
plished by  vigorous  voluntary  impulse  is  in  such  cases  oftentimes  considerable,  so 
that,  according  to  the  author's  experience,  the  Landolt  ophthalmodynamometer 
does  not  suffice  to  demonstrate  the  insufficiency  in  exophthalmic  goiter. 


838  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

6.  Nystagmus. 

In  examination  of  the  eyes  one  must  always  be  on  the  lookout  for 
nystagmus,  by  which  is  understood  a  rhythmic  oscillation  of  the  eye- 
ball, especially  marked  when  the  eyes  are  in  an  extreme  position.  It 
is  much  more  commonly  a  lateral  than  a  vertical  movement.  It  is 
generally  an  intention  tremor.  It  frequently  occurs  associated  with 
paralysis  of  the  eye  muscles  (see  p.  827),  and  without  demonstrable 
paresis  in  many  affections  of  the  eye  and  of  the  brain,  most  commonly, 
however,  in  multiple  sclerosis.  The  neurodiagnostic  importance  of 
nystagmus  is  not  so  great  as  has  been  supposed,  because  it  occurs  in  all 
sorts  of  ophthalmologic  affections,  especially  in  those  in  which  early  in 
life  the  sight  is  quite  defective — e.  g.,  in  corneal  opacity,  in  cataract, 
either  congenital  or  early  acquired,  in  congenital  iridochoroiditis  and 
retinitis  pigmentosa,  in  coloboma  of  the  choroid  and  of  the  retina,  and 
finally  in  albinismus.  [Oftener  than  true  nystagmus  in  these  last- 
named  conditions,  we  encounter  irregular  twitching  movements  of  the 
eyeballs,  to  which  the  designation  nystagmiform  movements  is  given. 
—Ed.] 

7.  Contractions  of  the  Ocular  Muscles. 

A  contraction  of  certain  of  the  external  ocular  muscles,  evidenced  by  anom- 
alous positions  of  the  eyeball,  plays  a  part  of  some  importance  in  hysteria.  These 
positions  change  so  constantly  that  it  is  impossible  to  confuse  them  with  paralyses 
or  with  concomitant  strabismus  ;  besides,  in  hysteria,  as  contrasted  with  the  latter 
condition,  a  voluntaiy  movement  fails  to  alter  to  any  considerable  extent  if  at  all 
the  position  of  the  deviated  eye  in  relation  to  the  lid  aperture.  The  history  will 
generally  aid  in  any  doubtful  case.  A  differential  diagnosis  between  spasm  and 
paralysis  might  be  difficult  in  some  instances  unless  the  pressure  of  contracture 
in  an  adjoining  muscle  (facial  spasm,  blepharospasm)  should  decide  the  question. 

(Compare  p.  836  in  regard  to  conjugate  deviation  of  both  eyes  as  a  spastic 
phenomenon.) 

The  so-called  "  Grafe's  sign,"  which  occurs  in  exophthalmic  goiter, 
is  probably  to  be  regarded  as  a  spasmodic  contractui*e  of  the  sympathetic 
superior  oblique  muscle  (p.  833).  This  sign  gives  the  patient  with 
exophthalmic  goiter  a  very  characteristic  appearance,  and  is  of  con- 
siderable diagnostic  importance.  It  is  elicited  by  having  the  patient 
look  down  gradually  ;  as  the  eyeball  lowers,  it  is  noticed  that  the  upper 
lid  does  not  follow  the  movement  of  the  eyeball,  but  either  remains 
still  or  only  moves  slightly,  thus  exposing  a  more  or  less  broad  band  of 
sclera  between  the  cornea  and  the  upper  lid.  For  its  demonstration  it 
is  important  to  avoid  a  dazzling  light,  because,  apparently  for  protection, 
this  seems  to  furnish  sufficient  stimulus  to  enable  a  patient  to  overcome 
the  phenomenon. 

8.  The  Pupillary  Phenomena. 

Diagnostically  these  are  of  the  greatest  importance. 

Diameter  of  the  Pupils. — The  size  of  the  pupils  varies  with  the 
illumination.  It  is  best  to  observe  them  in  illumination  of  medium 
intensity.  In  doubtful  cases  we  should  compare  the  pupils  of  the 
patient  with  those  of  a  healthy  man  under  the  same  light  conditions. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  839 

Schirmer*  found  that  the  diameter  of  the  puijil  under  physiologic  conditions 
varies  greatly  in  different  individuals,  and  particularly  at  different  ages.  In  an 
individual  case,  however,  the  diameter  is  constant  for  wide  ranges  of  illumination 
(from  100  to  1100  meter-candles),  provided  that  the  observation  be  made  after 
the  eye  has  fully  adapted  itself  to  the  particular  illumination,  as  it  does  within 
a  few  minutes.  If  we  bear  this  fact  in  mind  in  estimating  the  diameter  of  the 
pupil,  we  are  to  a  certain  extent  independent  of  the  existing  degree  of  illumina- 
tion. This  diameter  of  the  pupil,  determined  several  minutes  after  full  adapta- 
tion, must  consequently  be  employed  as  a  basis  for  the  recognition  of  pathologic 
variations.  Schirmer  obtains  the  necessary  degree  of  illumination  of  100  to  1100 
meter-candles  by  placing  the  jjatient  within  one  meter  of  a  window  which  is  well 
illuminated  by  the  sun,  and  yet  not  exposed  to  direct  sunlight.  The  pupillary 
diameter  is  then  determined  Avhile  the  patient  relaxes  his  accommodation  and 
convergence  by  looking  at  some  distant  object.  Schirmer  states  that  the  observa- 
tion should  not  be  made  when  passing  clouds  are  present,  since  the  illuminatioa 
will  vary  and  may  be  less  than  100  meter-candles.  Tange  found  by  observing 
these  conditions  that  the  pupillary  diameter  varied  between  2  and  4  mm.,  being 
dependent  upon  age,  refraction,  and  sex,  and  that  in  the  majority  of  cases  it  waj 
between  2. 5  and  3  mm.  In  advanced  life  the  pupil  is  usually  smaller  than  in 
youth. 

Pupillary  narrowing  (myosis)  is  found  physiologically  during  sleep 
and  old  age,  pathologically  as  an  early  symptom  in  tabes  dorsalis,  and 
in  progressive  paralysis.  Eserin,  pilocarpin,  opium,  morphin,  and 
chloroform  (the  latter  in  pronounced  narcosis)  narrow  the  pupil.  Sym- 
pathetic myosis  from  lesions  of  the  (pupillary)  dilating  iibers  of  the 
cervical  sympathetic,  from  disease  of  the  sympathetic  itself  or  of  the 
oculopupillary  jfibers  connecting  the  sympathetic  nerve  with  the  first 
dorsal  segment  of  the  spinal  cord,  is  of  local  diagnostic  importance. 

Pupillary  dilatation  (mydriasis)  occurs  in  complete  loss  of  conscious- 
ness, in  severe  pain,  in  dyspnea,  in  peripheral  blindness  (especially  from 
optic  atrophy  and  glaucoma),  in  general  oculomotor  paralysis,  and  in 
some  cases  of  tabes  dorsalis  and  progressive  paralysis.  Atropin, 
duboisin,  cocain,  chloroform  (in  the  early  stages  of  narcosis)  dilate  the 
pupil.     Children,  as  a  rule,  have  dilated  pupils. 

W.  Riegel  ^  describes  as  a  sign  of  neurasthenia,  under  the  name  of 
"  alternating  mydriasis,"  a  dilatation  appearing  sometimes  in  one,  some- 
times in  the  other  eye  with  a  normal  illumination. 

Irregularity  in  shape  of  the  pupils  may,  oif  course,  occur  in  diseases 
of  the  nervous  system,  but  in  most  cases  it  depends  upon  some  local 
disease  in  the  neighborhood  of  the  pupil  (synechia). 

Inequality  of  the  pupils  is  rare  in  health,  and  when  present 
most  frequently  depends  upon  an  unequal  refraction  of  the  two  eyes. 
It  is  not  uncommon  in  the  various  unilateral  cerebral  affections,  in 
progressive  paralysis,  in  tabes  dorsalis,  in  unilateral  disease  of  the 
sympathetic,  of  the  oculomotor  or  of  the  o|)tic  nerve,  and  in  migraine 
attacks.  An  inequality  of  the  pupils  is  fairly  common  in  neurasthenia, 
and  is  then  usually  of  a  vacillating  character. 

See  p.  846  et  seq.  concerning  an  inequality  of  the  ])upils  which 
depends  upon  the  loss  of  reaction  and  dilatation  of  one  pupil. 

•     1  Deulsch.  med.  Woch.,  1902,  No.  13. 

^  Zeits.f,  NervenheilL,  1900,  vol.  xvii.,  p.  169. 


840  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

On  account  of  the  crossed  pupillary  reaction  (compare  below),  both  pupils  are 
equally  contracted  when  only  one  is  exposed  to  light.  Yet,  not  rarely,  persons 
are  observed  in  whom  the  pupil  adjacent  to  the  source  of  light  is  narrower  than 
the  shaded  pupil.  Too  little  attention  is  paid  to  the  diagnostic  significance  of 
this  phenomenon.     It  may  be  that  it  is  a  stigma  of  neurasthenia. 

Anomalies  of  Pupillary  Contraction.  —  Pupillary  Light 
Reflex. — Exposure  of  the  pupil  to  illumination  narrows  not  only  the 
pupil  of  the  same  side,  but  also  the  pupil  of  the  other  eye,  thus  giving 
rise  to  a  direct-  and  a  crossed-light  reflex  or  reaction.  The  part  of  the 
oculomotor  nucleus  (iris  nucleus,  see  p.  833)  which  innervates  the  iris 
must  be  considered  as  the  center  of  this  reflex. 

A  convenient  method  of  testing  the  reaction  of  the  pupils  to  light  is 
as  follows  :  With  a  moderate  illumination  (candlelight)  in  front  of  the 
patient's  face  we  alternately  expose  and  then  shade  one  eye  with  the 
hand,  Avatching  the  effect  of  the  light  upon  that  pupil  and  upon  the 
other  pupil ;  then  we  do  the  same  thing  to  the  other  eye.  At  the  same 
time  the  patient  must  avoid  any  attempt  at  convergence  or  accommoda- 
tion. If  the  test  with  a  moderate  light  does  not  produce  the  pupillary 
contraction,  the  examination  should  be  repeated  with  a  dazzling  light 
(sunlight,  an  illumination  lens,  or  a  concave  mirror). 

This  customary  procedure  for  the  exact  quantitative  estimation  of  the  reaction 
of  the  pupil  to  light  is  subject  to  a  number  of  sources  of  error,  which  are  due  to 
the  fact  that  the  differences  between  the  effect  of  light  upon  the  macula  lutea  and 
upon  the  peripheral  portions  of  the  retina  are  disregarded,  and  also  to  the  fact  that 
the  narrowing  of  the  pupils  by  convergence  and  accommodation  cannot  be  posi- 
tively excluded.  As  the  result  of  minute  investigation,  Schirmer '  consequently 
o-ives  the  following  rules  for  the  accurate  study  of  the  reaction  of  the  pupils  to 
light:  "The  patient  should  be  seated  at. a  distance  of  one  meter  from  a  well- 
lighted  window  which  is  not  exposed  to  the  direct  rays  of  the  sun.  After  the 
eyes  have  adapted  themselves  to  this  illumination,  the  diameter  of  each  pupil 
is  observed  ;  the  reaction  of  each  pupil  to  light  is  now  determined  by  holding 
the  hands  in  front  of  the  open  eyes  and  then  rapidly  withdrawing  one  of  the 
hands.  The  reaction  of  each  pupil  to  light  is  next  determined  while  the  opposite 
eye  is  unshielded  from  illumination."  The  reaction  is  more  marked  with  the 
first  method  of  examination  (with  the  opposite  eye  shielded),  since  the  exclusion 
of  the  crossed  innervation  causes  the  pupil  to  dilate  before  the  reaction  occurs,  or, 
at  least,  to  be  more  susceptible  to  light.  This  procedure  is  consequently  the  one 
best  adapted  for  determining  the  vestiges  of  a  diminished  direct  pupillary  reac- 
tion. The  crossed  pupillary  reaction  is  then  determined  by  observing  the  eye 
while  the  opposite  one  is  alternately  shielded  and  exposed.  This  investigation  is 
repeated  for  each  eye.  The  sum  total  of  the  direct  and  uncrossed  pupillary  reac- 
tions, and  consequently  the  last  remnants  of  a  diminished  reaction  of  the  pupils 
to  light,  is  best  estimated  by  shielding  both  eyes,  simultaneously  exposing  them, 
and  then  observing  the  reaction  of  both  pupils. 

See  p.  843  et  seg.  concerning  the  so-called  "  hemiopic  reaction  " — 
i.  e.,  hemiopic  rigidity  of  the  pupil. 

Fig.  327  represents  the  course  of  the  light  reflex  which  was  for- 
merly "accepted  as  accurate.  It  was  based  upon  the  supposition  that  the 
stimulus  to  the  iris  nucleus,  causing  a  reflex  narrowing  of  the  pupil, 
originated  in  the  so-called  primary  optic  centers  (pulvinar,  anterior  cor- 
pora quadrigemina,  and  corpus  geniculatum  externum  see  Fig.  315). 
1  Deuisch.  med.  Woch.,  1902. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


841 


The  bilateral  character  of  the  light  reflex  was  attributed  not  only  to  the 
semi-clecussation  of  the  optic  fibers,  but  also  to  the  bilateral  connection 
of  the  iris  nuclei  (see  Fig.  327). 

Although  the  above  conception  was  advocated  in  the  earlier  German 
editions  of  this  work,  it  is  no  longer  tenable,  because  it  has  been  proved 
clinically,  as  well  as  experimentally,  upon  animals,  that  lesions  of  the 
primary  centers  do  not  cause  any  disturbances  of  the  pupillary  reflex. 
We  must  therefore  conclude  that  the  sensory  fibers,  which  transmit  the 
pupillary  light  reflex,  are  distinct  from  the  visual  fibers,  and  certainly 
leave  the  optic  tract  before  its  entrance  into  the  optic  centers.  Physio- 
logic examinations  and  clinical  observations  induced  Bechterew  ^  to  con- 


jfimary ohtic  centei 

f Rdmivir,cauadrani„ 

Corp  (/eniculfijctj 


Occipital  Cortex 


.  Fig.  327.— Old  diagram  of  the  pupillary  light  reflex,  which  no  longer  obtains  :  The  primary  optic 
centers  (pulvinar,  corpus  geniculatum  externum,  and  anterior  corpora  quadrigemina)  are  repre- 
sented as  a  single  center  for  the  sake  of  simplicity  (see  Fig.  315). 


elude  that  special  pupillary  fibers  exist  in  the  optics  and  that  these 
fibers,  after  separating  from  the  visual  fibers  at  a  certain  distance  behind 
the  chiasm,  run  through  the  gray  matter  near  the  third  ventricle  to  the 
iris  nucleus. 

Owing  to  the  occurrence  of  heraiopic  pupillary  immobility,  it  must  be 
a.ssumed  that  the  fibers  of  the  optic  nerve  which  are  involved  in  the 
])upillary  reflex  experience  a  semidecussation  in  the  chiasm  in  the  same 
manner  as  do  the  visual  fibers. 

Bechterew's  diagram  fi)r  the  pupillary  light  reflex,  which  was  repro- 
duced in  the  former  German  edition  of  this  work,  does  not  sufliciently 

^  DeuUch.  Zeiis.f.  Nervenheilk. ,  vol.  xvi.,  parts  3  and  4,  p.  193  et  seq. 


842 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


explain  physiologic  conditions  ;  it  contained  no  fibers  whatever  for  the 
direct  pupillary  reaction,  and  certain  of  its  details  had  not  been  posi- 
tively confirmed.  The  author  believes  that  the  following  diagram  (Fig. 
328)  of  the  pupillary  reaction  will  explain  the  physiologic  and  patho- 
logic facts  now  at  our  disposal,  and  that  it  is  not  based  upon  as  many 
unfounded  suppositions.  The  previously  mentioned  and  more  recent 
anatomic  postulates  have  been  regarded  in  its  construction. 

The  most  important  lesions,  clinically,  are  indicated  in  the  diagram 
by  the  letters  a,  h,  c,  d,  e,  f,  g,  and  A.  The  clinical  symptoms  of  these 
lesions  are  as  follows  : 

Lesion  a:  Transverse  section  of  one  optic    nerve.     Blindness  and 


Fig.  328.— Diagram  of  the  pupillary  light  refiex:  The  continuous  lines  represent  the  visual 
fibers;  the  dotted  lines,  the  centripetal  fibers  for  the  pupillary  light  reflex.  The  central  tract  for 
contraction  of  the  pupil  by  convergence  and  accommodation  is  not  indicated  in  the  figure ;  it 
might  be  imagined  as  passing  to  the  iris  nucleus  from  the  side. 


absence  of  the  direct  pupillary  reaction  in  the  eye  of  the  same  side,  with 
maintenance  of  the  crossed  pupillary  reaction.  The  crossed  reaction  is 
absent  in  the  opposite  pupil. 

Lesion  h:  Sagittal  section  of  the  chiasm.  Bilateral  temporal  hemi- 
opia.  The  direct  and  crossed  pupillary  reactions  are  normal  in  both 
eyes  when  tested  in  the  usual  manner  by  diffuse  light.  Direct  and 
crossed  hemiopic  pupillary  immobility  in  botli  eyes  (p.  843  et  seq.)  from 
involvement  of  the  nasal  halves  of  both  retinas. 

Lesion  c  .•  Section  of  one  optic  tract  in  front  of  the  ])rimarv  optic 
center  involving  the  centripetal  fibers  for  the  pupillary  refiex.  Homon- 
ymous hemiopia  and  homonymous  hemiopic  crossed  and  direct  pupil- 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  843 

lary  immobility  (see  below).  Maintenance  of  the  direct  and  crossed 
pupillary  reaction  by  the  ordinary  test  with  diifbse  light. 

Lesion  d :  Involvement  of  all  the  centripetal  fibers  of  the  pupillary 
light  reflex  upon  both  sides  after  their  separation  from  the  visual  fibers. 
Absence  of  the  crossed  and  direct  reactions  of  both  pupils  to  light  with 
maintenance  of  visual  power,  maintained  movements  of  the  eyeballs, 
and  maintained  reaction  of  the  pupils  by  convergence  and  accommoda- 
tion (Argyll-Robertson's  symptom  in  tabes  dorsalis  and  progressive 
paralysis,  p.  846). 

Lesion  e:  The  direct  and  crossed  pupillary  reactions  normal  in 
both  eyes  when  tested  with  diffuse  light.  As  a  result  of  the  injury  to 
the  fibers  connecting  the  iris  centers,  however,  only  the  direct  reflex  is 
present  when  the  temporal  halves  of  the  retinas  are  tested,  and  only  the 
crossed  reflex  is  present  when  the  light  falls  upon  the  nasal  halves. 

Lesion  /.•  Section  of  the  centripetal  fibers  for  the  pupillary  light 
reflex  proceeding  from  the  left  halves  of  both  retinas.  Homonymous 
hemiopic  pupillary  immobility  in  both  eyes  upon  illumination  of  the 
left  halves  of  both  retinas.  The  visual  power  and  the  pupillary  reac- 
tion to  convergence  and  accommodation  are  maintained  in  both  eyes 
(see  p.  847.) 

Lesion  g:  Section  of  the  motor  fibers  leading  from  the  left  iris 
nucleus  to  the  pupil  of  the  same  side.  Immobility  of  the  affected 
pupil  to  light,  both  direct  and  crossed,  and  also  during  convergence  and 
accommodation.  The  opposite  pupil  reacts  normally  both  to  direct  and 
crossed  impulses,  and  also  to  accommodation  and  convergence.  The 
sharpness  of  vision  and  the  visual  fields  are  normal  in  both  eyes. 

Lesion  h:  Destruction  of  the  left  iris  nucleus.  Immobility  of  the 
left  pupil,  both  to  direct-  and  crossed-light  impressions  and  also  to 
accommodation  and  convergence.  This  is  associated  with  hemiopic 
immobility  of  the  right  pupil  during  illumination  of  the  left  halves  of 
the  retinas. 

A  number  of  direct  observations  are  still  necessary  to  demonstrate 
the  complete  accuracy  of  this  diagram.  JN^o  observations  of  types  e  and 
/,  for  example,  have  as  yet  been  published.  In  type  h  investigations 
have  not  been  made  to  determine  whether  hemiopic  immobility  of  the 
opposite  pupil  is  really  present  from  an  involvement  of  the  retinal 
halves  corresponding  to  the  injured  side.  Not  until  positive  statistics 
have  been  obtained  in  reference  to  these  points  can  this  diagram  be 
defended  as  absolutely  correct.  If  it  be  found  that  the  lesions  e,  f,  and 
h  do  not  materialize  in  actual  practice,  the  diagram  must  be  modified. 

.  Hemiopic  Pupillarrj.  Immobility  {Hemiopic  Pupillary  Reflex). — Fig.  328  flir- 
nlshes  a  key  to  the  appreciation  of  the  so-called  hemiopic  pupillary  reaction 
(Wernicke)  or  hemiopic  pupillary  immobility.  When  one  side  of  the  ()i)tic  tract 
is  injured  at  the  jjoint  c,  or  when  the  centri])etal  fibers  of  the  light  reflex  proceed- 
ing from  homonymous  retinal  halves  are  injured  in  the  neighborhood  of  the  jioint 
/,  the  result  must  be  that  the  light  reaction  from  the  corresponding  homonymous 
retinal  halves  of  l^oth  eyes  will  be  entirely  destroyed,  whereas  from  the  opposite 
retinal  halves  the  reflex  will  remain  normal.  To  this  peculiar  condition  Wernicke 
gave  the  name  hemiopic  pupillary  reaction  ;  but  v.  Leyden  quite  properly  substi- 


844  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

tilted  for  this  expression  the  term  hemiopic  pupillary  immobility,  because,  as  a 
matter  of  fact,  when  this  condition  appears,  what  is  observed  is  certainly  an 
immobility  or  rigidity.  In  order  to  demonstrate  this  rigidity  it  is  essential,  while 
watching  the  pupillary  condition,  that  each  retinal  half  be  lighted  separately. 

The  ordinary  procedure  consists  in  projecting  a  cone  of  rays  into  the  eye  by 
means  of  an  ophthalmoscope  or  of  a  focusing  lens,  and  observing  the  reaction 
of  the  pupils,  according  as  the  light  impinges  upon  the  left  or  upon  the  right 
retinal  half.  A  darkened  room  is,  of  course,  very  desirable,  if  not  essential. 
The  difficulty  in  this  depends  upon  the  uncertainty  of  confining  the  illumination 
to  one  of  the  retinal  halves.  If  the  actual  apex  of  the  cone  of  light  does  not 
impinge  upon  the  retina,  anterior  or  posterior  circles — radiations — of  the  light 
picture  may  affect  the  other  retinal  half  or  even  the  macula,  and  so  spoil  the 
test.  According  to  Salomonsohn,  i  the  best  result  can  be  obtained  by  reflecting 
from  a  concave  mirror,  placed  horizontally  beside  the  eye,  a  very  sharp  and  ver- 
tical flame  picture  (the  latter  is  collected  by  the  mirror  from  an  illumination 
situated  at  one  side).  Then,  by  gently  rotating  the  mirror,  the  reflected  light 
winds  around  the  pupillary  edge  and  impinges  upon  the  retina,  at  one  time  from 
the  temporal,  at  another  from  the  nasal  side.  It  is  essential  that  the  patient 
should  always  focus  at  the  same  distance,  preferably  into  space.  On  account  of 
the  difficulties  mentioned  above  (the  dispersed  circles  of  light),  the  results  from 
this  method  are  oftentimes  not  very  conclusive  ;  hence  the  following  modifica- 
tion may  be  attempted:  A  black  screen,  at  least  a  meter  square  and  with  a  cen- 
tral opening,  is  placed  vertically  in  front  of  the  patient  in  the  dark  room,  at  a 
distance  of  about  60  cm.  (about  2  feet).  While  the  patient  focuses  upon  the 
opening,  an  assistant  in  front  of  the  screen  projects  a  very  bright  illumination 
(kerosene  lamp)  into  the  visual  field,  at  one  time  from  the  right  and  another  from 
the  left  side,  but  not  near  the  focusing  point  of  the  patient,  and  then  the 
behavior  of  the  pupils  is  noted  through  the  opening  in  the  screen.  The  lamp 
should  always  be  held  at  about  the  same  distance  from  the  eyes  as  a  focusing 
point,  in  order  to  be  sure  that  a  sharp  flame  and  not  dispersed  circles  are  pro- 
jected upon  the  retina;  with  this  method  the  test  can  be  made  as  well  with  one 
eye  as  with  two.  If  the  pupils  of  both  eyes  are  contracted  only  when  illumina- 
tion is  at  the  right  side,  or  only  when  it  is  at  the  left  side,  right  or  left  hemiopic 
homonymous  pupillary  rigidity  is  present.^ 

The  difficulty  of  both  these  tests  consists  in  the  fact  that  ordinarily  a  stimu- 
lation of  the  peripheral  portions  of  the  retina  by  a  circumscribed  light  picture 
excites  only  a  weak  pupillary  reaction  unless  the  region  of  the  macula  is  actually 
stimulated  as  well.  This  objection  applies  particularly  when  the  sensitiveness 
of  the  retina  has  been  difilisely  impaired, — e.  g.,  with  a  choked  disk.  In  such 
cases  the  following  device  may  be  helpful.  Place  in  front  of  the  patient  a  screen 
which  rotates  upon  a  sagittal  axis,  and  one-half  of  which  is  white,  the  other 
half  black;  then  instruc;  the  patient  to  focus  upon  a  small  mark  in  the  half  of 
the  screen  just  at  the  edge  of  the  border  between  the  black  and  white,  and  illu- 
minate the  screen  very  brilliantly  by  means  of  a  light  placed  behind  the  patient's 
head.  Now,  if  the  patient  opens  and  shuts  his  eyes,  hemiopic  pupillary  rigidity 
can  be  demonstrated  by  the  pupillary  reaction  occurring  only  when  the  white 
side  of  the  screen  corresponds  to  the  normal  retinal  half.  This  method  may  be 
employed  for  one  as  well  as  for  both  eyes. 

In  a  case  of  acromegaly  where  even  this  device  left  the  author  in  doubt,  he 
employed  the  following  method  with  considerable  success,  and  can  recommend  it 
as  being  the  best  he  has  thus  far  used.  While  the  patient  focuses  upon  some 
object — e.  g.,  his  own  finger — at  a  distance  of  about  30  cm.  (10  in.),  an  assistant 

'  Deutseh.  med.  Woch.,  1900,  No.  42. 

2  In  the  more  unusual  temporal  form  of  hemiopia,  which  characterizes  tumors  m 
the  neighborhood  of  the  chiasm  (acromegaly),  and  hydrocephalus  (in  which  the  chiasm 
is  compressed  by  the  enlarged  infundibulum),  we  are  compelled  to  examine  for  hemiopic 
pupillary  rigidity  in  the  corresponding  inner  retinal  halves  (see  Fig.  328,  lesion  6).  But 
as  a  matter  of  fact  the  demonstration  of  hemiopic  rigidity  hap  no  local  diagnostic  signifi- 
cance in  this  form  of  hemiopia,  as  it  can  arise  only  in  the  chiasm. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  845 

projects  in  front  of  Ms  eyes  an  electric-bulb  light  of  at  least  32-candle  power, 
and  stops  just  before  the  middle  of  the  visual  field;  this  light  must  be  held  so 
that  the  j^lane  in  which  the  carbon  thread  is  bent  remains  sagittal  to  the  eye 
examined.  With  hemiopic  rigidity  the  pupillary  reaction  can  be  obtained  only 
from  the  retinal  half  whose  pupillary  fibers  are  preserved.  The  advantage  of 
employing  such  an  illumination  is  that  by  virtue  of  the  linear  character  of  the 
source  of  light  it  remains  localized  enough,  even  despite  the  presence  of  dis- 
persed rays,  to  illuminate  only  one  retinal  half  so  long  as  the  lamp  does  not 
approach  too  near  the  focused  point.  The  great  intensity  of  the  illumination  is 
an  additional  advantage. 

The  best  method  of  demonstrating  hemiopic  pupillary  immobility  is  by 
means  of  the  "pupil  tester,"  described  by  v.  Fragstein  and  Kempner,^  which 
the  author  has  only  recently  had  an  opportunity  to  employ.  This  is  a  tubular 
instrument  in  which  the  rays  from  an  incandescent  lamp  of  8  volts  tension  are 
condensed  by  lenses  and  diaphragms  to  a  slender  but  most  intense  cone  of  light, 
the  focus  of  which  is  situated  4  cm.  in  front  of  the  anterior  extremity  of  the 
instrument.  With  this  cone  of  light  it  is  easy  to  illuminate  either  half  of  the 
retina  by  allowing  it  to  pass  through  the  pupil  from  the  temporal  or  the  nasal 
side.  Since  the  slightly  convergent  rays  cross  or  become  divergent  4  cm.  in  front 
of  the  instrument,  an  intense  and  quite  circumscribed  illumination  of  an  indi- 
vidual portion  of  the  retina  is  best  assured  by  holding  the  instrument  3.3  cm.  in 
front  of  the  cornea,  so  that  the  focus  of  the  cone  of  light  falls  about  7  mm. 
behind  the  convexity  of  the  cornea.  This  situation  corresponds  to  the  nodal 
point  of  Listing's  reduced  eye,  and  rays  passing  into  the  eye  and  directed  toward 
this  point  are  peculiar  in  that  they  pursue  their  original  direction  through  the 
vitreous  humor  as  though  they  had  not  been  refracted.  With  this  position  of  the 
instrument  the  cone  of  light  passes  into  the  eye  as  though  no  refracting  media 
were  present — i.  e. ,  the  slightly  convergent  rays  continue  their  original  course  into 
the  interior  of  the  eye  as  a  slender,  slightly  divergent  cone.  This  instrument  is 
probably  the  only  one  with  which  it  is  possible  to  illuminate  still  more  circum- 
scribed retinal  areas,  such  as  a  particular  quadrant. 

The  demonstration  of  hemiopic  pupillary  rigidity  permits  us  to  differentiate  a 
so-called  peripheral  from  a  central  homonymous  hemiopia.  While,  according  to 
Fig.  328,  peripheral  hemiopia  (location  of  the  lesion  at  c)  does  not  produce 
hemiopic  pupillary  rigidity,  this  is  not  the  case  with  central  hemiopia  (location 
of  the  lesion  at  e,  above  the  primary  optic  centers  Fig,  315).  The  hemiopic 
pupillary  rigidity  in  which  a  double  jjeripheral  blindness  occurs,  composed  of  two 
hemiopias,  one  side  of  which  is  peripheral  and  the  other  central,  is  of  special 
interest  and  has  often  been  observed.  An  individual  with  these  two  lesions  is 
completely  blind.  The  accurate  localization  and  significance  of  the  visual  dis- 
turbance is  then  furnished  by  the  presence  of  hemiopic  pupillary  rigidity  in  the 
pupil  which  reacts  only  to  one  retinal  half. 

In  those  cases  where  hemiopic  rigidity  is  present  both  a  direct  and  crossed 
pupillary  reaction  can  be  obtained  by  testing  the  pupils  in  the  ordinary  way,  so 
that  both  retinal  halves  receive  light.  The  reaction  may  be  diminished,  but  it  is 
still  plain  enough.  In  order  to  avoid  overlooking  hemiopic  rigidity  the  tests  men- 
tioned above  must  be  accurately  made,  especially  in  all  cases  of  homonymous 
hemiopic  and  bilateral  blindness  following  a  cerebral  affection.  Bechterew  has 
made  it  clear  (Fig.  328,  lesion/)  that  homonymous  pupillary  rigidity  may  occur 
without  any  visual  disturbance. 

Certain  other  hypotheses  in  reference  to  hemiopic  pupillary  immobility  have 
been  given  in  the  tabulation  of  the  various  lesions  of  the  pupillary  reflex  upon 
p.  842  et  seq. 

The  technical  difficulties  described  above  in  determining  homonymous  pupil- 
lary rigidity  are  perhaps  the  reason  that  the  phenomenon  has  been  so  rarely 
found. 

An  additional  difficulty  is  furnished  by  disturbances  of  Haab's  so-called  cor- 

^  Klin.  Monals.fur  Augenheilk.,  1899. 


846  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

tical  pupillary  reflex,  which  is  brought  about  by  concentration  of  the  attention 
upon  a  lateral  source  of  light  (see  p.  847).  All  of  the  procedures  for  testing 
hemiopic  pupillary  immobility  are  of  such  a  character  that  the  attention  of  the 
patient  is  apt  to  concentrate  upon  the  source.  But  this  is,  of  course,  the  case 
only  when  the  light  falls  on  the  seeing  retinal  half,  and,  therefore,  if  Haab's 
reflex  is  lacking,  hemiopic  pupil  rigidity  may  apparently  be  present  when  the 
blind  retinal  half  is  lighted. 

Loss  of  Pupillary  Light  Reaction  {Pupil  then  Ordinarily  Dilated) ;  Rigidity  of 
the  Pupil  to  Light. — A  failure  of  the  pupil  to  react  to  light  occurs  in  severe  dis- 
turbances of  consciousness  of  the  most  varying  kinds:  In  cerebral  pressure  (in 
these  cases  bilateral);  in  poisoning  from  the  substances  mentioned  above  as  dilating 
the  pupils  (these  unilateral  or  bilateral,  depending  upon  the  poison)  ;  in  focal 
lesions  which  interrupt  the  reflex  pupillary  arc  according  to  the  method  detailed 
in  Fig.  328  (e.  g.,  motor  lesions);  in  complete  peripheral  oculomotor  paralysis; 
in  nuclear  oculomotor  paralysis  which  affects  the  iris  nucleus,  but  does  not  attack 
the  other  branches  of  the  oculomotor  (see  p.  833);  in  sensory  lesions  ;  in  affections 
of  the  retina  ;  and  in  bilateral  optic  atrophy  or  marked  bilateral  choked  disk. 
Complete  loss  of  pupillary  reaction  from  choked  disk  is  a  comparatively  excep- 
tional occurrence,  and  observed  only  when  the  choked  disk  has  caused  at  the 
same  time  blindness.  The  visual  acuteness  is  frequently  very  well  preserved,  and 
corresponds  well  with  the  slight  injury  to  the  conduction  of  the  sensory  fibers 
belonging  to  the  pupillary  reflex.  Even  when  a  lesion  of  the  optic  nerve  dimin- 
ishes the  acuteness  of  vision  decidedly,  the  pupillary  reaction  need  not  be  seriously 
impaired.  This  is  evident  without  further  explanation  when  we  remember 
(p.  841)  that  the  centripetal  fibers  of  the  light  reflex  in  the  optic  nerve  are  dis- 
tinct from  the  visual  fibers.  A  unilateral  loss  of  reaction  is  usually  associated 
with  a  dilatation  of  that  pupil,  as  compared  with  the  opjjosite  side. 

Ordinarily  an  exact  examination  of  the  condition  of  the  optic  nerve,  on  the 
one  hand,  and  of  the  nerves  supplying  the  eye  muscles,  on  the  other  hand, 
facilitates  a  differential  diagnosis  between  pupillary  rigidity  depending  upon  a 
lesion  of  the  motor  and  that  depending  upon  a  lesion  of  the  sensory  limb  of  the 
reflex  arc.  Fig.  328  should  always  be  consulted  to  comprehend  the  diagnostic 
points.  In  addition  to  other  characteristics,  it  should  be  emphasized  that  with 
lesions  of  the  motor  limb  of  the  pupillary  reflex  (paralysis  from  the  muscles  of 
the  nucleus  of  the  iris  or  from  the  peripheral  oculomotor),  the  narrowing  of  the 
pupil  to  accommodation  and  the  power  of  convergence  (see  below)  is  lost;  whereas 
this  is  not  the  case  when  the  loss  of  jDupillary  reaction  depends  upon^a  lesion  of 
the  retina  or  of  the  optic  tr^ct.  In  case  the  lesion  is  recognized  as  motor,  the 
question  is  :  Does  this  lie  in  the  nucleus  or  its  immediate  neighborhood,  or 
in  the  peripheral  motor  fibers  of  the  oculomotor?  This  question  is  frequently 
decided  by  the  behavior  of  the  ciliary  muscle — i.  e.,  by  accommodation.  In 
lesions  of  the  nucleus  or  its  neighborhood,  accommodation  may  be  preserved  on 
account  of  the  arrangement  of  the  oculomotor  nucleus  (discussed  upon  p.  833); 
whereas  with  a  purely  peripheral  oculomotor  paralysis,  which  may  be  situated  in 
the  trunk  of  the  nerve  or  in  the  short  branches  of  the  ciliary  ganglion,  accom- 
modation will  probably  fail. 

Argyll- Robertson' s  Phenomenon. — This  is  an  early  symptom  of  tabes  dorsalis 
and  of  progressive  paralysis.  It  consists  in  a  preservation  of  the  pupillary  reac- 
tion to  convergence  and  to  accommodation  with  a  loss  of  the  reaction  of  the  pupil 
to  light,  and  is  not  associated  with  any  impairment  of  visual  acuteness  (see 
under  y).  For  some  unknown  cause  the  pupils  are  generally  narrowed  (the 
so-called  spinal  myosis  of  tabetics).^  Ordinarily  the  reaction  of  the  pupils  to 
pain  is  also  wanting.  Erb  called  Argyll-Robertson's  phenomenon  a  reflex  pupil- 
lary rigidity,  an  expression  in  which  the  words,  according  to  the  writer's  opinion, 
are  not  used  in  their  ordinary  sense,  since  from  it  one  might  conceive  of  a  rigidity 
occasioned  reflexly,  not  of  a  rigidity  of  the  reflex.  The  symptom  has  not  yet 
been  satisfactorily  explained  by  anatomic  researches.     According  to  Bechterew, 

^  It  has  not  yet  been  proved  that  this  is  of  spinal  origin. 


EXAMIXATIOy  OF  THE  NERVOUS  SYSTEM.  847 

Fig.  328,  however,  it  must  theoretically  depend  upon  a  lesion  of  all  the  centrip- 
etal fibers  of  the  pupillary  light  reflex,  after  their  separation  from  the  visual 
fibers  (lesion  d,  Fig.  328).  It  cannot  depend  upon  a  lesion  of  the  motor  limb 
(lesion  g  or  h,  Fig.  328),  because  the  pupillary  contraction  in  accommodation  and 
convergence  pei'sists. 

Paradoxic  FupiHart/  Reaction. — This  i^henomenon,  first  described  by  Ober- 
steiner  and  then  by  Bechterew,  consists  in  the  occurrence  of  a  dilatation  instead 
of  a  contraction  of  the  pupils  to  direct  and  crossed  illumination.  At  times  a 
very  insignificant  initial  contraction  precedes  the  dilatation.  Like  the  Argyll- 
Robertson  phenomenon,  this  sign  occurs  principally  in  tabes  dorsalis  and  joro- 
gressive  parcdysis. 

According  to  one  conception,  probably  erroneous,  this  dilatation  depends 
upon  unnoticed  movements  of  divergence  of  the  eyeball  at  the  moment  of  illumi- 
nation (as  contrasted  with  the  narrowing  of  the  pupils,  associated  with  convergence 
and  accommodation,  see  below,  7).  Bechterew,  however,  considers  that  it  is  a 
phenomenon  of  fatigue,  because,  under  the  pathologic  conditions  mentioned 
above,  a  brilliant  illumination  fatigues,  and  so  inhibits,  the  pupillary  tonus 
after  a  scarcely  noticeable  or  absent  narrowing. 

ji.  Pupillary  Pain  Reflex. — Severe  pain  stimulus  applied  to  various  parts 
of  the  body,  but  more  especially  painful  irritation  of  the  skin  of  the  neck,  will 
usually  dilate  the  pupils.  This  dilatation  is  produced  by  the  pupillary  dilator 
fibers  derived  from  the  sympathetic,  and  in  turn  from  the  VIII.  cervical  and  I. 
dorsal  segments  (see  Fig.  366,  p.  926).  The  reflex  is  sometimes  useful  in  diag- 
nosis, pointing  to  an  involvement  of  the  roots  or  of  the  sympathetic.  According 
to  the  author's  experience,  however,  the  pupillary  pain  reflex  is  so  inconstant 
that,  generally  speaking,  a  difference  between  the  two  sides  is  the  only  sign 
worth  heeding. 

7.  Narrowing  of  the  Pupils  to  Convergence  and  to  Accommodation. — 
Physiologically  the  pupils  are  decidedly  contracted  by  efforts  at  convergence  or 
accommodation  (it  is  difficult  to  separate  one  from  the  other).  This  consensual 
movement  is  diagnostically  significant;  m  the  first  place,  because  it  shows  that  in 
testing  the  other  pupillary  reactions  we  must  be  careful  to  have  the  patient  avoid 
convergence  or  accommodation.  Perhaps  the  best  plan  is  to  have  him  always 
focus  for  the  same  distance,  preferably  into  space.  A  further  diagnostic  interest 
is  furnished  by  the  retention  of  the  convergence  and  the  accommodation  reflex 
while  the  light  reflex  is  absent,  which  j^roves  that  the  light  reflex  is  not  affected 
by  a  lesion  of  the  motor  tract. 

(See  above  :  Loss  of  Pupillary  Reaction  to  Light,  p.  846  ;  Argyll-Robert- 
son's Phenomenon,  \>.  846.) 

^.  Westphal's  Pupillary  Phenomenon.' — This  consists  in  a  contraction  of 
the  pupil  when  the  examiner,  by  forcibly  holding  the  lid  open,  prevents  the 
patient's  attempt  to  close  the  eye  (Bell's  phenomenon,  p.  863).  To  appreciate 
this  reaction  it  is  generally  essential  that  the  pupilin  question  should  not  react 
to  light,  orj  at  least,  only  slightly,  and  should  not  be  markedly  narrowed.  It  is 
easier  to  recognize  the  appearance  with  dilated  pupils.  Westphal  never  found 
the  phenomenon  in  healthy  individuals,  and  only  once  in  the  pupils  of  an 
hysteric  person.  He  found  it  several  times,  on  the  contrary,  in  tabes,  and  in 
progressive  paralysis.     The  author  has  repeatedly  observed  it  in  tabes. 

f.  Haab's  So-called  Cortical  Pupillary  Reflex. — Thus  far  no  diagnostic 
significance  has  been  attached  to  this  reflex,  though  perhaps  it  may  yet  be  util- 
ized in  the  diagnosis  of  cortical  disturbances  of  vision.  It  consists  of  a  narrow- 
ing of  the  pupils  when  the  patient  in  a  dark  room,  without  any  alteration  in  the 
position  of  the  eye,  concentrates  his  attention  upon  a  flame  placed  at  one  side 
— i.  e.,  seen  indirectly. 

^  Neuroloyisches  CentralbL,  1899,  No.  4. 


848  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

9.  Condition  of  the  Accommodation. 

Before  testing  the  accommodation,  the  acuteness  of  vision  must  first 
be  determined  and  any  error  of  refraction  corrected.  To  correct  the 
latter,  if  the  patient  is  myopic,  we  employ  the  weakest  concave  lens  with 
which  he  sees  distant  objects  clearly;  if  hypermetropic,  the  strongest 
convex  lens.  The  acuteness  of  vision  is  then  determined  in  the  ordi- 
nary way.  The  accommodation  is  then  tested  by  placing  before  the 
eye  under  examination,  at  a  distance  of  25  cm.  in  a  good  light,  the 
finest  test  type  which  he  should  be  able  to  read  at  this  distance  with 
his  acuteness  of  vision.  (Perfect  accommodative  power  presupposed.) 
If  he  can  read  this  type  the  accommodation  is,  at  least,  normal.  If 
he  cannot  read  it  there  must  be  defective  accommodation.  Such  a  defect 
will  consist  of  the  physiologic  presbyopia  of  his  age  plus  whatever 
accommodative  paresis  may  exist.  The  convex  lens  which  the  patient 
requires  for  reading  the  selected  type  at  25  cm.  distance  (plus  the  glass 
which  corrects  the  refraction)  measures  the  defect  of  accommodation  in 
dioptrics.  By  comparing  this  defect  with  that  which  is  found  in  a 
patient  as  a  result  of  the  physiologic  presbyopia  for  his  age  (see  the 
accompanying  table),  we  can  decide  whether  there  is  a  paresis  or  paralysis 
of  accommodation.  Should  the  patient  need  a  +  4  D,  lens  to  read 
the  type  clearly,  there  exists  no  power  of  accommodation.^  Such  a 
total  defect  is  physiologic  after  the  age  of  seventy-five  years  (see  table) ; 
but  in  younger  individuals  it  would  indicate  a  complete  pathologic  par- 
alysis of  accommodation.  If  a  patient  forty-five  years  old  requires  a 
glass  of  4-  2  D.  he  has,  in  addition  to  his  physiologic  presbyopia 
(0.5  D.,  according  to  the  table),  a  paralysis  of  accommodation  of 
1.5  D.,  etc. 

Degree  of  presbyopia—!,  e., 
the  physiologic  defect  of  ac- 
Age.  cominodatioii  in  dioptries. 

Forty-five  years .     ...  0. 50  D. 

Fifty  " 1.50  D. 

Fiily-five  " 2.25  D. 

Sixty  " 3.00  D. 

Sixty-five  " 3.25  D. 

Seventy  " 3.75  D. 

Seventy-five  " 3.75  D. 

We  find  a  jparalysis  of  accommodation  in  total  oculomotor  paralysis, 
in  lesions  of  the  accommodation  nucleus  (p.  833),  and  also  in  diphtheric 
ptarolysis.  Despite  the  fact  that  many  of  the  last-named  (diphtheric) 
paralyses  are  probably  peripheral  in  their  localization,  they  are  quite  apt 
to  involve  the  fibers  of  the  oculomotor  nerve  which  supply  the  pupil 
and  the  ciliary  muscle. 

1  For  the  total  optical  effort  required  equals  that  which  is  necessary  to  focus  upon 
the  retina  rays  which  come  from  a  distance  of  25  cm.,  in  an  eye  rendered  emmetropic 
by  the  correction  of  its  refraction.  This  takes  place  when  the  convex  leus  in  question 
renders  parallel  the  rays  which  enter  the  eye  from  that  distance.  A  lens  of  +  1  D. 
renders  parallel  rays  which  come  fi-om  a  distance  of  1  m.,  a  lens  of  +  -i  D.  rendei-s  par- 
allel rays  which  come  from  one-fourth  of  that  distance — viz.,  25  cm. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  849 

V.   CRANIAL  NERVE;    TRIGEMINUS. 

1.  Motor  Trigeminus. — The  motor  branch  of  the  trigeminus 
supplies  the  muscles  of  mastication.  Their  power  is  tested  by  having 
the  patient  bite  upon  some  object,  such  as  a  piece  of  cork  or  wood,  or 
by  having  him  exert  vigorous  movements  of  the  jaw  while  the  examiner 
attempts  to  hold  the  jaw  still. 

In  connection  with  the  action  of  the  separate  chewing  muscles,  Vv'e  must 
remember  that  adduction  of  the  lower  jaw — i.  e.,  the  closure  of  the  teeth — is 
accomplished  essentially  by  the  temporal  and  masseter  muscles.  The  external 
pterygoid  pushes  the  lower  jaw  obliquely  forward  out  of  the  glenoid  fossa  upon 
the  articular  tubercle  (Gegenbauer).  The  bilateral  action  of  the  two  external 
pterygoids  protrudes  the  lower  in  front  of  the  upper  teeth.  The  unilateral  action 
of  one  external  pterygoid  pushes  the  jaw  to  the  opposite  side,  and  the  alternate 
action  of  the  two  external  pteiygoids — presupposing,  of  course,  that  the  temporal 
muscle  pulls  the  lower  jaw  back  again  into  the  glenoid  fossa — comprises  the  move- 
ment of  mastication.  The  external  pterygoid  also  aids  in  opening  the  mouth, 
and  this  is  farther  assisted  by  the  force  of  gravity,  and  by  the  digastric  ^  and  the 
I^latysma  myoides  muscles.'^  The  internal  pterygoid  muscle  aids  the  temporal  and 
the  masseter  in  add  acting  the  lower  jaw,  and  also  contributes,  to  a  certain  extent, 
in  the  movement  of  the  jaw  forward. 

Cerebral  jxiralyses  of  the  chewing  muscles  may  be  accurately  com- 
pared to  cerebral  paralyses  of  the  eye  muscles.  They  are  always  to  be 
attributed  to  a  cause  lying  in  the  neighborhood  of  the  trigeminus  nucleus 
or  affecting  the  efferent  trigeminus  fibers.  This  depends  upon  the  fact 
that  above  the  nucleus  the  central  fibers  of  each  trigeminus  are  distrib- 
uted to  both  hemispheres ;  in  consequence  of  which  a  unilateral  hemi- 
spheric lesion  does  not  necessitate  a  crossed  motor  trigeminal  paralysis, 
as  the  function  of  the  intact  hemisphere  is  sufficient  to  care  for  the 
innervation  of  both  sides.  To  comprehend  this  bilateral  innervation, 
the  reader  should  compare  Fig.  318,  for  that  diagram  applies  to  the 
muscles  of  mastication  in  the  same  way  as  to  the  eye  muscles.  On  the 
contrary,  a  bilateral  paralysis  of  the  chewing  muscles  can  be  brought 
about  by  bilateral  hemispheric  lesions,  such  as  pseudo-bulbar  paralyses 
(p.  876).  In  hemiplegia  a  l)ilateral  defect  of  innervation  of  the  chew- 
ing muscles  may  perhaps  be  demonstrated  dynamometrically. 

Spasms  of  the  chewing  muscles  occur  as  accompanying  phenomena 
of  general  spasms,  as  the  tonic  s]:»asms  in  tetanus  and  in  meningitis,  and 
reflexly  from  painful  affections  of  the  jaw,  producing  so-called  lockjaw. 

The  so-called  Jmv  reflex  depends  upon  both  the  motor  and  the  sensory  trigemi- 
nus. It  consists  in  a  contraction  of  the  chewing  nuiscles  which  lifts  the  lower 
jaw,  and  is  produced  by  striking  the  lower  jaw,  either  directly  with  a  percussion 
hammer  or  indirectly  through  some  object  applied  to  the  jaw.  It  can  be  elicited 
in  most  healthy  individuals,  but  is  not  absolutely  constant.  If  the  reflex  is 
increased,  a  clonus  can  frequently  be  elicited  by  simply  drawing  the  jaw  down- 
ward (jaw-clonus,  massetei'-clonus). 

2.  Sensory  Trigeminus. — The  sensory  division  of  the  trigem- 
inus supplies  the  skin  of  the  face,  the  mucous  membranes  of  the  mouth 
and  nasal  cavities,  the  conjunctiva,  and  the  cornea.      It  also  takes  part 

^  The  anterior  belly  is  innervated  by  the  third  branch  of  the  trio;eminns ;  the  pos- 
terior belly,  l)y  the  facial.  ^  Innervated  by  the  facial. 

54 


850  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

in  the  function  of  taste  (cliorda  tympani),  and  the  function  of  smell  in 
the  nasal  raucous  membranes.  The  sensibility  of  the  skin  (touch,  pres- 
sure, pain,  and  temperature)  is  tested  just  as  was  described  above  (p. 
756  et  seq.).  In  testing  the  trigeminus  taste  function,  a  soft  brush 
moistened  first  with  acid  (weak  acetic  acid)  and  afterward  with  salt 
solution  is  touched  to  the  tongue,  and  the  patient  asked  to  describe  what 
sense  of  taste  he  experiences.  The  two  sides  of  the,  tongue  are  com- 
pared, and  it  is  readily  determined  whether  the  appreciation  of  taste  is 
equally  active  and  equally  quick  upon  the  two  sides.  Since  the  trigem- 
inus practically  supplies  only  the  anterior  part  of  the  tongue,  the  test, 
should  be  made  there,  so  as  to  exclude,  so  far  as  possible,  the  taste  fibers 
of  the  glossopharyngeal.  The  patient  should  keep  his  tongue  protruded, 
and  reply  to  the  examiner's  questions  by  nodding  and  shaking  his  head. 
It  is,  of  course,  advisable  to  include  at  the  same  time  the  examination 
of  the  sense  of  taste  of  the  part  supplied  by  the  glossopharyngeal,  em- 
ploying the  same  method  as  above,  but  selecting  the  posterior  part  of 
the  tongue.  The  patient  should  not  breathe  during  the  test,  so  as  to 
avoid  a  confusion  between  the  sense  of  smell  and  that  of  taste.  The 
taste  fibers  of  the  trigeminus  (chorda  tympani)  may  be  injured  in  lesions 
of  the  lingual  muscle  (which  they  supply),  in  affections  of  the  middle  ear 
(through  which  they  pass),  in  certain  peripheral  paralyses  of  the  facial 
(see  pp.  858  and  860),  and  finally  in  lesions  of  the  root  of  the  second 
or,  according  to  other  authorities,  of  the  third  branch  of  the  trigeminus, 
in  which  the  taste  fibers  are  diverted  from  the  facial  (see  Fig.  337). 
Testing  the  sense  of  smell  supplied  by  the  trigeminus  has  been  described 
already  under  the  olfactory  nerve  (see  p.  821). 

The  corneal  sensibility  is  determined  by  touching  the  cornea  with  the 
head  of  a  pin.  Normally  this  procedure  is  very  painful,  owing  to  the 
fact  that,  according  to  v.  Frey's  researches,  the  cornea  possesses  no 
tactile  points,  but  merely  countless  pain  points  (see  p.  760  e^  seq.).  At 
the  same  time  we  should  determine  the  preservation  or  absence  of  the 
so-called  "corneal  reflex"  (lid-closure  in  touching  the  cornea).  The 
loss  of  this  may  depend  upon  a  lesion  of  the  sensory  limb  (trigeminus), 
or  upon  a  lesion  of  the  motor  limb  (facial)  of  the  reflex  arc.  Further 
examination  will  determine  which. 

Pareses  of  the  sensory  trigeminus  occur  in  peripheral  lesions  of  the 
nerve,  and  also  accompany  the  hemianesthesias  observed  both  in  hys- 
teria and  in  focal  lesions  at  the  most  posterior  part  of  the  internal  capsule. 
Disturbances  of  sensibility  which  appear  in  the  region  supplied  by  the 
trigeminus  from  spinal  cord  affections  involving  the  ascending  (spinal) 
trigeminus  roots  are  worth  noting  because  of  their  diagnostic  irnportance. 
They  may  occur  as  low  as  the  second  cervical  segments  (syringomyelia). 

(Compare  Fig.  356,  p.  915,  in  regard  to  the  distribution  of  the 
peripheral  skin  branches  of  the  trigeminus.) 

VII.   CRANIAL  NERVE  :    FACIAL. 

The  facial  nerve,  probably  purely  motor,  supplies  the  facial  muscles,  including 
the  muscle  which  closes  the  eye  (orbicularis  oculi),  Horner's  tear  sac  muscle,  the 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  851 

platysma  myoides,  the  muscles  of  the  skull  cap  (occipitalis  and  frontalis),  the 
retrahens,  attolleus,  and  transversus  auricuke/  the  stylohyoid,  the  posterior  belly 
of  the  digastric  ;  further,  in  connection  with  the  third  branch  of  the  trigeminus, 
the  buccinator,  and  finally,  by  means  of  the  descending  palatine  nerves,  which 
pass  through  the  sphenopalatine  ganglion  of  the  second  branch  of  the  trigeminus, 
it  supplies,  together  with  the  glossopharyngeus,  vagus,  and  accessory,  the  muscles 
of  the  soft  palate.  The  facial  takes  the  lion's  share  in  the  nerve  supply  of  the 
latter.  The  palatoglossal  and  palatopharyngeal  muscles  (palatine  arch  and  the 
azygos  uvulae)  seem  to  be  supj^lied  mostly  by  the  facial.  In  the  Fallopian  canal 
the  facial  nerve  supplies  the  stapedius  muscle  by  means  of  the  stapedius  nerves. 
At  one  part  of  its  course  in  the  temporal  bone  the  chorda  tympani  is  united  to 
the  facial  nerve,  and  so  brings  the  taste  fibers  to  the  facial,  and  from  it  receives 
the  salivary  secretory  fibers  for  the  submaxillary  and  sublingual  glands  (see  p. 
858).  From  its  motor  nucleus  the  facial  receives  fibers  for  sweat  secretion,  and, 
according  to  Goldzieher,  even  the  secretory  fibers  for  the  lacrimal  glands.  These, 
Koster^  thinks,  probably  start  from  the  nuclear  region  of  the  glossopharyngeal. 
At  the  periphery  the  facial  oftentimes  receives  sensory  fibers  of  the  trigeminus. 

(a)  Paralyses  of  the  Facial. 

General  Symptomatolog'y  of  Facial  Paralyses. — Upon  the 
paralyzed  side  in  facial  paralysis  we  notice  an  obliteration  of  the 
wrinkles,  a  loss  of  the  ordinary  voluntary  movements  or  their  very 
slight  preservation,  and  under  some  circumstances  even  the  loss  of  the 
emotional  movements,  the  associated  movements,  and  the  reflexes.  If 
the  paralysis  is  sufficiently  marked,  the  affected  cheek  flaps  with  respira- 
tion like  a  boat's  sail,  especially  during  sleep,  and  if  the  branches  to 
the  eye  are  affected,  the  eye  remains  more  or  less  open,  despite  attempts 
to  close  it,  and  even  during  sleep  (lagophthalmufi).  In  fresh  cases  the 
mouth  is  drawn  to  the  healthy  side.  If  the  palate  is  also  paralyzed,  it 
frequently  hangs  noticeably  lower  upon  the  diseased  side  and  seems  to 
crowd  to  the  healthy  side,  and  voluntary  or  reflex  innervation  pushes  it 
still  more  toward  the  latter.  The  depression  of  the  uvula  so  often 
occurs  normally  that  it  is  of  no  importance  for  the  diagnosis  of  palate 
paralysis.  A  unilateral  palate  paralysis  will  produce  neither  a  nasal 
character  in  the  voice  nor  regurgitation  through  the  nose ;  but  both 
phenomena  will  be  observed  if  the  palate  is  bilaterally  paralyzed  (diph- 
theric paralyses).  If  the  eye  is  prevented  from  closing  by  an  accom- 
panying involvement  of  the  ocular  branch  of  the  facial,  the  normal 
tear  secretion  will  be  affected  by  a  paralysis  of  Horner's  tear-sac  muscle  ; 
a  drooping  of  the  lower  eyelid  will  result  and  the  patients  will  suffer 
from  a  trickling  of  tears  (epiphora),  and  very  likely  later  from  ec- 
zematous  affections  of  the  eyelid.  They  may  also  complain  of  slight 
disturbances  of  vision  on  account  of  the  corneal  suffusion.  Blepharo- 
plegia  (automatic  winking)  is  exceptional  even  in  complete  facial  paralysis 
(including  the  orbicularis  oculi).  This  signifies  that  blepharoplegia 
depends  not  merely  upon  facial  innervation,  but  also  upon  atony  of  the 
levator  palpebne  superioris.  In  consequence  of  the  disturbances  of  tear 
secretion  the  nasal   mucous  membranes  become  drier  than   normal,  and 

'  According  to  Heitzmann,  the  attrahens  auriculae  is  supplied  by  the  auriculo-tem- 
poral  branch  of  the  tliird  branch  of  the  trigeminus. 
^  Arch.  J.  kl.in.  Med.,  vol.  Ixviii. 


852  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

the  sense  of  smell  is,  therefore,  often  aflfected.  The  nasal  opening  of 
the  diseased  side  often  seems  narrowed  from  paralysis  of  the  levator 
alse  nasi.  Because  of  the  paralysis  of  the  muscles  about  the  lips,  the 
saliva  frequently  trickles  from  the  corner  of  the  mouth  upon  the  para- 
lyzed side  and  patients  are  no  longer  able  to  whistle.  With  pronounced 
facial  paralysis  the  speech  may  be  altered,  especially  the  ability  to  articu- 
late the  labial  letters.  Statements  vary  considerably  in  regard  to  the 
condition  of  the  tongue  in  facial  paralyses.  Probably  facial  paralysis 
as  such  has  no  influence  upon  the  position  of  the  tongue,  although,  since 
the  facial  nerve  innervates  the  stylohyoid  and  the  posterior  belly  of  the 
digastric  muscle,  its  paralysis  may  have  a  certain  influence  upon  the 
position  of  the  hyoid  bone.  In  central  facial  paralysis  the  tongue  de- 
viates toward  the  paralyzed  side,  because  here  the  hypoglossal  territory 
anatomically  situated  so  near  by  is  always  more  or  less  affected  as  well. 
The  deflection  of  the  tongue  in  central  facial  paralysis  is,  therefore,  the 
result  of  a  paresis  of  the  genioglossus  muscle,  which  is  supplied  by  the 
hypoglossal  nerve  (see  XII.  Cranial  Xerve,  p.  875).  Deflections  of  the 
tongue  occur  in  peripheral  facial  paralysis,  but  these  have  only  an  indirect 
connection  with  the  facial  nerve  and  their  explanation  is  not  the  same 
in  every  case.  For  instance,  in  peripheral  paralysis  upon  first  glance 
one  would  think  that  the  tongue  was  protruded  obliquely,  but  more 
careful  observation  shows  that  it  is  really  protruded  in  the  middle  line, 
the  appearance  of  deviation  being  due  to  the  twisted  mouth.  In  other 
cases  the  tongue  is  actually  deflected  to  the  healthy  side,  which  is  exactly 
opposite  to  the  condition  in  central  facial  paralysis  accompanying 
genioglossus  paralysis.  Hitzig  has  proved  that  this  depends  upon 
the  patient's  effort  to  protrude  his  tongue  obliquely  in  order  to  keep  it 
in  the  middle  of  the  twisted  mouth.  This  can  be  confirmed  easily  by 
correcting  manually  the  assymetry  of  the  mouth.  The  patient  then 
protrudes  the  tongue  exactly  in  the  middle.  Paralysis  of  the  platysma 
myoides  is  most  readily  recognized  by  having  the  patient  attempt  to 
project  the  lower  lip  upwards  as  far  as  possible.  Normally  the  platysma 
assists  in  this  movement,  and  the  contracted  fibers  stand  out  quite  plainly 
under  the  skin  of  the  neck,  so  that  the  contrast  between  the  healthy  and 
paralyzed  side  can  be  readily  recognized.  A  paralysis  of  the  muscles 
of  the  ear  (retrahens,  attollens,  and  transversus  auriculae)  and  of  the 
frontalis  and  occipitalis  muscles  can  be  readily  recognized,  but  only  in 
those  patients  who  can  move  the  ears  and  the  scalp  voluntarily.  Yet, 
sometimes  a  paralysis  of  the  ear  muscles  of  one  side  causes  a  noticeable 
drooping  of  that  ear. 

The  clinical  picture  of  facial  paralysis  varies,  moreover,  according 
to  the  position  of  the  paralysis,  whether  above  the  nucleus — i.  e.,  in  the 
central  neuron,  or  in  or  IdcIow  the  nucleus — /.  e.,  in  the  peripheral 
neuron.  It  becomes  necessary,  therefore,  in  the  following  discussion,  to 
differentiate  accurately  the  symptomatology  of  these  two  types  of  facial 
paralysis,  and  to  defer  the  discussion  of  the  affections  of  secretion  and 
taste  as  w^ell  as  certain  accompanying  troubles  with  the  hearing,  until 
the  peripheral  type  (the  one  which  they  accompany)  is  taken  up. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


853 


Central  (Supranuclear)  Facial  Paralysis. — As  is  well  known, 
the  cortical  center  of  the  facial  nerve  lies  at  the  foot  of  the  central  con- 
volution, and  from  this  point  its  fibers  pass  intermingled  with  the  other 
pyramidal  fibers  through  the  internal  capsule  to  the  facial  nucleus  of 
the  opposite  side.  In  its  course  it  is  quite  frequently  injured  (cerebral 
hemiplegia).  Any  lesion  situated  above  the  nucleus  causes  what  we 
designate  as  central  facial  paralysis,  involving  the  muscles  of  expression 
of  the  lower  half  of  the  face,  and  the  corresponding  half  of  the  palate 
upon  the  affected  side,  whereas  the  secretory  and  taste  functions  of  the 
facial  are  not  affected  at  all,  because  the  fibers  supplying  them  do  not 


Fig.  329.— Facial  asymrrietry  simulating  hemiplegia  :  The  distorted  nose  and  a  groove  in  the 
lower  front  teeth  are  responsible  for  the  apparent  deviation  of  patient's  tongue  to  the  right  (New 
York  City  Hospital). 

join  the  facial  nerve  until  it  reaches  the  periphery  (see  Nuclear  or  Periph- 
eral Facial  Paralysis).  Nor  does  this  paralysis  include  the  upper 
branch  of  the  facial,  which  supplies  the  muscles  for  closing  the  eyes  and 
the  forehead  muscles,  for  reasons  about  to  be  mentioned.  In  regard  to 
the  condition  of  the  tongue  compare  above,  p.  852. 

The  most  weighty  factor  in  diflFerentiating  between  a  central  ^  and  a 
peripheral  paralysis  is  the  non-involvement  of  the  upper  facial  branch 
(for  the  forehead  and  eyes)    in  the  former.      This  peculiarity  is  to  be 

^"Central"  and  "cerebral"  sliould  not  be  confu.sed.  A  .siibnviclear  or  periphei-al 
facial  paralysis  may  be  located  within  the  brain — i.  p.,  still  be  cerebral,  although  it  is 
below  the  nucleus  and  therefore  not  central,  but  peripheral. 


854 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


explained  by  the  supposition  that  only  the  lower  part  of  the  facial  (the 
branch  to  the  face)  possesses  an  actual  crossed  innervation  from  the 
cerebral  cortex,  whereas,  the  upper  branch,  like  the  eye  muscles  (see 
p.  833)  and  the  motor  trigeminus,  is  equally  innervated  or  nearly  so  by 
both  hemispheres,  so  that  any  defect  of  innervation  from  one  hemi- 
sphere is  concealed  or  compensated  for  by  the  activity  of  the  other. 

A  diagram  of  the  central  facial  innervation  made  in  accordance  with 
this  supposition  is  given  in  Fig.  330.  This  clearly  explains  how  a 
unilateral  cerebral  lesion  at  (a)  paralyzes  only  the  lower,  not  the  upper 


Peribheral  iaeial 


Fig.  330.— DiagTam  of  the  central  innervation  of  the  facial  nerve.  The  upper  branch  is  sup- 
plied from  both  hemispheres,  more  from  that  of  the  opposite  side.  The  lower  branch  is  supplied 
almost  exclusively  from,  the  opposite  hemisphere. 

facial  of  the  opposite  side,  since  the  latter  is  still  sufficiently  inner- 
vated by  the  uncrossed  tract. 

The  hypothesis  responsible  for  Fig.  330,  viz.,  that  the  facial  possesses 
a  separate  nucleus  for  its  lower  and  another  for  its  upper  branch,  is 
really  not  based  upon  anatomic  proof.  But  experience  shows  that  a 
bulbar  paralysis,  a  disease  of  the  motor  nuclei  of  the  oblongata,  atfects 
almost  exclusively  the  lower  facial,  which  makes  it  probable  that  the 
nucleus  of  the  latter  exists  functionally  isolated,  even  though  it  is  im- 
possible to  demonstrate  this  macroscopically.  We  have  attempted  to 
express  this  individuality  as  simply  as  possible  in  Fig.  330,  by  repre- 
senting the  two  facial  nuclei  as  connected. 

It  is,  moreover,  incorrect  to  assume  that  in  a  central  paralysis  the 


EXAMINATION  OF  THE  NERVOUS  SYSTEM 


855 


Psychomotor  center  of 
the  facial 


u^^per  facial  escapes  entirely,  for  a  more  rainute  examination  shows  that 
a  slight  weakness  can  ordinarily  be  demonstrated.  This  consists  in  a 
less  vigorous  closure  of  the  eye  upon  the  aifected  side,  and  in  the 
patient's  inability  to  close  the  eye  of  the  paralyzed  side  alone,  although 
before  the  injury  this  was  possible  {Signe  de  Vorhiculaire,  Revilliod). 
From  this  it  is  evident  that  both  hemispheres  influence  the  upper  facial, 
but  that  the  effect  of  the  crossed  fibers  outweighs  that  of  uncrossed, 
although  perhaps  only  to  a  slight  extent.  Fig.  330  suggests  this  by 
the  heavier  line  representing  the  crossed  fibers  of  the  upper  facial. 

Probably  the  central  innervation  of  the  stapedius  muscle,  which  plays  a  r&le 
in  the  symptomatology  of  peripheral  facial  paralysis,  behaves  in  the  same  way  as 
that  of  the  upper  facial,  so  that  in  consequence  of  the  bilateral  innervation  of  the 
stapedius  the  symptom  of  hyperacusis  (p.  858)  cannot  be  attributed  to  central 
facial  paralysis. 

In  addition  to  the  escape  of  the  upper  facial  innervation,  a  central 
facial  paralysis  is  further  diiferentiated  from  a  peripheral  paralysis  by 
the  way  in  which  certain  voluntary  move- 
ments, the  emotional  and  the  reflex,  take 
part  in  the  paralysis.  To  explain  this 
point  we  must  assume  that  tracts  which 
are  separated  at  least  for  a  part  of  their 
course  are  responsible  for  each  different 
kind  of  movement.  Fig.  331  Avill  serve 
as  an  illustration. 

(a)  Represents  the  psychomotor  center 
of  the  facial,  (6)  represents  another  psy- 
chomotor center — {e.  g.,  the  arm-center), 
(c)  the  optic  thalamus,  {d)  the  facial  nu- 
cleus. 

The  tract  [ade)  represents  the  volun- 
tary facial  tract. 

It  has  been  assumed  oftentimes  that 
associated  movements — e.  g.,  grimaces  ac- 
companying movements  of  an  arm — de- 
pend upon  hypothetical  tracts  like  bd.  To 
prove  their  existence  it  has  been  argued 
that  a  slight  central  facial  paralysis  is  sometimes  evidenced  only  by  a 
weakness  of  the  associated  movements,  as  compared  with  those  of  the 
healthy  side,  thus  assuming  the  injury  of  a  tract  (bd)  while  the  actual 
facial  tract  (cuT)  is  unaffected.  But  this  manifestation  of  a  weakness  of 
the  associated  movements  in  the  facial  territory  in  certain  cerebral  facial 
paralyses  can  also  be  explained  in  another  way.  The  associated  move- 
ments can  be  assumed  to  pass  along  the  tract  (bad).  Then  with  a 
slight  lesion  of  the  voluntary  tract  (ad)  the  voluntary  impulse  suffers 
no  appreciable  opposition,  but  the  weaker  associated  impulse  running 
over  (bad)  does  exhibit  a  defect.  The  observation  that  a  similar 
effect  has  been  noted  in  mild  cases  of  peripheral  paralysis  argues  for 
this  explanation.     Hence  it  seems  to  the  author  superfluous  to  imagine 


Optic 
thalamus 


Fig.  331.— Diagram  of  the  three 
functionally  different  central  paths  of 
the  facial  nerve  and  of  its  reflex  arc. 


856  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

12  3 


Fig.  332.— Facial  palsy  of  left  side  :  1,  Bilateral  attempt  to  raise  eyebrows ;  2,  bilateral  attempt  to 
close  eyes ;  3,  smiling  (Church;. 

the  existence  of  tracts  like  (6c/)  in   order  to  explain  associated  move- 
ments. 


Fig.  333.— Facial  palsv  of  left  side  :  4,  Forced  effort  to  uncover  teeth  on  both  sides  ;  5,  protruded 
tongue  in  middle  line  ;  6,  mouth  open  more  widely  on  sound  side  in  bilateral  eifort  (Church). 

The  facial  innervation  of  mimicry  is  probably  from  the  tract  {cd) 
through  the  optic  thalamus.  This  is  determined  from  experience  in 
diseases  of  the  optic  thalamus  or  of  its  neighborhood,  which  cause 


Fig  334  —Facial  palsy  of  left  side :  7,  Effect  of  faradism  on  sound  side  ;  8,  non-eflfect  of  same- 
current  on  paralytic  side  (Church). 


EXAMINATION   OF  THE  NEEVOUS  SYSTEM. 


857 


isolated  paralysis  of  the  facial  mimetic  movements.  Moreover,  if  the 
thalamus  region  is  intact,  ordinarily  no,  or  only  a  very  slight,  involve- 
ment of  the  mimetic  movements  occurs  in  facial  paralysis. 

Besides  the  relative  freedom  from  involvement  of  the  upper  branch, 
a  central  facial  paralysis  is  characterized  by  intact  reflexes  and  by  the 
fact  that  the  actual  voluntary  movements  and  the  spontaneous  move- 
ments need  not  be  affected  to  the  same  degree,  whereas  without  question 
in  lesions  of  the  peripheral  neurons  situated  somewhere  along  the  line 
(de)  (i.  e.,  in  nucleoperipheral  paralysis),  every  single  function,  together 
with  the  reflexes,  appears  to  be  equally  affected.^ 

In  order  to  differentiate  a  central  from  a  nucleoperipheral  facial 
paralysis,  it  is  obviously  necessary  to  distinguish  separately  the  different 
kinds  of  facial  movements,  to  carry  out  the  electric  examination  in 
accordance  with  the  rules  mentioned  upon  p.  798  et  seq.,  and  to  deter- 
mine the  presence  or  absence  of  degenerative  atrophy  of  the  paralyzed 


Fig.  335.— Same  case  six  months  later :  9  Shows  late  contracture  on  the  paretic  side  while  the 
face  is  at  rest;  10,  contracture  in  the  lower  half  of  the  face  increased  by  gently  closing  the  eyes, 
and  at  the  same  time  shows  weakness  about  left  eye ;  11,  contracture  increased  by  raising  brows, 
showing  overaction  of  zygomatic!  and  weakness  of  frontalis  ou  left  side  (Church). 

muscles  in  accordance  with  p.  789  et  seq.  Of  course  neither  atrophy  of 
the  facial  muscles  nor  electric  changes  occur  in  central  facial  paralysis. 

Nucleoperipheral  Facial  Paralysis. — The  general  sympto- 
matology of  facial  paralysis  mentioned  above  (p.  851  et  seq.)  must  be 
amplified  in  the  case  of  nucleoperipheral  paralysis  by  the  description 
of  certain  other  disturbances  of  function  peculiar  to  this  type. 

As  most  important  may  be  mentioued  the  paralysis  of  the  stapedius 
muscle.  The  motor  fibers  for  the  supply  of  this  muscle  leave  the  facial 
nerve  within  the  petrous  bone  in  order  to  reach  the  tympanic  cavity 
(see  Fig.  337  p.  861).  Althougli  they  probably  also  accompany  the 
facial  in  its  intracranial  course,  a  stapedius  paralysis  is  actually  observed 
onlv  in  the  peripheral  form  of  facial  paralysis,   probably  because  the 

1  This  is  true,  however,  only  for  very  decided  and  complete  nucleoperipheral  facial 
paialyses.  In  incomplete  peripheral  paresis,  one  frecjuentlv  observes  merely  that  the  facial 
behaves  differently  for  different  kinds  of  movements — e.  r/.,  that  the  paralysis  is  recog- 
nized onlv  in  laughing  or  in  associated  movements.  Perhaps  this  can  be  explained  by 
supposing  that  in  the  different  kinds  of  movements  (voluntary,  spontaneous,  associated 
and  reflex  movements)  the  impulses  vary  in  their  strength. 


858  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

stapedius  muscle,  like  the  forehead  and  eye  branches  of  the  facial,  is 
innervated  by  both  cerebral  hemispheres  (see  p.  854).  This  paralysis 
of  the  stapedius,  observed  in  certain  localizations  of  peripheral  facial 
palsy  of  which  we  shall  speak  later  more  fully,  is  sometimes  manifested 
by  a  characteristic  peculiarity  of  hearing,  designated  as  hyperacusis.  In 
this  condition  the  patient  hears  the  deep  tones  (and  sometimes  others) 
louder  upon  the  paralyzed  side,  and  oftentimes  in  a  very  annoying 
fashion ;  sometimes  the  sound  impression  is  combined  with  a  sensation 
of  pain.  Lucae  has  attributed  this  phenomenon  to  an  increased  tension 
of  the  tympanic  membrane  producing  a  rise  of  the  labyrinth  pressure, 
because  the  action  of  the  tensor  tympaui  (innervated  by  the  trigeminus) 
can  be  no  longer  counteracted  by  its  antagonist,  the  stapedius.  This 
explanation  coincides  with  the  modern  conception,  introduced  by  Zim- 
mermann,  which  assumes  that  the  tympanic  membrane,  together  with 
the  chain  of  ear-bones  and  their  muscular  apparatus,  serves  much  less 
for  sound  transmission  than  for  a  so-called  accommodation  of  the  acous- 
tic organ  to  the  different  kinds  of  sound  impressions,  and  for  the  pro- 
tection of  the  internal  ear  against  too  intense  sounds,  associated  with 
marked  pressure  variations  in  the  labyrinth  fluid.  Patients  with 
paralysis  of  the  stapedius  muscle  also  occasionally  complain  of  experi- 
encing subjective  noises  in  the  ear  from  movements  of  the  facial  or 
chewing  muscles. 

Other  characteristic  appearances  arise  in  peripheral  facial  paralysis 
when  the  fibers  of  the  chorda  tympani  are  injured.  These  consist  partly 
of  disturbances  in  the  sense  of  taste  upon  the  anterior  half  of  the  tongue, 
partly  of  disturbances  in  the  salivary  secretion  of  the  submaxillary 
and  sublingual  glands.  Patients  frequently  complain  of  a  defective 
sense  of  taste  upon  one  side  of  the  tongue,  or  of  an  abnormal  dryness 
of  the  corresponding  half  of  the  mouth  (see  p.  850  et  seq.  for  the  more 
exact  method  of  testing  the  sense  of  taste).  To  examine  the  chorda 
tympani's  function  of  salivary  secretion  more  accurately  the  following 
procedure  is  advisable  :  The  patient  opens  his  mouth  and  lifts  the  tip  of 
his  tongue  so  as  to  expose  the  openings  of  the  ducts  of  the  submaxillary 
and  sublingual  glands  (ordinarily  united  at  the  sublingual  caruncle). 
In  case  he  is  unable  to  do  this,  the  tip  of  the  tongue  is  held  up  by  a 
pair  of  forceps  such  as  are  used  in  chloroform  narcosis.  The  sublingual 
caruncle  is  then  carefully  dried  upon  both  sides  of  the  frenum  with 
absorbent  cotton,  and  while  the  examiner  watches  carefully  the  open- 
ings of  the  ducts,  the  patient  inhales  deeply  the  fumes  from  a  sponge 
saturated  with  acetic  acid,  and  held  close  to  the  nose.  If  the  chorda 
functionates  normally  the  saliva  flows  from  both  sides  freely,  as  a 
result  of  the  reflex  ;  if  the  chorda  is  paralyzed  upon  one  side  the  flow 
occurs  only  upon  the  healthy  side  or  much  more  profusely  upon  that 
than  upon  the  injured  side. 

The  excretory  ducts  are  occasionally  so  close  together  that  the  above  method 
will  not  enable  us  to  determine  whether  saliva  comes  from  one  or  both  openings. 
In  these  cases  the  author  has  succeeded  in  gently  clamping  the  excretory  duct  upon 
the  unaffected  side  with  a  cilia-forceps,  after  which  it  is  easy  to  observe  whether 
saliva  escapes  from  the  opposite  opening. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  859 

In  connection  with  the  anatomic  relations  of  these  two  functions 
of  the  chorda  to  the  facial,  we  should  emphasize  the  fact  that  the  func- 
tion of  secreting  saliva  belongs  to  the  facial  from  its  origin  at  the  base 
of  the  brain  up  to  the  exit  of  the  chorda  tympani.  According  to 
Koster^  it  probably  does  not  arise  from  the  facial  nucleus  itself,  but 
from  the  nuclear  region  of  the  portis  intermedia  Wrisbergi  belonging 
to  the  glossopharyngeal.  The  taste  fibers  of  the  chorda  tympani,  on 
the  contrary,  accompany  the  facial  from  the  periphery  through  the  tym- 
panic cavity,  merely  a  tiny  distance  apart,  and  leave  the  latter  again 
near  the  geniculate  ganglion  in  the  petrous  bone  (Fig.  337),  according 
to  one  supposition  (continuous  blue  line)  in  order  to  connect  with  the 
sphenopalatine  ganglion  by  means  of  the  superficial  large  petrosal  nerve, 
and  from  there  with  the  second  branch  of  the  trigeminus,  but  according 
to  another  less  probable  view  (dotted  blue  line)  in  order  to  connect 
with  the  third  branch  of  the  trigeminus  or  with  the  glossopharyngeal 
by  means  of  the  communicating  nerve  to  the  tympanic  plexus. 

Our  knowledge  of  the  functions  of  the  peripheral  facial  has  been 
still  further  perfected  by  Goldzieher.  He  found  that  at  the  base  of  the 
brain  the  trunk  of  this  nerve  contains  fibers  for  the  secretion  of  tears, 
and  that  therefore  an  injury  to  the  facial  at  this  point  results  in  drying 
up  the  tear  secretions  '^  upon  the  paralyzed  side.  These  secretory  fibers 
must  emerge  from  the  facial  further  down  in  the  region  of  the  genicu- 
late ganglion  and  pass  by  means  of  the  greater  superficial  petrosal  nerve 
to  the  sphenopalatine  ganglion  and  from  there  to  the  lacrimal  glands 
by  means  of  the  communication  between  the  subcutaneous  malar  and 
the  lacrimal  nerves.  Goldzieher's  suppositions  have  been  confirmed 
by  an  observation  of  Franke,^  as  well  as  by  the  extensive  clinical  and 
experimental  work  of  Koster.  According  to  the  latter  the  lacrimal 
secretory  fibers,  like  the  salivary  secretory  fibers,  probably  arise  from 
that  part  of  the  glossopharyngeal  nucleus  belonging  to  the  portio 
intermedia  Wrisbergi,  and  mingle  with  the  facial  directly  at  its  exit 
from  the  brain.  To  test  the  lacrimal  secretion,  he  recommends  tick- 
ling the  nasal  mucous  membrane  with  a  feather  or  with  a  fine  brush, 
and  then  observing  the  secretion.  The  amount  of  the  tear-flow  secreted 
can  be  best  estimated  by  collecting  it  upon  a  piece  of  filter  paper  intro- 
duced into  the  conjunctival  sac. 

Koster,  in  addition,  showed  that  disturbances  of  the  sweat  secretion 
upon  the  paralyzed  half  of  the  face  appear  not  uncommonly  in  periph- 
eral facial  paralysis.  This,  too,  is  to  be  attributed  to  the  fact  that 
from  its  nucleus  the  facial  conducts  fibers  for  the  secretion  of  sweat. 
In  peripheral  facial  paralysis,  these  fibers  may  be  stimulated  (hyperhi- 
drosis)  as  well  as  paralyzed  (anhidrosis).  These  phenomena  may  be 
confused  with  the  influence  of  the  sympathetic  upon  the  sweat  secretion 
of  the  face. 

^  Deutsch.  Arch.  f.  klin.  3Ted.,  vol.  Iw'm.,  1900. 

2  Only  intermittent  secretion  from  the  tear  glands,  such  as  occurs  in  weeping  or  in 
reflex  tears,  not  a  continued  conjunctival  secretion. 
^  Deutsch.  med.  Woch.,  1895,  p.  33. 


860 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


Slight  disturbances  of  hearing  which  occur  in  lesions  of  the  facial 
nerve  in  the  neighborhood  of  the  geniculate  ganglion  are  worth  men- 
tioning ;  these  depend  upon  the  proximity  of  the  internal  ear  to  the 
facial  nerve  at  this  point  (the  cochlea  is  separated  by  a  bone  about 
1  mm.  thick).  Hence  inflammatory  changes  of  the  facial  can  easily  have 
an  effect  upon  the  internal  ear. 

The  distinctions  between  nucleoperipheral — i.  e.,  facial  paralysis  in 
the  region  of  the  peripheral  neurons — and  central  facial  paralysis  have 


^^r 


Fig.  336.— Diagram  of  the  peripheral  nerve  fibers  of  the  facial  for  clinical  use. 

already  been  emphasized  in  describing  the  latter  (p.  853  et  seq.).  From 
this  it  is  evident  that  the  essential  factors  in  the  distinction  are  the  defi- 
nite paralysis  of  the  forehead  and  eye  branch  of  the  facial  in  the 
nucleoperipheral  forms,  disturbances  in  the  secretory  and  taste  func- 
tions, the  condition  of  the  tongue  (p.  852),  the  condition  of  the  reflex 
and  spontaneous  movements  (p.  855),  and  the  electric  and  trophic  con- 
ditions of  the  muscles.  After  the  nucleoperipheral  nature  of  a  facial 
paralysis  has   once  been  recognized,  the   essential   interest  centers  in 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


861 


determining  the  exact  location  of  the  lesion  in  the  course  of  the 
nucleoperipheral  tract.  This  is  best  made  out  by  referring  to  the 
diagrams  (Figs.  336  and  337).  Fig.  336  serves  for  general  orien- 
tation;  Fig.  337,  for  a  comprehension  of  the  anastomoses  of  the 
facial  nerve. 


'EaurLCwt 
fjosC. 


®  Gangl.syijnajCLlL.  nfihi. 

Glcmd.Suhmax.  UpP^^^^-^''J^        //^^ 

/J 


Fig.  337— Diagrammatic  plan  of  the  periplieral  facial  nerve  and  its  connection  with  other 
nerves:  _    .  , 
Motor  fibers  of  facial. 

Other  cranial  nerves.  ,      ,  ,.  ,    i      j        j    ^  <.!,„ 

Secretory  fibers  of  the  facial  to  the  submaxillary  and  sublingual  glands  and  ot  the 

glossopharyngeal  to  the  parotid. 

Taste  fibers  of  the  facial  from  the  chorda  tympaui.  »,  ,  ,„ 

Central  course  of  the  same  from  the  geniculate  ganglion  to  another  less  prpbabie 

connection.  (Termination  through  the  nervus  tympanicus  (Jacobson  s)  m  the 
glossopharyngeal  or  through  the  otic  ganglion  iii  the  third  branch  ot  tlie  tri- 
^geminal.) 

In  Fig.  336  it  is  evident  that  a  lesion  situated  at  («)  Avill  aifect  the 
so-called  mimic  branches  of  the  facial,  including  the  platysma  myoides ; 
if  it  is  situated  at  (6),  above  the  exit  of  the  facial  from  the  stylomastoid 
foramen,  the  posterior  auricular  nerve  will  also  be  paralyzed  (this  sup- 
plies the  occipital  muscle  and  the  attolens,  retrahens,  and  transversus 


862  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

auricular  muscles).^  As  many  people  cannot  move  these  muscles  vol- 
untarily, paralysis  of  them  is  oftentimes  shown  only  by  an  electric 
examination,  and  then,  of  course,  only  when  the  electric  irritability 
of  the  paralyzed  muscle  has  been  affected.  If  the  lesion  is  situated  at 
(c),  the  taste  and  the  salivary  secretory  fibers  of  the  chorda  tympani  are 
also  paralyzed.  This  becomes  evident  in  a  diminution  of  the  trigem- 
inus taste  appreciation  upon  half  of  the  tongue  in  its  anterior  portion 
and  possibly  in  a  dryness  of  half  of  the  mouth  (see  below  for  a  more 
exact  method  of  testing  this  function).  The  sensations  of  touch  and 
pain  in  the  anterior  half  of  the  tongue  are  sometimes  diminished,  since 
the  chorda  tympani  also  contains  fibers  for  the  appreciation  of  touch 
and  pain  in  the  tongue.  With  a  lesion  at  (d),  the  stapedius  muscle, 
supplied  by  the  stapedius  nerve  from  the  facial,  shares  in  the  paralysis 
(see  above,  p.  857,  in  relation  to  appearances  so  caused).  Should  the 
lesion  be  situated  still  farther  above  at  (e),  that  is  above  the  geniculate 
ganglion,  the  disturbances  of  taste  just  mentioned  .escape,  because  the 
taste  fibers  have  left  the  facial  at  this  point,  but  the  palate  half  will  be 
paralyzed  to  voluntary  and  to  reflex  (see  below)  impulses,  and  the  secre- 
tion of  tears  (see  above)  may  be  affected.  Disturbances  of  hearing  from 
an  extension  of  the  process  to  the  cochlea  may  result  from  lesions  in 
the  neighborhood  of  the  geniculate  ganglion.  If  the  paralysis  is  situ- 
uated  at  (/),  at  the  base  of  the  brain,  where  the  acoustic  and  facial  nerves 
are  so  closely  approximated,  the  former  is  oftentimes  involved  with  the 
latter,  and  in  addition  to  the  involvement  of  the  tear  secretion,  diminu- 
tion of  hearing  and  disturbances  of  equilibrium  from  lesions  of  the 
fibers  of  the  ramus  vestibuli  are  added  to  the  symptoms  of  facial 
paralysis.  When  the  lesion  is  localized  still  higher  above — i.  e.,  is 
nuclear — at  least  in  its  most  usual  form  (bulbar  paralysis),  the  coinci- 
dent involvement  of  other  bulbar  nerves,  the  bilateral  character  of  the 
paralysis,  and  the  very  unequal  involvement  of  the  individual  branches 
of  the  facial  make  the  picture  sufficiently  characteristic.  In  bulbar  paral- 
ysis, the  territory  of  the  lower  facial  (see  p.  854)  is  most  affected,  espe- 
cially the  lip  musculature.  The  facial  palsy  due  to  a  lesion  in  the  pons, 
another  nucleoperipheral  palsy  since  the  peripheral  motor  neuron  is 
also  affected,  is  usually  characterized  by  paralysis  of  the  extremities 
upon  the  opposite  side  (alternating  or  crossed  paralysis).  This  is  due 
to  the  involvement  of  the  psychomotor  tract  for  the  extremities  (the 
pyamidal  tract)  before  its  decussation,  although  at  this  point  the  facial 
fibers  have  already  crossed.  Between  this  location  and  the  cortex  is 
the  region  for  central  facial  paralysis. 

In  addition  to  these  local  diagnostic  points  (in  regard  to  the  special 
symptomatology  of  nucleoperipheral  facial  paralysis),  the  following 
facts  will  be  of  assistance  in  completing  the  clinical  picture  : 

Lagophtlialmus,  due  to  paralysis  of  the  eye  branch,  is  a  very  char- 
acteristic sign  in  most  cases  of  peripheral  facial  paralysis,  and  one 
which  furnishes  a  sharp  contrast  to  central  facial  paralysis.     This  con- 

^  According  to  Heitzmann,  the  attrahens  auricular  muscle  is  supplied  by  the 
auriculotemporal  nerve  from  the  third  branch  of  the  trigeminus. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  863 

sists  in  the  eyes  remaiuing  open  upon  the  paralyzed  side,  despite 
attempts  to  close  it.  In  fruitless  endeavors  to  close  the  eye  the  globe 
assumes  the  so-called  sleeping  position,  upward  and  outward,  more 
rarely  upward  and  inward,  beneath  the  upper  lid,  so  that  patients 
believe  that  they  have  completely  closed  the  eye. 

This  so-called  "Bell's  phenomenon,''  just  described,  is  to  be  attributed  to  an 
associated  movement  of  the  globe,  whose  object  is  to  protect  the  eye.  It  occurs 
physiologically,  as  is  shown  by  its  appearance  during  sleep  in  a  healthy  indi- 
vidual, as  well  as  by  the  fact  that  it  also  occurs  when  a  healthy  person  attempts 
to  close  the  eye  when  the  closure  is  mechanically  prevented.  The  sign  is  more 
evident  in  paralysis  of  the  eye  branch  of  the  facial,  not  only  because  the  eye 
remains  open,  and  so  we  see  it  more  plainly,  but  also  because  the  movement 
appeared  to  be  increased,  probably  because,  after  interruption  of  conductivity  in 
the  domain  of  the  facial  branches,  the  motor  impulses  radiate  more  intensely 
through  the  pathway  of  the  associated  movement  in  a  way  very  analogous  to 
other  associated  movements.  Bell's  phenomenon  has  some  prognostic  signifi- 
cance, as  one  of  the  earliest  signs  of  improvement  in  facial  paralyses  is  a  retro- 
gression of  this  sign.  This  is  probably  to  be  attributed  to  an  improvement  in 
the  conduction  function  of  the  facial  fibers,  whereby  a  smaller  proportion  of  the 
motor  impulses  are  diverted  into  the  branch  for  associated  movements  ;  with  this 
improvement  of  transmission  the  strength  of  the  motor  impulses,  corresponding 
to  the  better  effect,  is  diminished. 

Although  patients  with  peripheral  paralysis  protect  themselves  against 
a  painful  sensation  in  touching  the  cornea,  nevertheless  the  usual  lid- 
closure  (corneal  reflex,  p.  850)  either  fails  entirely  or  occurs  very  in- 
completely. On  the  contrary,  automatic  winking  (blepharoplegia)  is 
retained  (see  p.  851). 

The  true  corneal  reflex  must  not  be  confused  (although  the  mistake  is  com- 
mon) with  the  ordinary  eye  closure  excited  reflexly  by  the  visual  appreciation 
of  an  approaching  object  even  before  the  cornea  has  been  touched.  This  latter 
is  really  an  opticofacial  reflex — i.  e.,  the  optic  nerve  constitutes  the  sensory 
limb  ;  and  physiologically  it  is  a  most  useful  process,  since  it  frequently  protects 
the  eye  by  closing  the  lid  in  time  to  prevent  the  injury,  whereas  the  true  corneal 
reflex  would  occur  too  late  to  be  of  any  service.  The  optic  reflex,  like  the 
genuine  corneal  reflex,  is  evidently  either  lost  or  diminished  in  perii^heral  facial 
paralysis.  It  is  of  some  diagnostic  importance  in  determining  the  condition  of 
the  facial  in  those  cases  where  the  true  corneal  reflex  is  absent  as  a  result  of 
anesthesia  of  the  cornea  (sensory  trigeminus  paralysis). 

When  a  lesion  is  situated  at  (e),  the  palate  reflex  may  be  lost.  This 
can  be  recognized  by  tickling  the  patient's  pharynx  with  a  brush, 
although  in  unilateral  facial  paralysis  it  is  often  very  difficult  to  be 
sure  of  it,  as  the  paralyzed  half  is  passively  moved  by  the  healthy  half 
of  the  palate. 

Characteristic  appearances  of  irritation  are  not  infrequently  observed 
in  the  partially  paralyzed  territory  of  old  severe  peripheral  facial  paraly- 
ses which  have  recovered  completely.  These  consist  either  of  contrac- 
tures, which  may  lead  to  the  erroneous  supposition  of  a  facial  paresis 
of  the  opposite  side,  or  of  associated  movements  and  of  fibrillary  con- 
tractions in  the  paretic  and  atrophic  territories. 

Hitzig  assumes  that  these  phenomena  depend  upon  irritation  in  the  facial 
nucleus  as  a  result  of  degenerative  processes  proceeding  from   the   periphery, 


864  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

which  hypothesis  coincides  with  Darkschewitsch's  explanation.  The  latter  has 
discovered  that  peripheral  lesions  of  the  motor  nerves  lead  to  changes  in  the 
nuclear  cells.  These  irritative  phenomena  in  the  facial  territory  may  persist 
through  life. 

The  electric  irritability  is  generally  altered  in  nucleoperipheral  facial 
paralyses.  In  mild  cases  there  is  a  more  or  less  diminished  exci- 
tability and  in  severe  cases  a  complete  or  partial  reaction  of  degenera- 
tion, resulting  in  a  degenerative  atrophy  of  the  paralyzed  muscles  (see 
pp.  812  and  816). 

Severe  peripheral  facial  paralyses  commonly  lead  to  vasomotor  phenomena, 
as  shown  by  the  occurrence  of  coolness,  cyanosis,  and  frequently  some  edema  of 
the  affected  side.  It  has  not  yet  been  accurately  determined  whether  this  depends 
upon  a  connection  between  the  peripheral  facial  and  the  vasomotor,  or  upon  a 
lesion  of  the  sympathetic  fibers  which  are  united  to  the  facial  branches  in  the 
periphery.  Xeither  hypothesis  is  absolutely  necessary,  since  the  muscular  action 
of  the  affected  side  is  sufficiently  impaired  to  produce  some  stasis  (p,  795  et  seq.). 

The  diminished  senmbility  of  the  affected  half  of  the  face,  not  infrequently 
observed  in  facial  jsaralysis,  has  led  to  A-arious  hypotheses.  Some  authors,  con- 
trary to  the  general  opinion,  assume  that  the  facial  contains  some  sensoiy  fibers. 
This  is,  however,  unnecessary  in  order  to  explain  the  disturbances  of  sensibility, 
for  certainly  sensory  trigeminus  fibers  do  anastomose  at  the  periphery  with  the 
facial,  and  these  may  quite  well  be  injured  by  the  same  cause.  The  absolute 
immobility  of  the  affected  half  of  the  face  and  the  associated  circulatory  disturb- 
ances are  alone  sufficient  to  dull  the  sensibility'.  Such  disturbances  are  most  fre- 
quently discovered  while  the  muscles  are  being  tested  by  the  electric  current ;  for 
this  procedure  is  found  to  be  more  painful  upon  the  healthy  side,  especially  in 
severe  paralysis,  than  upon  the  injured  side.  The  observation  certainly  sug- 
gests that  the  degeneration  of  the  muscles  may  alone  be  responsible  for  a  dis- 
turbance of  the  sensory  nerve  terminations.  In  many  cases  an  hysterical  cause 
may  explain  the  difficulty. 

The  j)ains  accompanying  rheumatic  facial  paralysis  in  the  affected  half  of  the 
face  are  probably  due  to  coincident  involvement  of  the  peripheral  trigeminus 
fibers  running  with  the  facial. 

Bulbar  paralysis,  which,  as  has  been  already  mentioned,  includes  a  partial 
nuclear  facial  paralysis,  sometimes  exhibits  an  increased  scdivary  secretion ;  and 
this  is  j^eculiar  in  so  much  as  there  is  actually  more  saliva  secreted  than  normally, 
and  not  merely  an  excessive  flow  on  account  of  imperfect  closure  of  the  lips. 
We  may  assume  that  this  increased  secretion  falls  under  the  heading  of  a  so- 
called  paralytic  secretion.  Physiologists  have  noted  it  in  animals  after  they  have 
cut  the  several  nerves  leading  to  the  submaxillary  glands.  Such  an  assumption, 
however,  hardly  seems  justified,  in  the  first  place  because  the  fibers  supplying 
the  sublingual  and  submaxillary  glands  really  come  from  the  trigeminus,  and  in 
bulbar  paralysis  the  latter  nerve  is  one  of  the  last  to  be  involved,  and  in  the 
second  place  because  the  paralytic  secretion  is  rather  a  transitory  condition,  and 
even  if  continued  is  never  very  decided.  The  more  rational  explanation  seems 
to  the  author  to  be  that  the  swallowing  mechanism  is  affected  in  bulbar  paralysis, 
the  saliva  accumulates  in  the  mouth,  and  its  presence  reflexly  stimulates  the 
secretion. 

(6)  Spasms  of  the  Facial. 

Spasmodic  phenomena  in  the  facial  territory  are  not  rare,  but  their  descrip- 
tion belongs  to  special  pathology,  so  that  here  we  need  only  mention  their  occur- 
rence in  the  so-called  "  mimic  facial  sjiasm,"  tetanus,  tetany,  epilepsy,  and  chorea. 
The  peculiar  twitching  of  the  lid  depending  upon  fibrilhiry  contractions  of  the 
facial,  is  worth  mentioning  from  the  diagnostic  standpoint.  It  occurs  in  neuras- 
thenics when  they  attempt  to  close  the  eyes  at  command.    Such  an  attempt,  as  has 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  865 

been  frequently  noted,  causes  some  degree  of  difficulty  in  many  cases.  This 
twitching  is  quite  an  important  sign  of  neurasthenia.  Irritative  appearances  in 
the  territory  of  old  facial  paralyses  have  been  mentioned  in  preceding  paragraphs 
(p.  863  et  seq.). 

VIII.    CRANIAL  NERVE  :  AUDITORY   (Acusticus). 

(a)  Paralysis  of  the  Auditory  Nerve. 

Auditory  paralyses  occur  in  diseases  of  the  internal  ear,  of  the 
petrous  bone,  in  affections  of  the  base  of  the  brain  and  of  the  medulla 
oblongata,  and  finally  as  a  part  of  cerebral  hemianesthesias. 

A  unilateral  acoustic  j^aralysis  in  hemianesthesia  is  never  absolute,  except  in 
hysteric  affections  ;  there  is  much  more  apt  to  be  only  a  moderate  impairment 
of  hearing.  This  may  be  accounted  for  by  the  fact  that  the  central  innervation 
of  the  acoustic  is  not  entirely  crossed,  and  coincides,  so  far  as  the  author  knows, 
with  the  fact  that  in  unilateral  lesions  of  the  auditory  center,  situated  in  the 
temporal  lobes,  no  instance  of  comx^lete  crossed  deafness  has  as  yet  been  observed. 

In  examining  the  auditory  nerve,  a  procedure  which  should,  of  course, 
be  carried  out  in  as  quiet  a  room  as  possible,  the  perception  of  sound  by 
air  conduction  must  be  sharply  distinguished  from  that  by  bone  con- 
duction. In  testing  the  former,  a  ticking  watch  or  vibrating  tuning- 
fork  is  held  near  the  external  auditory  canal,  the  maximum  distance  de- 
termined at  which  one  or  both  can  be  heard,  and  the  two  sides  then  com- 
pared. In  testing  the  latter,  the  perception  of  sound  by  bone  conduc- 
tion, the  watch  or  tuning-fork  is  held  upon  the  mastoid  process,  and 
any  difference  between  the  two  sides  determined  from  the  patient's 
statements.  Since  neither  watches  nor  tuning-forks  emit  sounds  of 
definite  intensity,  PolitzerV  has  constructed  a  sound-meter  with  which 
a  sound  of  constant  intensity  may  be  produced  by  allowing  a  small 
hammer  to  fall  upon  a  metallic  bar.  Politzer's  sound-meter  may  be 
employed  to  test  the  perception  not  only  of  sounds  transmitted  through 
the  air,  but  also  of  sounds  conducted  by  bone,  in  which  case  the  instru- 
ment is  brought  into  contact  with  the  cranial  bones  l^y  means  of  a  rod- 
shaped  attachment. 

Rinne's  test  is  also  of  some  importance.  It  consists  in  holding  a 
vibrating  tuning-fork  to  the  mastoid  process,  until  the  patient  can  no 
longer  appreciate  any  sound  ;  then  the  tuning-fork  (which  is  still  vibra- 
ting) is  quickly  approached  to  the  external  ear.  If  the  auditory  trans- 
mitting apparatus  h  functionating  ^vell,  the  tuning-fork  is  heard  again 
(positive  result  of  Rinne's  test) ;  should  this  not  he  the  case  (negative 
result  of  Rinne's  test)  there  must  exist  some  disease  of  this  apparatus. 
If  the  issue  of  the  test  is  positive  the  transmitting  apparatus  is  not 
necessarily  perfect,  because  air  conduction  permits  a  better  auditory 
impression  than  bone  conduction,  and  slight  affections  of  the  sound- 
transmitting  mechanism  might  escape  notice. 

To  determine  a  disturbance  of  hearing  independent  of  the  otoscopic  findings 
and  Weber's  and  Schwabach's  tests  (see  below),  Rinne's  test  must  be  employed 
in  a  more  exact  quantitative  manner  by  determining  the  degree  of  superiority 

'  Pnlitzer,  Lehrb.  der  Ohrenheilfcuncle,  Stuttgart,  1887. 
55 


866  EXAMINATION   OF  THE  NERVOUS  SYSTEiM. 

of  air-conduction  over  bone-conduction  by  measuring  the  time  during  which 
a  vibrating  tuning-fork  is  heard  at  the  external  auditory  meatus  after  it  has 
become  inaudible  upon  the  mastoid  process.  Under  normal  conditions  this  time 
for  an  A^  tuning-fork  amounts  to  about  30  seconds.  If  Rinne'  s  test  gives  a  negative 
result,  we  may  proceed  in  the  opi^osite  manner  by  determining  the  time  during 
which  the  tuning-fork  upon  the  mastoid  process  is  heard  after  it  has  become 
inaudible  Avhen  held  in  front  of  the  external  auditory  meatus. 

Zimmermann  has  recently  objected  to  the  principles  involved  in  Rinne's  test, 
believing  that  in  placing  the  tuning-fork  upon  the  bone  we  test  the  energy  of 
movement  of  the  handle  of  the  fork,  and  that  in  holding  the  tuning-fork  at  the 
external  auditory  meatus  we  test  the  much  greater  energy  of  movement  of  the 
prongs.  From  this  he  concludes  that  the  diagnostic  importance  of  Rinne's  test  is 
doubtful  and  that  the  normal  positive  result  cannot  be  employed  as  an  argument 
for  Helmholtz's  theory,  according  to  which  the  membrana  tympani  and  the  audi- 
tory ossicles  are  assumed  to  aid  in  the  transmission  of  sound.  According  to 
Zimmermann's  theory,  (see  p.  858  et  seg.),  the  normal  positive  result  of  Rinne's 
test  is  due  to  the  fact  that  the  auditory  ossicles  may  really  be  an  accommoda- 
tion mechanism  for  the  acoustic  organ,  or,  in  other  words,  a  sound-dulling  rather 
than  a  sound-transmitting  apparatus.  These  views  of  Zimmermann 'have  been 
successfully  combated  by  v.  Bezold,  who  has  suggested  a  new  method  of  per- 
forming Rinne's  test.  Performed  in  this  way,  the  test  is  free  from  objection  and 
rehabilitates  Helmholtz's  theory.  He  provides  the  a^  tuning-fork  with  a 
rounded  handle  and  after  the  vibrations  have  become  inaudible,  both  upon  the 
mastoid  process  and  at  the  external  auditory  meatus,  he  introduces  this  handle 
into  the  meatus  so  that  an  air-tight  closure  of  the  canal  is  effected.  It  then 
becomes  manifest  that  the  audibility  of  the  tuning-fork,  introduced  in  this 
manner,  is  increased  by  about  12  seconds  over  the  ordinary  perception  by  means 
of  air  conduction ;  the  vibrations  are  consequently  perceived  by  air  conduction, 
about  30+12  seconds  longer  than  by  bone-conduction  (the  positive  normal 
result  of  Rinne's  test  carried  out  in  this  manner).  In  this  test  air  conduction 
and  bone  conduction  are  both  measured  with  the  handle  of  the  fork,  so  that  the 
results  may  be  absolutely  and  directly  compared. 

The  so-called  Weber's  test  has  a  similar  significance  for  the  differ- 
entiation of  impaired  hearing  due  to  disturbances  of  the  conducting 
apparatus  from  that  dependent  upon  affections  of  the  nervous  portion 
of  the  acoustic  organ.  The  handle  of  a  vibrating  tuning-fork  is  placed 
upon  the  middle  of  the  vertex,  and  the  patient  is  required  to  state  upon 
which  side  he  perceives  the  louder  sound.  In  affections  of  the  conduct- 
ing apparatus  the  sound  is  usually  more  distinctly  perceived  upon  the 
affected  side,  while  the  reverse  is  true  in  affections  of  the  auditory  nerve 
or  of  the  labyrinth.  The  chief  obstacle  to  Weber's  test  is  the  uncer- 
tainty of  the  localization  of  the  auditory  perception  in  one  ear. 

Schivabach's  test  consists  in  determining  whether  the  vibrating  tuning-fork  is 
perceived  by  bone  conduction  for  an  abnormal  period  of  time.  If  it  be  heard 
longer  than  normal,  Schwabach  supposes  a  disturbance  of  the  conducting  appa- 
ratus; if  not  so  long  as  normal,  an  affection  of  the  nervous  mechanism.  If  the 
investigator  be  possessed  of  normal  hearing  this  comparison  is  best  made  by 
removing  the  tuning-fork  from  the  patient's  mastoid  process  as  soon  as  he  declares 
it  to  be  inaudible  and  placing  it  upon  the  mastoid  process  of  the  investigator; 
the  result  is  then  to  be  compared  with  that  obtained  by  reversing  the  process. 

The  results  of  all  these  tests,  however,  should  be  utilized  with  caution,  since 
the  pitch  and  intensity  of  the  sound  employed  may  sometimes  cause  them  to  vary 
and  even  be  the  direct  opposite  of  what  the  formulated  rules  would  lead  us  to 
expect. 

The  usual  method  adopted  in  ear  clinics  for  testing  the  auditory  nerve  is  by 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  867 

means  of  determining  which  of  a  series  of  tuning-forks,  comprising  the  entire 
tone  scale,  can  be  appreciated!  This  method  has  not  yet  been  adopted  in  clinical 
medicine,  because  only  gross  disturbances  can  be  utilized  in  the  local  diagnosis  of 
cerebral  diseases. 

The  acuteness  of  hearing  should  be  tested  by  means  of  the  whispered  voice, 
as  well  as  by  means  of  the  above-described  instrumental  test.  In  a  quiet  room 
the  examiner  notes  at  what  distance  from  each  ear  (the  other  being  closed) 
the  whispered  voice  can  be  heard;  experience  has  shown  that  such  a  method  fre- 
quently furnishes  quite  different  results  from  the  instrumental  test.  The  whis- 
pered voice  is  preferable  to  the  loud  voice,  not  only  because  the  latter  would  be 
too  intense  in  a  closed  space,  but  also  because  the  individual  sounds  and  words 
are  more  uniformly  adapted  for  auditory  perception  when  whispered  than  when 
loudly  spoken. 

{b)  Irritative  Phenomena  of  the  Auditory  Nerve. 

Subjective  sound  perceptions  result  from  various  cerebral  diseases,  from  gal- 
vanic stimulation  of  the  brain,  and  especially  from  affections  of  the  internal  and 
middle  ear.  The  most  familiar  are  the  ear  noises  heard  in  chronic  sclerotic  otitis 
media,  the  "crux"  of  the  otologists.  This  acoustic  phenomenon  of  irritation 
does  not  possess  in  cerebral  disease  any  very  important  local  diagnostic  signifi- 
cance, because  even  the  most  exact  otoscopic  examinations  cannot  differentiate 
with  certainty  the  subjective  perceptions  of  peripheral  from  those  of  central  origin. 
A  peripheral  origin  is  much  more  probable,  on  the  one  hand,  on  account  of  the 
great  frequency  of  middle-ear  diseases,  and,  on  the  other  hand,  on  account  of  the 
generally  applicable  law  that  the  terminal  organs  of  sensory  nerves  are  the  most 
irritable  parts  of  the  sensory  apparatus.  Pathologic  appearances  of  the  drum 
argue  for  a  peripheral  origin  of  the  ear  noises.  A  normal  drum,  however,  does 
not  necessarily  exclude  such  an  origin. 

Auditory  Vertigo  {Meniere's  Disease). — Since  the  vestibular  branches  of  the 
acoustic  nerve  supply  the  semicircular  canals,  and  since  the  latter  are  regarded 
as  the  organs  of  equilibrium,  it  is  easy  to  understand  that  vertigo  will  result  from 
affections  of  the  acoustic  nerve.  Vertigo  is  in  fact  most  usually  observed  accom- 
panying affections  of  the  labyrinth  and  of  the  middle  ear.  Cerebellar  vertigo 
must  be  closely  identified  with  auditory  vertigo  on  account  of  the  anatomic  prox- 
imity of  the  auditory  nerve  to  the  cerebellum. 

(c)  Otoscopic  Examinations. 
Disease  of  the  hearing  apparatus  is  frequent,  even  in  people  who 
consider  themselves  perfectly  well.  Hence,  under  all  circumstances  in 
which  a  disturbance  of  hearing  has  been  determined,  it  is  important  to 
make  an  otoscopic  examination.  In  no  other  way  can  we  differentiate 
between  disturbance  of  hearing  dependent  upon  disease  of  the  auditory 
nerve  and  that  depending  upon  the  ear  itself.  This  distinction,  as  was 
mentioned  above,  cannot  always  be  determined  by  the  Rinne  test  nor 
in  some  instances  even  by  an  otoscopic  examination,  so  that  a  disturb- 
ance of  hearing  will  not  always  assist  much  in  the  diagnosis  of  cerebral 
disease. 

The  reader  is  advised  to  consult  the  otoscopic  pictures  in  Politzer's  "Atlas  der 
Beleuchtungsbilder  des  Trommelfells"  Wien,  Braumiiller,  1896. 

{d)  Demonstration  of  Simulated  Deafness.' 
When  ioioX  (leaf aess  of  both  earix  is  simulated  a  more  prolonged  obser- 
vation in  a  hospital  is  usually  all  that  is  necessary  to  determine  it. 

'  Partly  taken  from  Siebermann,  "  Untersuchung  atif  Simulation  von  Schwerhorig. 
keit  oder  Taubheit,"  Schweizerischer  Medlcinalkaknder,  1895,  p.  76  f. 


868  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

The  simulation  of  bilateral  or  unilateral  impairment  of  hearing  becomes 
evident  when  we  test  the  patient's  hearing  (that  of  each  ear)  with  his 
eyes  closed,  so  that  he  cannot  see  the  distance  from  which  the  sound 
comes.  He  will  then  express  contradictory  statements  in  regard  to 
rapidly  repeated  tests. 

Simulation  of  unilateral  total  deafness  may  be  discovered  in  various 
ways: 

1.  The  patient's  normal  ear  is  closed,  and  the  examiner  speaks 
directly  in  front  of  the  supposedly  deaf  ear.  If  the  patient  claims  not 
to  hear  this,  either  simulation  or  exaggeration  exists,  since  under  such 
conditions  even  the  closed  healthy  ear  would  appreciate  the  conversational 
voice. 

2.  One  end  of  a  flexible  rubber  tube,  about  4  feet  long,  is  inserted 
into  the  external  canal  of  the  patient's  ear,  another  similar  tube  into 
the  other  ear.  Funnels  are  affixed  to  the  other  ends  of  each  tube. 
The  examiner,  speaking  in  a  whisper  behind  the  patient,  talks  a  tone 
moment  into  the  one,  and  at  another  moment  into  the  other  funnel, 
alternating  as  quickly  as  possible,  and  the  patient  is  required  to  repeat 
what  is  said.  In  consequence  of  the  confusion  and  the  fatigue  which 
this  process  produces,  if  simulation  exists  the  patient  finally  repeats 
what  is  spoken  into  the  supposedly  deaf  ear.  The  examiner  must  be 
trained  for  the  test.  The  best  plan  is  to  write  down  beforehand  what  is 
to  be  said  in  two  columns,  one  marked  L  for  the  left  ear,  and  the  other 
E,  for  the  right  ear.  This  procedure  is  to  a  certain  extent  analogous  to 
the  stereoscopic  method  of  investigating  simulated  unilateral  blindness 
(p.  825). 

3.  An  A'  tuning-fork  is  set  in  vibration  and  placed  vertically  upon  the 
middle  of  the  skull ;  if  even  one  ear  is  normal  the  patient  must  hear 
the  tone.  The  test  is  then  repeated  with  the  normal  ear  closed,  and  if 
the  patient  says  that  he  no  longer  hears  the  tone,  it  is  evident  that  he  is 
simulating,  since  by  bone  conduction  the  normal  ear,  even  if  it  is  closed, 
must  hear  the  tuning-fork. 

4.  Many  malingerers  are  exposed  by  the  fact  that  they  insist  upon 
their  inability  to  determine  whether  the  tuning-fork  vibrates  or  not, 
when  the  examiner  places  a  large  vibrating  tuning-fork  (A  or  C  or  A') 
upon  the  skull  in  the  neighborhood  of  the  supposedly  deaf  ear,  whereas 
the  vibrations  of  such  a  type  of  tuning-fork  can  be  felt  even  by  the 
deaf. 

Siebemann  quite  correctly  calls  attention  to  the  danger  of  confusing 
exaggeration  and  complete  simulation,  and  emphasizes  the  advisability 
of  never  placing  any  reliance  upon  the  results  of  one  method  of  exam- 
ination. 

In  resrard  to  the  demonstration  of  the  simulation  of  disturbances  of 
hearing,  the  reader  is  referred  to  Burchardt's  works,  referred  to  upon 
p.  826. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  869 

IX.,  X.,  XI.    CRANIAL  NERVES  :    GLOSSOPHARYNGEAL,  VAGUS,  SPINAL 
ACCESSORY  (VAGUS  GROUP;. 

Physiologic  Introduction. 

These  three  nerves  are  so  intimately  connected  at  their  origin  in  the  oblon- 
gata, and  both  during  and  after  exit  from  the  jugular  foramen,  and  they  pos- 
sess so  many  anastomoses,  that  experimental  physiology  has  not  yet  succeeded  in 
isolating  the  functions  of  each.  This  is  especially  so  in  the  case  of  the  vagus 
and  spinal  accessorj'.  Clinical  investigations  are  made  exceptionally  difficult, 
because,  as  a  result  of  the  anatomic  relations  of  these  nerves,  pathologic  con- 
ditions frequently  affect  the  three  simultaneously,  both  centrally  and  peripherally. 

The  ijeripheral  glossopharyngeal  nerve  supplies  motor  fibers  to  the  muscles  of 
the  pharynx,  to  the  pharyngeal  constrictors,  and  to  the  stylopharj'ngeus  muscle; 
and  it  participates  with  the  facial  and  the  accessory  in  the  supply  of  the  muscles 
of  the  soft  palate.  In  addition  the  glossopharyngeal  is  the  secretory  nerve  of  the 
parotid  gland.  From  the  petrous  ganglion  it  gives  off  these  secretory  fibers  by 
means  of  the  tympanic  nerve  (Jacobson's)  to  the  otic  ganglion,  and  from  there 
by  means  of  the  auriculotemporal  nerve  of  the  third  trigeminal  branch  to  the 
parotid  gland  (Fig.  337,  p.  861).  The  glossopharyngeal  also  contains  sensory 
fibers,  which  are  distributed  to  the  back  of  the  tongue,  to  the  pharynx,  and  to 
the  soft  palate.  These  fibers  are  responsible  for  the  sensation  of  taste — i.  e.,  for 
bitter  and  sweet — and  they  also  i^revent  breathing  during  the  act  of  swallowing. 

The  peripheral  vagus  includes  both  motor  and  sensory  fibers.  The  motor 
fibers,  with  the  help  of  the  glossopharyngeal  and  accessor}^,  supply  the  muscles 
of  the  pharynx,  the  soft  palate,  and  the  esophagus,  so  that  the  vagus  has  with 
the  glossopharyngeal  an  important  function  in  the  act  of  swallo^^ing.  In  addi- 
tion it  furnishes  motor  fibers  to  the  larynx  in  its  inferior  or  recurrent  laryngeal 
branch,  and  there  supplies  all  the  laryngeal  muscles,  except  the  cricothyroid  and 
the  two  epiglottis  muscles  (the  thyro-  and  ary-epiglottis).  The  last  three, 
although  not  innervated  by  the  recurrent  laryngeal  nerve,  are  supplied  by  fibers 
derived  from  the  vagus,  through  the  superior  laryngeal  nerve.  The  vagus  is  fur- 
thermore the  motor  nerve  of  the  stomach  and  of  part  of  the  intestines;  it  is  also 
the  inhibitory  nerve  of  the  heart,  for,  as  is  well  known,  a  centrifugal  irritation  of 
one  or  both  vagi  slows  the  action  of  the  heart  and  at  the  same  time  diminishes  the 
cardiac  power,  whereas  sectioning  one  or  both  vagi  increases  the  cardiac  rapidity. 
The  vagus  is  further  assumed  to  innervate  the  bronchial  muscles  and  the  vessels 
of  the  lungs.  Sensory  branches  :  It  gives  off  a  small  sensory  branch  (auricular 
branch  of  the  vagus)  to  the  posterior  wall  of  the  external  auditor^"  canal.  Thus 
the  mucous  membrane  of  the  pharynx,  larynx,  trachea,  and  bronchi  is  supplied 
by  the  vagus,  as  well  as  the  heart  and  probably  also  the  stomach  and  intestines. 
The  sensory  nerves  for  the  upper  part  of  the  larynx  run  in  the  so-called  superior 
laryngeal  branch,  those  for  the  lower  part  of  the  larynx  in  the  inferior  or  recur- 
rent'laryngeal.  The  sensory  fibers  of  the  vagus  exert  an  important  regulatory 
control  over  the  breathing;  their  best-known  effect,  perhaps,  is  the  action  of  the 
superior  larj-ngeal  in  centripetal  stimulation — the  respiration  ceases  in  the  condi- 
tion of  expiration.  The  sensory  A^agus  branches  to  the  lung  itself  influence 
breathing  to  the  extent  that  distention  or  inflation  of  the  lung  excites  expira- 
tion, while  compression  or  collapse  of  the  lung  excites  inspiration.  The  auto- 
matic regulation  of  breathing,  as  explained  by  Hering  and  Breuer,  should  be 
understood  to  mean  merely  that  the  sensory  irritation  of  the  pulmonary  branches 
of  the  vagus  endeavors  to  accomplish  a  median  position  of  pulmonary  distention, 
whereas  the  rhjfthm  of  breathing  is  independent  of  such  regulation,  but  is  much 
more  an  automatic  function  of  the  respiratory  center.  In  reality  the  only  influ- 
ence that  the  centripetal  vagus  fibers  have  upon  the  rhythm  is  that  sectioning 
the  vagus  slows  the  respiration,  while  weak  centripetal  vagus  irritation  increases 
it.  The  vagus  is  the  most  important  sensory  nerve  for  coughing,  which  can  be 
induced  by  any  one  of  its  sensory  branches  (even  including  the  auricular  branch). 
The  vagus  branch  coming  from  the  heart,  which  can  be  demonstrated  in  animals. 


870  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

is  called  Ludwig  Cyon's  depressor.  It  is  of  some  clinical  interest,  because  its 
centripetal  irritation  produces  a  marked  diminution  of  blood  pressure  without 
affecting  the  heart,  probably  from  vascular  dilatation. 

The  peculiar  sensation  of  nausea  and  the  reflex  vomiting  depending  upon 
such  sensation  may  start  from  the  sensory  branches  of  the  vagus  to  the  pharynx 
and  stomach.  Vomiting  does  not,  however,  depend  upon  intact  vagi,  for  in 
animals  the  vomiting  paroxysm  can  still  be  excited  from  the  stomach,  even  after 
bilateral  section  of  the  vagus.  Other  tracts  for  the  vomiting  reflex  probably 
must  exist,  although  they  are  unknown.  The  vagus  is  supposed  to  have  some 
secretory  influence,  but  it  has  not  yet  been  accurately  demonstrated. 

The  functions  of  the  peripheral  accessory  nerve  are  simple;  they  are  purely  motor. 
Its  internal  branch  anastomoses  with  the  pharyngeal  branches  of  the  vagus  and 
the  glossopharyngeal,  thus  sharing  in  the  motor  innervation  of  the  soft  palate, 
while  its  external  branch  supplies  the  sternocleidomastoid  and  trapezius  muscles.  ' 

The  determination  of  the  central  origin  of  fibers  which  are  limited  to 
individual  functions  is  much  more  difficult  than  the  study  of  the  peripheral 
branching  and  fiinctions  of  these  three  nerves.  Two  points  are  sure — that 
the  taste  fibers  are  derived  from  the  glossopharyngeal  nucleus,  and  that  the 
innervation  of  the  sternocleidomastoid  is  exclusively  a  function  of  the  accessory 
nucleus.  From  reasons  which  have  been  detailed  above,  we  are  still  undecided 
whether  many  functions  executed  in  the  peripheral  tracts  of  the  vagus  and 
glossopharyngeal  do  not  depend  upon  fibers  which  in  reality  are  derived  from  the 
accessory  nucleus,  but  which  at  the  periphery  have  been  attached  to  the  two 
other  nerves.  For  instance,  the  heart-accelerating  fibers  of  the  vagus,  and  espe- 
cially the  motor  fibers  for  the  larynx,  are  supjiosed  by  many  authors  to  be 
derived  from  the  accessory  nucleus.  Grabower  has  recently  denied  this  relation 
of  the  accessory  to  the  larynx.  At  all  events  the  question  is  not  settled.  Nor  is 
it  yet  possible  to  determine  with  certainty  how  far  the  accessory  nucleus  shares  in 
the  innervation  of  the  glossopharyngeal  and  vagus  fibers  which  supply  the  swal- 
lowing and  palate  musculature. 

In  regard  to  the  anatomic  relations  of  the  nuclei  of  the  three  nerves  of  the 
vagus  group  see  Figs.  343,  344. 

Pathologic   Relations. 

The  fibers  of  the  three  nerves  of  the  vagus  group  may  be  affected 
either  in  their  peripheral  course  or  within  the  cranium — i.  e.,  the 
oblongata.  The  same  peculiarities  are  true  in  regard  to  their  central 
(supranuclear)  innervation,  as  in  the  case  of  the  nerves  to  the  eye 
muscles,  of  the  motor  trigeminus,  and  of  the  superior  branch  of  the 
facial,  viz.  :  that  their  central  innervation  is  not  exclusively  contralateral, 
but  that  the  hemisphere  of  each  side  takes  part  in  innervating  the  two 
nerves  (see  Fig.  318,  p.  829).  As  a  result  a  hemispheric  lesion  occa- 
sions very  little  or  no  disturbance  in  the  nerves  of  the  vagus  group, 
because  the  other  hemisphere  then  performs  the  function  sufficiently 
w^ell ;  and  therefore  without  further  discussion  unilateral  affections  can 
for  the  most  part  be  attributed  to  a  lesion  at  the  base  of  the  brain 
or  in  the  oblongata,  provided,  of  course,  that  the  trouble  is  situated 
within  the  skull.  This  is  exactly  the  same  condition  as  in  unilateral 
paralysis  of  the  eye  muscles  (see  p.  832  et  seq.)  and  motor  paralysis  of  the 
trigeminus  (p.  849).  With  a  cerebral  hemiplegia,  such  as  is  usually 
localized  in  the  cerebrum,  there  is  practically  never  any  affection  of  the 
vocal  cords,  of  the  muscles  of  swallowing,  nor  of  the  sternocleidomastoid, 
.whereas  a  paresis  of  the  trapezius  is  apt  to  be  noticed  upon  the  hemi- 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  871 

plegic  side,  because  the  innervation  of  this  muscle  is  for  the  most  part 
entirely  crossed.  The  clavicular  portion  of  the  trapezius,  however, 
which  aids  in  respiration,  is  bilaterally  innervated  and  so  exempt  from 
this  paresis.  A  bilateral  paralysis  of  the  nerves  of  the  vagus  group 
may,  of  course,  arise  in  pseudobulbar  fashion  from  bilateral  hemispheric 
lesions  (see  876). 

Symptomatology  of  I^esions  of  the  Three  Nerves  of 
the  Vagus  Group. — Disturbances  of  the  motor  innervation  of  the 
.soft  palate  may  occur  in  paralysis  not  only  of  the  facial,  but  also  of 
the  glossopharyngeal  and  vagus,  as  well  as  of  the  nuclear  and  trunk 
portions  of  the  accessory.  In  regard  to  the  phenomena  of  unilateral  or 
bilateral  paralysis  of  the  palate,  compare  the  section  upon  the  facial 
nerve  (see  pp.  850  and  (reflex)  863).  In  a  similar  way  the  peripheral 
glossopharyngeal  and  vagus,  and  even  the  region  of  origin  of  the  acces- 
sory, are  to  be  considered  also  in  connection  Nvith  the  other  movements 
of  swallowing.  A  patient's  subjective  complaints  and  the  examiner's 
observation  of  the  act  of  swallowing,  will  disclose  any  affection  of  that 
function.  A  unilateral  vagus  paralysis,  such  as  is  observed  surgically, 
does  not  noticeably  affect  swallowing.  Disturbances  in  the  motor  inner- 
vation of  the  larynx,  proceeding  from  the  vagus  or  the  accessory, 
become  evident  either  during  phonation,  or  by  the  exhibition  of  deficient 
laryngeal  closure  or  laryngeal  stenosis  (in  posticus  paralysis,  see  below). 
Imperfections  in  phonation  depend  upon  a  lesion  of  fibers  running  to 
the  vocal-cord  musculature  in  the  inferior  laryngeal  nerve.  Deficient 
closure  of  the  glottis  depends  upon  a  paralysis  of  the  glottis  constrictors 
(crico-arytenoideus  lateralis  and  interarytenoidei),  as  well  as  of  the 
ary epiglottic  muscle.  The  two  former  are  supplied  by  the  inferior 
laryngeal,  and  the  latter  by  the  superior  laryngeal  nerve.  The  conse- 
quence of  deficient  laryngeal  closure  is  that  patients  readily  choke  in 
swallowing,  and  can  no  longer  effectually  cough  or  exert  abdominal 
pressure.  Traube  has  proved  that  paralysis  of  the  glottis  closure,  with 
inability  to  cough  and  expectorate,  is  the  most  essential  cause  of  the 
disastrous  results  (vagus  phenomena)  of  bilateral  section  of  the  vagus 
in  animals  and  of  bilateral  vagus  paralysis  in  men.  Whether  or  not 
paralysis  of  the  bronchial  muscles  and  of  the  pulmonary  vessels  plays  any 
role  in  this  is  not  yet  accurately  determined.  In  unilateral  vagus  par- 
alysis phonation  and  glottis  closure  are  not  always  so  markedly  affected 
as  one  would  think,  because  a  more  pronounced  movement  of  the  healthy 
vocal  cord  will  offset  to  a  great  extent  the  paralyzed  cord.  Still,  the 
hoarse  feeble  voice  of  unilateral  vocal  paralysis  is  so  very  characteristic 
that  such  a  diagnosis  may  often  be  ventured  by  the  skilled,  even  before  a 
laryngoscopic  examination.  A  gradually  developing  paralysis  of  the 
recurrent  nerve  (it  is  quite  immaterial  whether  this  is  of  peripheral  or 
of  nuclear  origin)  almost  always  particularly  involves  the  crico-ary- 
tenoideus posticus.  This  muscle  widens  the  glottis.  Hence  the  earliest 
symptoms  of  an  increasing  motor  laryngeal  paralysis  is  a  narrowing  of 
the  glottis,  because  the  constrictors  overpower  the  weakened  posticus. 
The  corresponding  vocal  cord  assumes  a  position  of  adduction.    Should 


872  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

the  paralysis  be  bilateral,  there  may  result  a  serious  obstacle  to  breathing 
with  all  the  appearances  of  laryngeal  stenotic  dyspnea  (see  p.  86  et  seq.), 
even  necessitating  tracheotomy.  This  condition  is  generally  described 
briefly  as  "  posticus  paralysis."  This  remarkable  selection  of  the  crico- 
artenoideus  posticus  in  the  beginning  of  recurrent  paralysis  has  led  to 
countless  discussions.  No  satisfactory  explanation  has  yet  been  given. 
One  theory  is  that  those  neurons  which  preside  over  glottis  widen- 
ing suffer  on  account  of  a  greater  sensitiveness,  but  this  seems  to  the 
author  arbitrary  and  superfluous.  A  much  simpler  explanation  is  that, 
quantitatively,  the  musculature  of  the  glottis  constrictors  overpowers 
the  dilators  very  decidedly.  This  preponderance  is  in  keeping  with 
the  fact  that  in  phonation,  coughing,  exerting  abdominal  pressure,  and, 
in  short,  in  all  forms  of  glottis  closure,  the  constrictors  accomplish  very 
much  more  than  the  dilators.  As  a  matter  of  fact,  all  laryngeal  muscles, 
with  the  single  exception  of  this  "posticus,"  subserve  the  function  of 
narrowing  the  glottis,  and  therefore  it  is  not  surprising  that  the  crico- 
arytenoideus  posticus  is  the  first  to  suffer,  and  that  in  partial  pharyn- 
geal paralysis  the  constrictors  overpower  it.  Evidently  then,  as  the 
paralysis  increases,  the  narrowing  of  the  glottis  recedes,  while  the  vocal 
cord  (or  cords)  from  a  position  of  adduction  assume  more  and  more  the 
so-called  cadaveric  position.  The  exact  diagnosis  of  a  motor  laryngeal 
paralysis  can  be  accomplished  only  by  means  of  the  laryngoscope. 
(Compare  the  chapter  upon  Laryngoscopy  and  the  illustrations  of  the 
larynx  reproduced  there,  p.  696).  A  normal  laryngoscope  picture  is 
characteristic  of  hysteric  aphonia  :  the  larynx  resembles  that  of  a  person 
voluntarily  whispering.  There  is  no  actual  paralysis  in  the  territory 
of  the  vagus  and  accessory,  but  merely  a  psychic  inability  to  control 
the  speech  volition.  Spasm  of  the  glottis  and  the  spastic  form  of 
hysteric  aphonia  may  be  mentioned  here,  as  motor  vagus  accessory 
symptoms  ;  but  for  their  explanation  the  literature  of  special  pathology 
should  be  consulted. 

Compare  p.  850  et  seq.  (trigeminus)  concerning  derangements  of  taste 
peculiar  to  lesion  of  the  glossopharyngeal  (especially  for  bitter  and 
sweet).  Affections  of  the  sensory  innervation  of  the  larynx  (superior 
and  inferior  laryngeal  nerves)  can  be  demonstrated  by  touching  the 
mucous  membrane  of  the  larynx  by  means  of  a  curved  laryngeal  sound 
under  the  control  of  a  mirror,  and  noting  the  absence  of  sensitiveness, 
and  finally  the  loss  of  the  cough  reflex. 

The  determination  of  disturbances  in  function  of  the  cardiac  and 
pulmonary  branches  of  the  vagus  is  very  difficult,  because  all  the 
changes  which  irritative  and  paralytic  conditions  of  these  nerves  for  the 
circulation  and  respiration  produce  can  take  place  pathologically  in  other 
ways,  especially  in  affections  of  the  heart  and  of  the  lungs  themselves, 
and  also  reflexly  from  almost  any  nerve  territory.  The  establishment  of 
less  ambiguous  symptoms,  especially  the  determination  of  the  phenomena 
described  above  in  connection  with  the  act  of  swallowing  and  the 
laryngeal  innervation,  as  well  as  the  establishment  of  lesions  whose 
nature  and  position  can  be  definitely  attributed  to  the  vagus,  will  gener- 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  873 

ally  be  sufficient  to  attribute  certain  respiratory  and  circulatory  disorders 
to  paralytic  or  irritative  vagus  phenomena.  The  cases  of  traumatic 
vagus  paralysis  are  the  easiest  to  understand. 

The  results  of  surgical  or  other  accidents,  such  as  cutting  the  vagus 
nerve  during  operations,  or  the  results  of  injury  to  both  vagi  from  the 
pressure  of  tumors,  prove  that  a  unilateral  vagus  paralysis  need  not 
influence  the  pulse  very  materially.  At  first  it  may  be  accelerated,  but 
later  on  it  will  become  equalized.  A  double  vagus  paralysis  will,  how- 
ever, generally  induce  a  permanent  acceleration,  up  to  160  beats  in  a 
minute.  Dilatation  of  the  heart  has  not  yet  been  observed  to  depend 
upon  unilateral  or  bilateral  vagus  paralysis.  Nor  is  there  any  founda- 
tion for  the  frequent  assumption  that  irregularity  of  the  pulse  is  to  be 
attributed  to  paralyzing  affections  of  the  vagus.  On  the  contrary,  physi- 
ology teaches  that  irritation  of  the  vagus  may  cause  irregularity  in  the 
pulse. 

The  rule  formulated  by  Gerhardt  in  connection  with  the  diagnosis  of  the 
cause  of  tachycardia  should  be  mentioned  here:  "Taken  all  in  all,  the  majority 
of  nervous  tachycardias  are  to  be  attributed  to  vagus  paralysis,  those  with  very  rapid 
pulse  (above  200)  to  a  combination  of  vagus  paralysis  with  sympathetic  irritation, 
a  few  rather  milder  forms  to  the  latter  alone."  Martins  adds:  "This  rule 
coincides  with  well-known  physiologic  facts.  In  unpoisoned  animals  an  accel- 
eration of  the  heart  pulsation,  30  to  70  per  cent,  (not  more,  Aubert)  can  be 
brought  about  by  stimulating  the  accelerating  nerve  of  the  sympathetic.  After 
bilateral  sectioning  of  the  vagus,  the  acceleration  of  the  pulse-frequency  in  mam- 
mals is  not  very  great.  According  to  v.  Bezold  it  may  rise  to  120  to  180  beats.  The 
following  conclusions  maybe  drawn:  Acceleration  up  to  about  120  beats  (30  to  70 
per  cent.)  depends  upon  irritation  of  the  sympathetic;  from  120  to  180  beats,  upon 
paralysis  of  the  vagus;  more  than  that,  upon  a  combined  action  of  both  causes."  ^ 
Martins  objects  to  the  assumption  of  a  vagus  paralysis  or  of  a  sympathetic 
irritation  to  explain  tachycardia.  He  assumes  neither  a  vagus  paralysis  nor 
sympathetic  irritation  to  interpret  the  characteristic  clinical  picture  of  paroxysmal 
tachycardia,  but  considers  that  it  depends  upon  a  temporary  acute  cardiac  insuffi- 
ciency with  dilatation,  in  which  the  tachycardia  is  one  of  the  secondary  symp- 
toms, probably  for  the  sake  of  compensation.  But  this  conception  of  Martins 
does  not  seem  logical  to  the  author.  For  in  these  cases  of  paroxysmal  tachy- 
cardia evidence  of  cardiac  insufficiency  is  so  much  in  the  background  that  one 
might  better  assume  a  sort  of  epileptic  discharge  in  the  territory  of  the  acceler- 
ating nerve  of  the  heart.  Nothnagel  has  also  made  an  attempt  to  formulate  rules 
for  diagnosticating  the  cause  of  tachycardia.  He  says:  1.  "If  a  very  decided 
acceleration  of  the  pulse  occurs  in  paroxysmal  tachycardia,  if  the  rhj^thm  of  beats 
is  quite  regular,  and  the  cardiac  impulse  is  very  weak,  if  other  symptoms  are 
absent  or  are  developed  first  as  consequences  of  incomplete  cardiac  emptying,  if, 
finally,  the  paralysis  of  other  nerve  tracts  accompanying  the  vagus  can  be  coin- 
cidentally  confirmed,  then  one  can  assume  a  vagus  paralysis  as  a  cause  in  this 
special  case.  2.  If  during  the  attacks  of  tachycardia  the  cardiac  impulses  are 
vigorous,  if  the  peripheral  arteries  are  well  filled,  and  the  tension  is  preserved 
(but  this  is  not  in  any  sense  a  necessity),  if  other  marked  evidence  of  irritation  in 
vasomotor  nerve  tracts  appears  in  paroxysms,  then  the  assumption  of  a  condition 
of  irritation  of  the  accelerating  nerve  (sympathetic)  is  justified."  This  position 
seems  to  the  author  arbitrary  and  untrustworthy. 

The  statements  which  are  to  be  found  in  literature  concerning  the 
behavior  of  the  breathing  in  vagus  paralysis  are  of  little  use.     Accord- 

*  Martins,  Tachycardia,  Stuttgart,  Enke,  1895. 


874  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

iug  to  physiologic  experiments  it  is  fair  to  assume  here,  as  with  the 
heart,  that  only  bilateral  lesions  can  cause  serious  difficulties.  Edin- 
ger's  statement  is  worth  noting  that  v^agus  paralysis  may  be  associated 
with  pulmonary  distention  and  consequently  with  dyspnea.  Vagus 
pneumonia  (as  we  saw  upon  p.  871)  depends  essentially  upon  incom- 
plete laryngeal  closure,  and  is  therefore  merely  an  indirect  pulmonary 
symptom  of  vagus  paralysis. 

As  yet  there  is  very  little  known  about  the  effect  of  vagus  paralysis 
upon  disturbances  of  the  functions  of  the  stomach  and  intestines  in  man. 
This  alone  appears  certain — a  unilateral  vagus  paralysis  does  not  notice- 
ably influence  these  functions. 

We  now  come  to  the  mention  of  the  symptomatology  of  the  affec- 
tions of  the  so-called  external  branch  of  the  accessory,  which  supplies 
the  sternocleidomastoid  and  trapezius  muscles.  A  unilateral  paralysis 
of  the  sternocleidomastoid  causes  a  moderate  twisting  of  the  head  toward 
the  paralyzed  side,  associated  with  a  slight  elevation  of  the  chin,  due  to 
the  action  of  the  antagonists.  Turning  the  head  to  the  healthy  side, 
although  performed  less  vigorously  than  normally,  is  not  prevented, 
because  this  movement  is  accomplished  not  exclusively  by  the  sterno- 
cleidomastoid but  also  by  the  deep  muscles  of  the  neck,  especially  the 
oblique  capitis  inferior,  and  the  splenius  of  the  other  side.  The  clonic 
and  tonic  wry  neck  (tic  rotatoire,  caput  obstipum  spasticum)  depends 
partly  upon  a  unilateral  irritation  of  the  spinal  accessory  nerve  leading 
to  the  sternocleidomastoid.  Yet  the  unsatisfactory  results  following 
myotomies  of  the  sternocleidomastoid  alone,  and  the  very  much  better 
results  when  the  opposed  splenius  and  the  oblique  capitis  inferior  have 
also  been  cut,  show  that  the  name  "  accessory  cramp  "  for  this  condition 
is  not  absolutely  justified.  In  reality  the  condition  depends  much  more 
upon  spasm  of  a  central  extensive  area  which  supplies  functionally  sim- 
ilar muscles.  The  symptoms  of  unilateral  paralysis  of  the  trapezius 
vary  according  to  whether  the  entire  muscle  or  only  separate  portions 
of  it  are  involved.  If  complete  the  affected  shoulder  hangs  lower  ;  the 
shoulder-blade  is  thrust  out  obliquely  upwards  and  outwards  ;  and  the 
power  to  lift  the  arm  is  somewhat  impaired,  but  not  nearly  so  markedly 
as  in  serratus  paralysis.  If  only  the  central  portion  (acromial)  is  para- 
lyzed, the  upper  half  of  the  median  edge  of  the  shoulder-blade  is  de- 
pressed outwards  (3Iouvement  de  bascule,  Duchenne).  According  to 
Schlodtmann,  if  the  origin  of  the  accessory  is  affected,  this  central  por- 
tion of  the  muscle  should  remain  exempt  because  it  is  entirely  or  partly 
supplied  by  the  cervical  plexus.  This  point  has  not  yet  been  definitely 
decided,  nor  has  the  extent  to  which  the  cervical  nerves  assist  in  the 
innervation  of  other  parts  of  the  trapezius.  It  is  worth  noting  that 
in  juvenile  muscular  atrophy  the  clavicular  bundle  of  the  trapezius, 
whose  function  is  essentially  respiratory,  remains  intact  longest,  so  that 
Duchenne  has  described  it  as  the  ultimum  moriens  of  the  muscle. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  875 

XII.    CRANIAL   NERVE:    HYPOGLOSSUS. 

The  hypoglossus  is  the  motor  nerve  of  the  tongue,  and  therefore  aids 
in  chewing,  swallowing,  and  especially  in  speaking.  Its  function  is 
tested  by  observing  whether  coarse  movements  of  the  tongue  are  per- 
formed equally  well  upon  both  sides,  and  by  watching  the  patient  while 
chewing  and  swallowing.  With  a  unilateral  hypoglossal  paralysis  or 
paresis  the  tongue,  when  protruded,  deviates  towards  the  paralyzed  side 
because  the  healthy  genioglossus  muscle  overpowers  its  paralyzed  fellow. 

Further  evidence  proving  tliat  the  genioglossus  muscle  is  at  fault  in  unilateral 
hypoglossal  paralysis  is  furnished  by  observing  the  tongue  as  it  rests  naturally 
upon  the  floor  of  the  mouth.  As  a  result  of  the  preponderance  of  the  unafiected 
muscle,  the  tip  will,  in  this  position,  be  deviated  toward  the  healthy  side;  and, 
in  addition,  a  more  prominent  arching  of  the  dorsum  of  the  tongue  will  be  noted 
upon  the  paralyzed  side.  This  curving  shows  that  the  pushing  of  the  genioglossus 
forward  has  ceased. 

In  unilateral  hypoglossal  paralysis,  we  by  no  means  always  notice 
any  pronounced  affection  either  in  chewing  or  swallowing.  Even  artic- 
ulation may  be  carried  out  reasonably  well,  especially  after  some  prac- 
tice. 

In  old  peripheral  paralyses  of  the  hypoglossus  the  affected  half  of  the 
tongue  is  flaccid,  thin,  and  wrinkled  and  often  shows  fibrillary  contrac- 
tions in  the  shape  of  peculiar  peristaltic  wavering.  Electric  stimulation 
of  the  lingual  nerve  (chorda  tympani  fibers)  will  oftentimes  intensify 
this  wavering  so  decidedly  that  an  actual  movement  of  the  tongue  occurs 
(pseudomotor  action,  Heidenhain),  The  tongue  is  frequently  more 
coated  upon  the  paralyzed  than  upon  the  healthy  side. 

With  bilateral  hypoglossal  paralysis  the  disturbances  of  function 
are  naturally  very  marked.  The  tongue  then  lies  flaccid  upon  the  floor 
of  the  mouth  and  can  be  protruded  only  very  incompletely,  if  at  all. 
Speech  becomes  incomprehensible,  and  mastication,  chewing,  and  swal- 
lowing finally  impossible.  The  patient  cannot  even  swallow  the  saliva 
but  must  either  spit  it  out  frequently  or  constantly  drool. 

In  a  peripheral  hypoglossal  paralysis  the  muscles  attached  to  the  hyoid  bone 
and  supplied  by  the  descending  branch  of  the  hypoglossus  are  also  frequently 
involved  in  association  (sternothyroid,  thyrohyoid,  sternohyoid,  and  the  inferior 
belly  of  the  omohyoid).  The  fibers  for  these  muscles  originate  in  the  second  and 
third  cervical  nerve  roots.  Part  of  them  join  the  root  of  the  hypoglossus  nerve 
and  later  leave  it  again  as  the  descending  branch;  part  of  them  terminate  further 
down  in  the  latter  branch.  When  in  conjunction  with  a  lingual  paralysis  these 
muscles  are  found  to  be  affected,  it  is  natural  to  conclude  that  the  lesion  is  situ- 
ated in  the  hypoglossal  trunk  below  the  anastomosis  with  the  superior  cervical 
nerves.  The  paralysis  of  the  inferior  hyoid  muscle  can  be  recognized  by  an 
atrophy  of  the  musculature  over  the  thyroid  cartilage  and  by  a  more  noticeable 
prominence  of-  the  latter.  If  the  paralysis  is  unilateral,  the  larynx  will  be  seen 
to  be  laterally  dislocated  during  the  act  of  swallowing.  Under  some  circum- 
stances such  paralysis  may  be  demonstrated  by  an  electrical  examination  (motor 
points,  see  p.  801,  Fig.  305). 

The  electric  examination  of  the  tongue  itself  should  be  carried  out 
in  the  ordinary  way  (p.  798  et  seq.).  The  motor  point  of  the  hypo- 
glossus is  situated  just  behind  and  above  the  horn  of  the  hyoid  bone. 


876  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

In  many  individuals,  the  nerve  can  be  stimulated  alone  at  this  point  by 
deep  pressure  of  the  fine  electrode.  The  hypoglossus  of  each  side  is 
innervated  by  both  hemispheres,  and  therefore  unilateral  cerebral  lesions 
causing  a  hemiplegia  give  very  little  evidence  of  hypoglossal  paralysis. 
The  same  conditions  apply  as  in  the  behavior  of  the  superior  facial 
branch  with  a  hemiplegia  of  central  origin  (see  p.  853  et  seq.').  The 
crossed  influence  is,  however,  responsible  for  a  more  or  less  plain  devia- 
tion of  the  tongue  towards  the  paralyzed  side  in  an  ordinary  hemiplegia, 
depending,  as  has  already  been  said,  upon  a  weakness  of  the  genioglossus 
muscle  upon  the  paralyzed  side.  This  deviation  of  the  tongue  in  hemi- 
plegia ordinarily  runs  a  parallel  course  with  the  facial  paralysis,  and  for 
this  reason  was  formerly  attributed  to  the  facial  nerve.  Such  a  supposi- 
tion is,  of  course,  incorrect,  but  the  coincidence  of  central  facial  paralysis 
and  hypoglossal  paresis  does  depend  upon  the  intimate  proximity 
of  the  central  tracts,  or  even  of  the  cortical  centers,  of  these  two  nerves. 
Ordinarily  no  particular  difficulty  in  chewing,  swallowing,  or  speaking 
results  from  this  hemiplegic  hypoglossus  paresis ;  at  most  it  has  only  a 
transitory  eflPect  on  these  functions. 

n.  THE  CHARACTERISTICS  OF  MOTOR  HEMIPLEGIA:  PSEUDa 
BULBAR  SYMPTOMS. 

In  the  preceding  paragraphs  (see  the  diagram  Fig.  318,  p.  829)  we  have  em- 
phasized the  fact  that  most  of  the  cranial  nerves  are  supplied  by  both  hemispheres, 
so  that  a  unilateral  hemispheric  lesion  producing  a  hemiplegia  of  the  extremities 
does  not  cause  any  marked  crossed  paralysis  of  the  cranial  nerves.  This  rule 
applies  particularly  to  the  nerves  of  the  eye  muscles  (except  in  the  conjugate 
tract  for  the  lateral  movement),  to  the  motor  trigeminus,  to  the  motor  glossophar- 
angyeal,  to  the  vagus,  and  to  most  fibers  of  the  accessory — i.  e. ,  the  vocal  cord 
fibers  and  the  fibers  of  the  sternocleidomastoid.  As  was  mentioned  above, 
a  unilateral  hemispheric  lesion  has  a  slight  crossed  effect  upon  the  upper  branches 
of  the  facial,  upon  the  hyoglossus  (genioglossus)  and  upon  the  fibers  of  the 
trapezius,  with  the  exception  of  the  clavicular  portion,  which  remains  intact. 
The  fibers  of  the  inferior  facial  branch  are,  on  the  contrary,  very  decidedly  affected, 
because  crossed.  Therefore  the  typical  clinical  picture  of  cerebral  hemiplegia 
includes  a  hemiplegia  of  the  extremities  and  of  the  muscles  supplied  by  the  lower 
branch  of  the  facial,  while  those  supplied  by  the  other  motor  cranial  nerves  are 
either  intact  or  slightly  and  partially  paralyzed. 

In  a  similar  way  the  muscles  of  breathing  and  abdominal  pressure,  apparently 
innervated  bilaterally,  present  merely  a  slight  negligible  weakness  on  the  paralyzed 
side. 

A  bilateral  defective  innervation  is,  however,  present  in  any  unilateral  hemi- 
spheric lesion,  but  escapes  notice  because  it  is  very  difficult  to  detect  any  objec- 
tive evidence  of  a  moderate  degree  of  bilateral  paralysis  (this  was  alluded  to  in 
the  case  of  the  eye  muscle  upon  p.  831  et  seq.,  and  is  quite  as  true  for  other 
muscle  territories  innervated  bilaterally). 

Wernicke  and  Mann  undertook  not  long  ago  a  more  accurate  analysis  of 
motor  hemiplegia  in  order  to  compare  the  degree  of  involvement  of  the  individual 
muscles  of  the  extremities.  They  demonstrated,  what  had  been  well  known  for 
a  long  time,  that  the  leg  is  always  affected  less  than  the  arm,  and  formulated  the 
following  rules  in  regard  to  the  amount  of  involvement  of  the  individual  muscle 
groups  of  the  arm  and  leg. 

Arrn  i;    The  movements  most  affected,  and  in  milder  and  less  distinctive  par- 

'  Wernicke,  Berlin,  klin.  Woch.,  1889,  p.  45,  and  Lehrbueh  der  Gehirnkrankheiten, 
1881.     Cassel,  Fischer. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


871 


alysis  oftentimes  the  only  ones,  are  extension  in  all  joints  (elbow,  hand,  and  finger 
joints),  supination  of  the  hand,  ab-  and  adduction  and  the  opposition  of  the 
thumb,  and  spreading  of  the  fingers.  All  other  movements,  especially  those  of 
flexion,  are  less  affected.  The  ordinary  position  of  the  paralyzed  arm  is  therefore 
flexed  at  all  joints  and  slightly  pronated. 

Leg^ :  The  muscles  most  decidedly  paralyzed,  and,  in  milder  and  less  distinc- 
tive paralysis,  the  only  ones  affected  are  those  shortening  the  leg  in  walking — 
i.  e. ,  those  which  flex  the  leg  and  are  thereby  efficient  at  the  first  stage  of  the 
movement.  The  more  important  muscles  for  walking — those  which  elongate  the 
leg  and  so  push  the  body  forward — are,  on  the  contrary,  either  less  paralyzed  or 
in  milder  cases  not  at  all  afi'ected.     The  ileopsoas,  the  gracilis,  the  sartorius,  and 


Fig.  338.— Left  hemiplegia  showing  contractures  and  distortion  of  mouth  (Dr.  E.  G.  Cutler, 

Massachusetts  General  Hospital).  ■ 

the  dorsal  flexors  of  the  foot — i.  e.,  the  tibialis  anticus  and  extensor  digitorum 
communis — are  therefore  conspicuously  paralyzed.  Although  the  long  head 
of  the  biceps  and  the  semitendinosis  and  semimembranosis  can  act  as  flexors  of 
the  leg,  they  are  less  paralyzed.  This,  however,  does  not  argue  against  the  above 
rule,  because;  on  account  of  their  extensor  action  upon  the  hip  joint  in  walking, 
they  functionate  not  as  flexors  of  the  leg,  but  as  extensors  of  the  thigh  ;  in  other 
words,  as  elongators  of  the  leg.  In  the  same  way  the  gastrocnemius  does  not  act 
as  a  flexor  of  the  leg  in  walking,  but  as  an  extensor  of  the  foot,  therefore  elon- 
gating the  leg,  and  so,  in  accordance  with  the  above  rule,  remains  comparatively 
free  in  hemiplegias.     It  may  be  added  that  in  hemiplegias,  flexion  of  the  thigh 

^  Mann,  Vollcmavns  Sammlvng  klin.  Vortrage.  Nene  Folge,  No.  132,  Leipzig,  1895,  and 
D.  Zeits.  f.  Nervenheilkunde,  1896,  vol.  x.,  parts  1  and  2,  p.  1. 


878  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

is  often  found  to  be  less  affected  than  Mann's  rules  would  lead  us  to  think,  because 
the  quadriceps  acting  as  an  extensor  aids  the  ileopsoas  in  this  movement. 

To  explain  this  peculiarity  in  distribution  of  motor  paralysis  in  hemiplegias, 
which  applies  both  to  cerebral  and  to  spinal  hemiplegias,  we  must  assume 
that  the  seriously  paralyzed  muscles,  like  the  muscles  supplied  by  the  inferior 
branch  of  the  facial,  depend  for  their  innervation  upon  the  opposite  hemisphere, 
whereas  the  groups  of  muscles  less  affected  by  the  hemiplegia,  like  those  sup- 
plied by  the  upper  branch  of  the  facial  and  most  motor  cranial  nerves,  are  sup- 
plied by  both  sides  and  therefore  exhibit,  perhaps  a  weakness,  but  never  any 
decided  paralysis.  The  researches  of  Pitres  and  Dignat  ^  completely  corroborate 
this  assumption  of  bilateral  innervation,  for  in  cerebral  hemiplegias  they  found  a 
diminution  in  the  power  of  the  healthy  leg  up  to  about  50  per  cent.,  in  the 
healthy  arm  up  to  about  38  per  cent.  Therefore  what  we  call  hemiplegias  are 
not  hemiplegias  at  all,  accurately  speaking,  but  paraplegias  with  a  preponderating 
crossed  paralysis.^ 

In  bilateral  hemispheric  lesions  we  observe  very  characteristic  appearances 
upon  the  part  of  the  motor  cranial  nerves,  as  a  result  of  their  bilateral  innerva- 
tion. Since  each  lesion  affects  fibers  for  both  sides,  a  bilateral  deficiency  of 
innervation  must  result,  which  would  remain  latent,  except  that  under  these 
circumstances  there  is  nothing  to  hide  it.  A  glance  at  Fig.  818,  p.  829  (suppos- 
ing a  coincident  existence  of  lesions  x  and  z),  will  make  this  clear.  If  these 
bilateral  hemispheric  areas  involve  especially  the  motor  fibers,  they  may  by 
summation  cause  a  marked  bilateral  paralysis  of  the  motor  cranial  nerve  which 
would  not  be  much  paralyzed  were  the  trouble  unilateral.  Since  bulbar  nerves 
(like  the  motor  trigeminus,  accessory,  hypoglossus,  and  upper  branch  of  the 
facial)  are  affected,  the  clinical  picture  will  closely  simulate  the  paralyses  origi- 
nating in  the  nuclear  regions  of  the  oblongata  and  the  pons.  The  symptoms  of 
this  summation  of  hemiplegias  are,  therefore,  spoken  of  as  pseudobulbar  symp- 
toms. Pseudobulbar  symptoms  may  be  occasioned  either  by  two  hemispheric 
lesions  coming  on  simultaneously,  or  by  the  addition  of  a  fresh  lesion  of  one 
hemisphere  to  an  old  hemiplegic  lesion  of  the  other  side. 

Similarly,  in  complete  conformity  with  the  theory  of  bilateral  innervation, 
experience  teaches  that  as  soon  as  a  hemiplegia  of  the  other  side  is  added  to  the 
first  hemiplegia  of  patients  who  have  retained  but  slight  residual  effects  of  such 
a  hemiplegia,  the  former  affected  side  promptly  becomes  more  seriously  paralyzed. 
This,  together  with  the  explanation  furnished  upon  p.  831,  could  account  for  the 
fact  that  the  bilaterally  innervated  muscle  territories  (in  the  arm  the  flexors,  in 
the  leg  the  extensors)  overpower  their  antagonists  and  give  rise  to  contractures  in 
descending  degeneration. 

m.  CEREBRAL  DISTURBANCES  OF  SENSATION. 

The  sensory  tract  in  the  brain  may  be  involved  in  a  number  of  entirely  differ- 
ent locations,  as  a  clinical  result  of  which  there  will  be  a  mrire  or  less  distinctly 
unilateral  disturbance  of  sensation.  A  portion  of  the  cerebral  sensory  tract,  how- 
ever, is  so  diffused  that  a  circumscribed  lesion  producing  marked  sensory  disturb- 
ances can  be  situated  only  in  certain  locations.  These  places  are  found  exclusively 
in  the  compact  portion  of  the  sensory  tract  which  is  formed  by  the  fillet.  The 
sensory  fibers  of  the  fillet  arise  from  the  nucleus  gracilis  and  nucleus  cuneatus  in 
the  medulla,  partly  cross  to  the  opposite  side  in  the  so-called  decussation  of  the 
fillet,  run  through  the  tegmentum  of  the  crus  cerebri  to  the  ventral  nucleus  of 
the  optic  thalamus,  and  finally  reach  the  parietal  lobe  by  passing  through  the 

^  Cited  bv  Pierre  Marie,  T.egons  sur  les  maladies  de  la  moelle,  1892,  p.  26. 

^  The  rules  proposed  by  Mann  in  regard  to  the  behavior  of  the  elongators  and 
shorteners  of  the  leg  frequently  apply  in  spinal  cord  lesions  which  partially  interrupt 
the  motor  conduction  upon  both  sides  ( incomplete  crossed  lesions,  motor  systemic  dis- 
eases). Perhaps  this  peculiarity  may  be  explained  by  assuming  that,  in  addition  to  their 
bilateral  innervation,  the  elongators  possess  other  more  favorable  conditiqns  of  innerva- 
tion— e.  g.,  possibly  a  greater  number  of  fibers  in  their  conduction  tracts. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  879 

posterior  third  of  the  internal  capsule.  ^  Hemianesthesia  may  consequently  be 
observed  as  the  result  of  lesions  :  in  the  posterior  columns  of  the  medulla  ;  in  the 
pons  where  the  region  of  the  fillet  is  affected  ;  in  the  tegmentum  of  the  cms, 
when  the  legion  is  situated  between  the  red  nucleus  and  the  substantia  nigra  ; 
in  the  subthalamic  region  and  the  adjacent  posterior  portion  of  the  internal  cap- 
sule ;  in  the  fibers  of  the  corona  radiata  proceeding  from  the  optic  thalamus  ;  and 
in  extensive  lesions  of  the  parietal  lobe,  particularly  when  they  involve  the  inferior 
parietal  lobule  and  the  central  convolutions. 

Cerebral  hemianesthesia  is  most  frequently  dependent  upon  a  lesion  in  the 
posterior  portion  of  the  internal  capsule.  Milder  degrees  of  sensory  disturbances 
may  originate  in  the  most  varied  locations  in  the  brain,  dependent  upon  the 
diffusion  of  that  portion  of  the  sensory  tract  which  is  not  contained  in  the  fillet, 
but  little  typically  is  known  about  them. 

The  Character  of  Cerebral  Hemianesthesia  Produced  by  Anatomic 
Lesions  and  Its  Differentiation  from  Hysterical  Hemianesthesia  and 
Spinal  Hemianesthesia. — The  cerebral  hemianesthesia  due  to  anatomic  causes 
is  characterized  by  the  fact  that  it  involves  the  spinal  sensory  tracts  together 
with  the  cutaneous  area  supplied  by  the  trifacial  ;  in  some  cases  the  opjtic  tract 
may  also  be  involved  and,  in  rare  instances,  the  acoustic  tract.  Involvement  of 
the  optic  tract  occurs  when  the  lesion  affects  the  sensory  fibers  in  the  region  of 
the  posterior  portion  of  the  internal  capsule  or  those  in  the  corona  radiata  of  the 
optic  thalamus,  when  it  involves  the  optic  radiation  passing  through  the  sub- 
thalamic region  from  the  pulvinar  and  external  geniculate  body  to  the  cerebral 
cortex,  or  when  it  implicates  the  primary  optic  centers  themselves.     The  acoustic 

.  tract  is  affected  when  the  lesion  involves  the  internal  geniculate  body  and  pos- 
terior corpus  quadrigeminum,  or  the  fibers  w'hich  connect  these  structures  with 
the  temporal  lobe.  Visual  disturbances  in  cerebral  hemianesthesia  dependent 
upon  anatomic  causes  are  always  hemiopic  in  character,  since  the  visual  center 
is  cut  off  from  the  retinal  halves  corresponding  to  the  side  of  the  lesion.  Hearing 
is  simply  impaired  and  never  abolished  upon  the  side  opposite  to  the  lesion,  since 
each  acoustic  nerve  is  connected  with  both  temporal  lobes.  Smell  and  taste  are 
always  intact,  because  the  lesion  is  at  some  distance  from  the  olfactory  and  gus- 
tatory fibers.  These  fibers  from  each  side  are  connected  with  both  hemispheres 
and  do  not  run  in  a  compact  bundle,  so  that  it  will  be  readily  understood  that 
they  could  not  easily  be  destroyed  by  a  circumscribed  lesion.  Cerebral  hemian- 
esthesia is  further  characterized  by  the  fact  that  all  of  the  sensory  powers  may  be 
involved — touch,  pressure,  pain,  temperature,  bone-sensation,  the  perception  of 
the  position  and  of  pjassive  motions  of  the  extremities,  and  stereognostic  sensa- 
tion, although  they  are  usually  very  incompletely  affected.  The  perception  of 
the  position  and  of  passive  motions  of  the  extremities  and  the  stereognostic  recog- 
nition of  objects  are  most  affected  and  may  be  completely  abolished,  while  the 
sensations  of  touch,  pain,  and  temperature  are  usually  simply  diminished.  The 
disturbance  is  most  marked  at  the  distal  ends  of  the  extremities,  possibly  because 
this  region  is  supplied  by  a  comparatively  larger  number  of  crossed  fibers  from 
the  opposite  hemisphere,  while  the  proximal  portions  of  the  extremities  are  pre- 
sumably supplied  by  fibers  from  both  hemispheres.  If  the  cause  of  the  hemian- 
esthesia be  situated  in  the  pons  or  in  the  uppermost  portion  of  the  medulla,  a 
fjo-called  alternating  hemianesthesia  may  be  produced,  since  the  sensor  trigeminus 
is  involved  below  its  decussation   and  its  sensation   is  abolished  upon  the  side 

I  opposite  to  the  anesthetic    extremities.      The  hemianesthesia  frequently  extends 

I  somewhat  beyond  the  median  line  of  the  body. 

I  Since  the  cerebral  hemianesthesia  is  crossed — ?".  e.,  situated  upon  the  side  oppo- 
site to  the  lesion — it  must  be  assumed  that  the  sensations  for  one-half  of  the  body 

'  The  cerebral  course  of  the  sensoiy  fibers  from  the  anterolateral  columns  of  the  cord 
(see  Fig.  362,  page  921,  and  Fig:.  355,  page  907),  which  in  physiologic  and  pathologic 
importance  are  second  only  to  those  of  the  posterior  columns,  is  as  yet  unknown.  Clinical 
experience  would  lead  us  to  suppose  that  at  least  some  of  these  fibers  become  associated 
..;■',  .'T^«e  of  the  fillet. 


880  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

are  received  by  the  opposite  half  of  the  brain.  Since  a  triple  decussation  is 
improbable,  we  are  led  to  suppose  that  the  cerebral  decussation  (occurring  chiefly 
in  the  decussation  of  the  fillet)  involves  only  those  fibers  which  do  not  decussate  at 
lower  levels.  This  fact  explains  why  the  complicated  conditions  of  spinal  hemian- 
esthesia (see  p.  904  ef  seq.)  are  absent  in  hemianesthesia  of  a  cerebral  type. 

Hysteric  hemianesthesia  differs  from  anatomic  cerebral  hemianesthesia  in 
that  the  higher  senses  are  usually  involved,  not  only  sight  and  hearing,  as  may  be 
the  case  with  a  cerebral  lesion,  but  also  smell  and  taste.  The  visual  disturbance 
is  amblyopic  rather  than  hemiopic,  and  consists  of  diminished  sharpness  of  vision, 
together  with  narrowing  and  weakening  of  the  visual  field  upon  the  hemianesthetic 
side.  The  auditory  jjhenomena  may  consist  of  a  complete  unilateral  deafness, 
such  as  does  not  occur  in  anatomic  cerebral  hemianesthesia.  It  must,  neverthe- 
less, be  noted  that  the  higher  senses  may  not  be  involved  in  hysteric  hemian- 
esthesia. It  is  rather  characteristic  of  this  form  of  hemianesthesia  that  the 
most  markedly  disturbed  sensation  is  that  of  pain. 

Sensory  Disturbances  with  Cortical  Lesions. — Sensory  disturbances  with 
cortical  lesions  require  particular  consideration,  since  there  is  a  conflict  of  views 
in  reference  to  this  subject.  As  the  sensory  terminals  extend  over  a  very  large 
cortical  area  and  are  more  diffused  than  the  terminals  of  the  motor  tract,  it  is 
apparent  that  a  localized  cortical  lesion  can  produce  only  a  partial  disturbance  of 
sensation.  These  sensory  disturbances  are  most  marked  in  lesions  situated  in  the 
so-called  motor  region  and  in  lesions  of  the  parietal  cortex.  These  areas  receive 
the  termination  of  the  thalamic  radiation  which  conducts  the  fibers  of  the  fillet  to 
the  cortex.  It  is  likely  that  sensory  fibers  of  different  qualities  terminate  hetero- 
geneously  in  both  these  areas,  and  that  the  location  and  extent  of  the  pathologic 
lesion  is  indicated  by  the  degree  rather  than  by  the  nature  of  the  sensory  disturb- 
ance. The  character  of  the  sensory  disturbances  in  lesions  of  the  so-called  motor 
area  has  a  sjjecial  practical  interest,  since  such  disturbances  play  an  important, 
though  still  somewhat  uncertain  role  in  the  localization  of  these  lesions.  In  the 
first  place  it  should  be  noted  that  sensory  disturbances  are  not  constantly  observed 
with  lesions  of  the  motor  area  From  what  has  previously  been  said,  we  are  led  to 
sui^pose  that  they  are  absent  when  the  lesion  is  quite  circumscribed.  In  large  lesions 
of  the  motor  area,  however,  the  motor  symptoms  are  usually  accompanied  by 
sensory  disturbances.  They  are  almost  always  most  i^ronounced  and  sometimes 
present  exclusively  in  the  distal  portions  of  the  extremities,  particularly  in  the 
terminal  phalanges  of  the  hand.  This  peculiarity,  which  has  been  previously 
referred  to  as  characteristic  of  cerebral  hemianesthesia  in  general  (p.  879),  is 
probably  due  to  the  fact  that  the  proximal  portions  of  the  extremities  receive 
sensory  fibers  fi'om  both  hemispheres.  It  is  well  known  that  the  analogous 
statement  is  true  in  reference  to  motor  disturbances  (see  p.  878).  A  farther 
characteristic  of  cortical  disturbances  of  sensation  is  that  they  affect  those  sensory 
functions  which  are  dependent  ujjon  the  correlation  of  sensory  impulses  rather 
than  upon  the  im^oulses  themselves.  The  sensations  for  j^ain,  touch,  and  temper- 
ature are  usually  but  slightly  if  at  all  affected,  while  there  are  distinct  disturb- 
ances of  the  perception  of  the  position  and  of  passive  movements  of  the  extremi- 
ties, as  well  as  impaired  localization  of  the  sensations  of  touch  and  pain.  This 
correlation  of  sensory  impulses  is  a  complicated  function  of  the  cortex,  and 
cortical  lesions  consequently  may  give  rise  to  these  peculiar  symptoms,  although 
the  elementary  sensations  are  fairly  well  preserved. 

IV.  VERTIGO. 

Vertigo  is  a  peculiar  pathologic  phenomenon  which  plays  a  great  role  in 
neurology  and  is  characterized  clinically  by  a  feeling  of  uncertainty  as  to  the 
position  of  the  body.  With  this  there  is  ijhysiologically  associated  the  discomfort 
attendant  uj^on  disturbed  equilibrium;  in  severe  cases  there  are  also  motor  dis- 
turbances of  equilibrium.     Other  physiologic  sequelae  of  vertigo  are  the  ajsparent 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  881 

movement  of  objects,^  due  chiefly  to  the  involvement  of  visual  perceptions  (rotary 
vertigo)  and  affections  of  other  sensorial  perceptions,  particularly  of  the  sensation 
of  contact  between  the  soles  of  the  feet  and  the  floor  (oscillation  of  the  floor). 
More  remote  sequelae,  produced  by  reflex  action,  are  nausea  and  vomiting,  a 
sense  of  faintness,  palpitation,  and  even  loss  of  consciousness. 

The  Pathogenesis  and  Clinical  Significance  of  Vertigo.— The  origin  of 
vertigo,  in  many  instances,  is  to  be  sought  in  the  function  of  the  semicircular 
canals  of  the  labyrinth.  At  the  present  time  it  may  be  regarded  as  established 
that  the  function  of  these  structures  is  to  acquaint  the  individual  with  the  position 
of  his  body  in  space.  The  sensory  tract  involved  is  the  vestibular  nerve,  which 
innervates  the  semicircular  canals;  the  other  sensory  nerves  are  not  involved  in 
this  function.  The  perception  of  equilibrium  is  simply  a  special  instance  in 
which  this  function  is  employed,  and  the  author  does  not  believe  we  are  justified 
in  regarding  the  semicircular  canals  as  the  mechanism  of  a  special  "sense  of 
equilibrium"  or  of  a  "static  sense."  It  would  seem  more  correct  to  designate 
them  as  an  apparatus  for  the  perception  of  space.  It  is  equally  erroneous  to 
speak  of  the  cerebellum  as  the  organ  of  equilibrium,  simply  because  it  is  the  first 
central  station  for  the  impulses  coming  from  the  semicircular  canals.  Equi- 
libration is  but  one  of  a  number  of  functions  of  the  cerebellum.  The  cerebellum 
serves  rather  for  general  orientation  in  space  and  for  the  adaptation  of  motor 
innervation  to  the  position  of  the  body;  as  the  first  central  station  it  receives  and 
conducts  to  higher  levels  the  impulses  from  the  vestibular  nerve,  and  from  the 
direct  cerebellar  and  Gowers's  tracts.  The  peculiar  and  wonderful  arrangement  of 
the  mechanism  for  the  perception  of  space  need  not  be  discussed  in  detail;  it  is 
enough  simply  to  point  out  that  the  three  semicircular  canals  are  arranged  in  the 
three  planes  of  space  and  surely  are  concerned  with  orientation,  since  every 
movement  of  the  body — i.  e.,  the  labyrinth — is  analyzed  into  its  three  com- 
ponents, each  of  which  exerts  an  exciting  influence  upon  the  nervous  elements 
of  one  of  the  semicircular  canals.  The  exciting  influence  is  doubtless  due  chiefly 
to  the  displacement  of  the  endolymph  upon  the  walls  of  the  labyrinth,  which 
occurs  with  every  movement  as  a  result  of  the  inertia  of  rest.  But  since  we  are 
conscious  of  our  position  even  during  rest,  it  must  be  assumed  that  static  pressure 
effects  may  also  act  as  the  exciting  influence  which  serves  as  a  basis  for  the  per- 
ception of  space.  The  nervous  impulses  arising  in  this  manner  are  first  conducted 
to  the  cerebellum  by  that  portion  of  the  auditory  nerve  called  the  vestibular 
nerve.  The  apparent  double  function  of  the  auditory  nerve  seems  to  justify 
Ewald's  suggestion  that  it  be  named  the  nervus  octavus  ;  we  should  not  elevate 
the  vestibular  nerve  to  the  dignity  of  a  special  cranial  nerve  for  the  reason  that 
the  current  terminology  of  these  nerves  is  too  firmly  fixed  in  our  literature. 
The  nervous  impulses  received  by  the  cerebellum  are  possibly  metamorphosed 
and  then  conducted  to  the  cerebrum. 

From  these  physiologic  facts  it  will  be  understood  that  a  sensation  of  vertigo 
always  arises  when  there  is  a  contradiction  between  the  nervous  imjmlses  from  the 
semicircular  canals  and  the  position  of  the  body  (i.  e.,  the  labyrinth)  as  indicated 
by  the  other  sense-organs.  This  contradiction  causes  the  symptoms  of  vertigo — 
uncertainty  of  judgment,  together  with  the  resulting  consequences  for  the  motor 
innervation  of  the  body,  particularly  for  the  maintenance  of  equilibrium,  con- 
comitant discomforts,  and  the  characteristic  secondary  reflexes.  In  this  manner, 
the  majority  of  the  clinical  symptoiiis  of  vertigo  are  easily  explainable. 

Vertigo  occurs  particularly  in  affections  of  the  labyrinth  which  paralyze  or 
irritate  the  end  organs  in  the  semicircular  canals  and  thus  lead  to  a  pathologic 
distribution  of  the  exciting  influence  and  to  a  consequent  faulty  perception  in 
reference  to  the  position  of  the  body.  The  classical  example  is  Meniere's  dis- 
ease, in  which  the  violent  pathologic  excitation  of  the  semicircular  canals  pro- 
duces such  marked  vertigo  that  the  patient  cannot  maintain  the  erect  i)Osition. 
In  some  of  these  cases  the  sensorial  perception  of  space  may  be  suddenly  and 

^  As  we  shall  subsequently  learn  (p.  882  et  seq.)  this  may  also  he  tlie  cause  of  the 
vertigo. 

56 


882  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

completely  abolished,  and  this  may  result  in  an  interruption  of  some  of  the  asso- 
ciation-fibers so  that  unconsciousness  is  produced.  The  vertigo  which  is  observed 
with  innocent  middle-ear  affections  is  also  to  be  referred  to  an  associated  involve- 
ment of  the  labyrinth,  either  in  the  form  of  circulatory  disturbances  or  of  varia- 
tions in  the  intralabyrinthine  pressure.  All  these  cases  are  characterized  as 
otogenic  on  account  of  the  simultaneous  disturbances  of  the  acoustic  function 
of  the  auditory  nerve,  disturbances  which  take  the  form  of  either  impaired 
hearing  or  the  presence  of  subjective  auditory  sounds.  In  these  cases,  condi- 
tions either  of  excitement  or  paralysis  within  the  semicircular  canals  may  pro- 
duce the  phenomena  of  vertigo  if  all  the  semicircular  canals  are  not  equally 
afiected. 

The  vertiginous  symptoms  which  give  such  a  characteristic  stamp  to  cere- 
bellar disease  are  evidently  due  to  the  fact  that  the  stimuli  for  the  sensorial  per- 
ception of  space  are  correctly  originated  but  not  properly  conducted,  becoming 
blocked  in  the  cerebellum.  The  so-called  cerebellar  ataxia,  so  frequently 
observed  associated  with  vertigo  in  cerebellar  disease,  is  made  up  of  two  com- 
ponents. One  of  these  has  nothing  whatever  to  do  with  the  sensorial  perception 
of  space,  but  is  associated  with  that  disturbance  of  muscle-tones  which  Luciani 
has  demonstrated  in  cerebellar  lesions.  The  other  component  is  to  be  regarded 
as  the  motor  effect  of  the  vertigo — i.  e. ,  the  result  of  the  defective  correction  of 
movements  on  account  of  faulty  sensorial  perceptions  of  space  (see  p.  756).  Since 
the  sensorial  perceptions  of  space  are  prepared  in  the  cerebellum ,  but  do  not 
become  conscious  sensations  and  concepts  until  they  reach  the  cerebrum,  it  will 
readily  be  understood  that  affections  of  the  cerebrum,  as  well  as  those  of  the  cere- 
bellum, may  lead  to  vertigo.  The  frequent  and  marked  clinical  similarity 
between  tumors  of  the  frontal  lobe  and  those  of  the  cerebellum  indicates  that  the 
frontal  lobe  contains  centers  which  receive  the  sensorial  perceptions  of  space  by 
means  of  fibers  radiating  from  the  cerebellum  and  passing  through  the  superior 
cerebellar  peduncles  and  red  nucleus. 

The  vertigo  which  occurs  as  a  functional  symptom  of  circulatory  disturbances, 
cardiac  diseases,  arteriosclerosis,  anemia,  etc.,  is  possibly  due  to  abnormal  excita- 
tion of  the  semicircular  canals  or  of  their  co-ordinated  centers.  The  same  is 
true  of  neurasthenic  vertigo. 

The  vertigo  associated  with  paralysis  of  the  ocular  muscles  is  evidently  due 
to  a  false  projection  of  the  retinal  images,  as  a  result  of  which  disturbances  of 
space-orientation  might  naturally  give  rise  to  vertigo.  These  disturbances  of 
space-orientation  are  due  not  only  to  the  occurrence  of  double  images  but  also  to 
the  fact  that  these  retinal  images  become  abnormally  displaced  during  ocular 
movement — i.  e.,  they  do  not  conform  with  the  motor  im23ulses,  so  that  the 
objects  apparently  seem  to  move.  In  unilateral  ocular  paralysis  the  vertigo  may 
be  controlled  to  a  variable  degree  by  having  the  patient  concentrate  his  attention 
upon  the  image  produced  in  the  sound  eye  and  disregard  the  faulty  projection  of 
the  image  in  the  paralyzed  organ.  Even  in  bilateral  paralysis  of  the  ocular 
muscles  the  vertigo  may  be  eliminated  if  the  patient  can  learn  to  disregard  the 
visual  sense  in  the  formation  of  his  conceptions  of  space.  In  all  cases  the  ver- 
tigo produced  by  paralysis  of  the  ocular  muscles  may  be  made  to  disappear  by 
closing  either  one  or  both  eyes. 

A  special  variety  of  vertigo,  partly  also  of  ocular  origin,  is  that  which  is 
experienced  upon  rapid  rotation  of  the  body  or  upon  the  sudden  arrest  of  a  pas- 
sive movement  involving  the  body,  such  as  the  stopping  of  a  train.  In  the  first 
instance  the  phenomenon  is  probably  dependent  upon  the  fact  that  a  physiologic 
excitation  is  produced  in  the  semicircular  canals  by  the  motion  imparted  to  the 
body,  which  results  in  reflex  stimuli  to  the  ocular  muscles  so  that  the  eyes  follow 
external  objects  in  spite  of  the  movement  of  the  body.  When  the  particular 
motion  is  very  rapid,  the  excitation  of  the  semicircular  canals  becomes  so  strong 
that  the  reflex  stimulation  of  the  ocular  muscles  is  excessive;  since  these  ocular 
movements  are  unconsciously  executed,  the  objects  themselves  apparently  move 
and  vertigo  is  consequently  produced.  The  inability  to  fix  the  eyes  permanently 
upon  any  object,  together  with  the  violence  and  rapid  change  in  the  excitation 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  883 

of  the  individual  semicircular  canals  may  also  be  a  factor  in  producing  the  dis- 
turbance of  space-orientation  in  this  variety  of  vertigo.  The  vertigo  which  is 
experienced  by  many  individuals  upon  the  sudden  stopping  of  a  train  is  probably 
due  to  the  fact  that  the  unconscious  reflex  ocular  movements,  produced  through 
the  agency  of  the  semicircular  canals,  are  continued  somewhat  longer  than  the 
motion  of  the  train,  and  the  apparent  motion  of  external  objects  results  in  vertigo 
as  before. 

Mountain  vertigo,  or  the  vertigo  of  elevation,  is  not  a  pure  vertigo,  but  is 
partly  due  to  a  sensation  of  fear.  The  other  factor  is  probably  an  ocular  vertigo 
dependent  upon  a  strong  concept  of  falling,  which  by  autfjsuggestion  innervates 
the  nervous  mechanism  of  space-orientation  to  an  abnormal  degree. 

Agarophobia. — Vertigo  jiroduced  by  the  fear  of  space  is  brought  about  by 
an  analogous  mechanism  which  is  excited  by  autosuggestion. 

Seasickness  is  probably  nothing  else  than  a  violent  vertigo  with  numerous 
irradiations  (to  the  vomiting  center,  etc.),  produced  by  pathologic  excitation  of 
the  semicircular  canals  as  a  result  of  the  oscillations  of  the  ship.  Ocular  vertigo 
plays  an  important  role  in  seasickness  and  originates  in  the  labyrinth,  just  as  is 
the  case  in  the  vertigo  produced  by  rapid  rotation  of  the  body  or  upon  the  sudden 
stopping  of  a  train.  This  is  borne  out  by  the  fact  that  a  large  number  of  the 
phenomena  of  seasickness  disappear  when  the  eyes  are  closed.  Since  the 
symptoms  by  no  means  completely  disappear,  however,  it  is  quite  likely  that  a 
further  cause  is  to  be  found  in  the  inability  of  the  mind  and  the  movements  of 
equilibration  to  follow  the  rapidly  changing  and  violent  excitations  of  the  semi- 
circular canals. 

Galvanic  vertigo,  produced  by  the  application  of  a  galvanic  current  to  the 
head,  is  doubtless  dependent  upon  a  direct  and  unequal  excitation  of  the  nerve- 
terminals  of  the  semicircular  canals,  which  does  not  correspond  with  the  position 
of  the  body. 

The  existence  of  the  so-called  gastric  vertigo  of  Trousseau  (vertigo  e  stomacho 
laeso)  in  affections  of  the  stomach  is  doubtful.  The  majority  of  the  cases  answer- 
ing to  Trousseau's  description  have  been  shown  to  be  other  varieties  of  vertigo 
(particularly  aural  vertigo),  the  origin  of  which  were  unknown  in  the  time  of  this 
distinguished  clinician.  In  many  such  cases  the  only  symptom  suggestive  of 
gastric  disease  is  the  vomiting  produced  by  the  vertigo. 


884 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


V.  CEREBRAL  LOCALIZATION. 

Without  intending  to  enter  minutely  into  the  question  of  cerebral  localization, 
which  belongs  more  properly  to  the  province  of  special  diagnosis,  the  author 
wishes  to  submit  the  following  diagrams  to  be  utilized  as  a  sort  of  guide  in  the 
problems  of  cortical  and  nuclear  diagnosis: 


Fig.  339.— Cortical  localization  :  1,  Trunk  ;  2,  shoulder:  3.  elbow  ;  4,  wrist  joint ;  5,  the  three 
last  fingers;  6,  index  fingers;  7,  thumb;  S,  "writing  center"  (see  p.  894i  (assumed  by  French 
-writers) ;  9,  larynx  ;  10,  Broca's  speech  center  (motor)  ;  11,  tongue  ;  12,  mouth  ;  13,  lower  facial ; 
14,  upper  facial";  15,  eve  muscle  ;  16,  vision  ;  17,  hearing  (Wernicke's  sensory  speech  center);  18, 
taste;  19,  conjugate  movements  of  eves  and  head;  20,  movements  of  hip  joint;  21,  movements  of 
knee  joint!;  22,  movements  of  ankle"  joint ;  23,  movements  of  great  toe;  24,  movements  of  little 
toes  (from  Debove  and  Achard). 

Compare  p.  831  in  regard  to  the  dispute  which  is  still  going  on  concerning  the  central  inner- 
vation of  the  conjugate  movements  of  the  eyes.  Wernicke  has  assumed  that  the  center  for  these 
movements  is  situated  in  the  inferior  parietal  convolution,  because  he  found  but  few  projection 
fibers  in  this  region.  He  supposes  that  the  conjugate  deviation  of  the  eyes,  which  arises  in  case 
of  lesions  in  this  area,  is  due  to  lesion  of  an  association  tract,  demonstrated  by  himself  to  exist 
between  the  visual  area  and  the  motor  area. 

Flechsig  disputes  this.  He  locates  the  "  visual  center  "  almost  exclusively  in  the  median  sur- 
face of  the  hemispheres,  especially  in  the  region  of  the  calcarine  fissure.  The  visual  disturbances 
so  frequently  met  with  clinicallv"  in  lesions  of  this  region  (16)  may  be  explained  partly  by  the 
fact  that  such  lesions  often  also"  involve  the  visual  fibers  situated  deeper  and  connecting  the 
central  fibers  of  the  optic  tract  to  the  visual  center. 

According  to  Flechsig,  the  center  or  area  for  smell  in  man  has  allotment  both  in  the  frontal 
and  temporal  portion  of  the  brain.  The  former  embraces  the  entire  posterior  portion  of  the  base 
of  the  frontal  lobes  and  the  basal  portions  of  the  gT,-rus  fornicatus,  the  latter  embraces  the  unci- 
nate gyrus  and  a  part  of  the  adjoining  inner  pole  of  the  temporal  lobe.  Both  portions  are  funda- 
mientallv  connected  with  the  island. 

Flechsig,  who  has  recently  investigated  the  localization  of  the  sense  of  taste,  does  not  furnish 
anv  definite  statements  about"  its  seat.    18  in  the  diagram  is,  therefore,  placed  provisionally. 

"  Munk  locates  the  region  for  stomatic  sensibility  in  the  territory  of  the  centraF convolutions 
and  the  parietocentral  lobule  supplied  with  motor  centers  (see  Flechsig,  Gehini  und  Seele.  Leipsic, 
Veit  &  Co.,  1896).  That  is  to  say,  these  areas  contain,  in  addition  to  the  motor  centers,  the  central 
apparatus  for  sensory  apprecia'tions  in  so  far  as  they  do  not  belong  to  the  '■  higher"  senses  (sight, 
hearing,  etc. ),  which  "possess  special  centers.  The  area  for  corporeal  feeling,  according  to  Flechsig, 
also  includes  the  lobus  limbicus— t.  e.,  the  gyrus  fornicatus,  gyrus  uncinatus,  and  the  gyrus  hip- 
pocampus. 

The  white  unshaded  areas  and  the  shaded  area  of  the  parieto-occipital  brain,  16.  according 
to  Flechsig  wrongly  credited  with  the  visual  center,  contain  the  Flechsig  associatirm  centers. 
He  differentiates  three,  viz.,  the  frontal  or  anterior,  the  parieto-occipito-temporal  or  posterior 
great  association  center,  and  finally  the  Island  of  Reil.  These  areas  are  anatomically  character- 
ized by  containing  no  projection  fi'bers,  or  very  few,  and,  on  the  contrary,  very  many  association 
fibers.  Lesions  of  the  anterior  association  center  should  cause  a  loss  of  interest  and  a  change  of 
character;  lesions  of  the  posterior  association  center,  a  loss  of  collective  representations,  initia- 
tion, and  mental  capacity. 


EXAMINATION  OF  TEE  NERVOUS  SYSTEM. 


885 


JitqionofiiJ}f)ereitrei'i^y    \  ^^^io''^  "/^"'"er  extremtfyt 


J^terdettructSuitf 
th!iur(a.Ottfimr 

fillers  Cdruuith* 

moiKditittietktuab 
5  not  iniKtindL 


fieyion  of  head 
(FaceJ 

Fig  840.— The  lateral  aspect  of  the  human  cerebral  hemisphere.    The  motor  areas  according  to 
Allen,  Starr,  Keen,  Mills,  Horsley,  and  v.  Monakow,  as  arranged  by  the  latter. 


Fig.  341.— The  motor  areas  in  the  ape,  according  to  Beevor  and  Horsley. 


886 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


Fig.  342.— Base  of  the  brain  showing  the  origin  of  tlie  cranial  nerves  (from  Heitzmann). 


(See  Figs,  on  opposite  page  for  the  following  legends) : 

Fig.  343.— Transparent  surface  view  of  the  medulla  oblongata  from  behind.  Upon  the  right 
side  the  nerve  nuclei  are  put  in  diagrammatically  and  numbered  with  Roman  figures  :  V,  Motor 
nucleus  of  the  trigeminus;  U' and  V" .  middle  and  lower  sensory  nuclei  of  the  trigeminus; 
VT,  abducens  nucleus ;  VII,  facial  nucleus  ;  TT//,  posterior  median  acoustic  nucleus  ;  VHP,  anterior 
median  acoustic  nucleus  ;  VIII",  anterior  lateral  acoustic  nucleus  ;  IX,  glossopharyngeal  nucleus  ; 
X,  vagus  nucleus;  ,17,  accessory  nucleus;  XII,  hypoglossal  nucleus;  1,  brachium  pontis ; 
2,_brachium  conjunctivae:  3,  cerebellar  peduncle;  4."  eminentia  teres  ;  .5.  strife  acousticse ;  6,  ala 
cinerea.    The  large  numerals  represent  the  corresponding  nerve  roots  (Erb). 

Fig.  344.— Transparent  lateral  view  of  the  right  half  of  the  medulla  oblongata.  To  show  the 
relations  of  the  most  important  nuclei.  The  nuclei  situated  nearest  are  shaded  darker  (dia- 
grammatic):  Py,  Pyramidal  tract ;  P//.A>,  decussation  of  pyramidal  tract ;  0,  olive;  0..s,  superior 
olive;  F,  motor  nucleus  of  trigeminus;  V,  middle  sensory  nucleus  of  trigeminus;  V",  lower 
sensory  nucleus  of  trigeminus;  IT",  nucleus  of  abducens;  "G./.,  knee  of  the  facial;  VII,  facial 
nucleus;  VIII,  posterior  middle  acoustic  nucleus;  IX,  glossopharyngeal  nucleus;  -V,  vagus 
nucleus  ;  XI,  accessory  nucleus  ;  XII,  hvpoglossal  nucleus  ;  Kz,  nucle'us'gracilis  :  RV,  trigeminus 
root;  RVI,  abducens  root ;  RVII,  facial  root  (Erb). 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


887 


Fig.  344. 


888  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

VI.  THE  DISTURBANCES  OF  SPEECH. 

I.    THE  CONCEPTION  OF  THE  SPEECH  TRACT. 

Speech  arises  from  the  elaboration  of  motor  speech  conceptions  in  the  so-called 
motor  speech  center  situated  in  the  left  hemisphere.  When  the  will  is  exerted, 
these  conceptions  are  responsible  for  the  co-ordinated  impulses  proceeding  through 
the  so-called  central  speech  tract  to  the  bilateral  cortical  centers  for  the  muscles 
of  speech  and  generating  the  spoken  word. 

The  speech  tract  (Fig.  345)  originates  in  the  motor  speech  center,  the  so-called 
Broca's  area  (a,  Fig.  345),  runs  to  the  cortical  centers  for  the  oral,  laryngeal,  and 
respiratory  muscles,  some  of  the  fibers  possibly  passing  through  the  corpus  cal- 
losum,  and  finally  enters  the  pyramidal  tract  to  reach  the  nuclei  for  the  muscles 
of  speech.  From  the  cortical  centers  to  the  nuclei  of  these  muscles,  the  impulses 
travel  through  the  same  fibers  that  are  utilized  for  the  other  functions  of  the 
muscles,  so  that  an  actual  special  tract  does  not  exist  after  the  impulse  leaves  the 
cortical  centers. 

2.  THE    DISTURBANCES   OF  SPEECH    FROM    LESIONS  OF  THE   SPEECH  AREA 
OR    OF   THE  CONDUCTING  FIBERS. 

The  innervation  for  the  movements  of  speech  may  be  inteiTupted  by  a  lesion 
situated  in  any  portion  of  its  course.  The  clinical  picture  is  subject  to  great  varia- 
tion, according  to  whether  the  lesion  affects  the  speech  center,  the  actual  speech 
tract  (the  heavy  line  in  Fig.  345),  or  simply  the  connection  of  the  cortical  centers 
of  the  muscles  of  speech  with  the  nuclei  of  the  latter  (the  light  lines  in  Fig.  345). 
In  the  first  instance,  even  though  the  lesion  be  circumscribed,  the  ability  to  form 
words  will  be  more  or  less  completely  abolished.  When  the  lesion  affects  the 
connection  between  the  cortex  and  the  nuclei  of  the  muscles,  however,  the  only 
result  is  a  mutilation  of  the  syllables,  a  disturbance  of  pronunciation ;  if  the 
lesion  be  of  moderate  extent  the  disturbance  is  but  slight,  since  owing  to  the 
commissural  fibers  the  speech  impulse  is  conducted  downward  from  both  hemi- 
spheres. As  a  result  of  the  bilateral  quality  of  this  portion  of  speech  innervation, 
the  disturbance  of  pronunciation  can  be  extreme  only  when  the  lesion  is  situated 
low  down  in  the  vicinity. of  the  nuclei  for  the  muscles,  where  the  fibers  of  both 
hemispheres  are  simultaneously  more  or  less  involved. 

The  disturbances  having  as  their  cause  some  lesion  in  the  speech  center  or  in 
the  actual  speech  tract  of  the  left  hemisphere  are  called  aphasias  ;  those  due  to 
some  lesion  between  the  cortex  and  the  nuclei  for  the  muscles  of  speech  are  called 
anarthrias. 

Although  in  typical  cases  the  clinical  distinction  between  these  two  conditions 
is  quite  marked,  the  differentiation  between  them  is  not  sharp,  since  lesions  of  the 
speech  center  and  of  the  actual  speech  tract  may  give  rise  to  symptoms  resem- 
bling anarthria,  providing  that  the  lesion  is  neither  large  nor  destructive  (see 
Anarthria).  Such  a  disturbance,  which  might  be  called  a  "  central  anarthria," 
may,  nevertheless,  be  differentiated  from  a  peripheral  anarthria,  and  jiarticularly 
from  that  localized  in  the  vicinity  of  the  nuclei,  by  the  fact  that  in  the  latter 
the  other  functions  of  the  muscles  of  speech  (deglutition,  mastication)  are  also 
involved. 

The  sharpest  differentiation  between  aphasia  and  anarthria  consequently  con- 
sists of  the  fact  that  the  former  is  a  pure  and  exclusive  disturbance  of  speech, 
while  the  latter  is  always  accompanied  by  a  disturbance  of  the  other  functions  of 
the  muscles  of  speech. 

(a)    Anarthria. 

In  anarthria  there  is  an  affection  of  individual  fibers  of  the  speech  tract  in  the 
neighborhood  of  the  nuclei.  Hence  the  following  peculiarity :  The  speech  im- 
pulse is  correctly  formed  in  the  speech  area  and  correctly  despatched  to  the 
periphery;  but,  as  the  result  of  partial  interruption  of  cond^^ction  in  the  neighbor- 
hood of  the  nuclei,  each  of  its  ganglion  cells  no  longer  receives  the  measure  of 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


889 


innervation  essential  to  co-ordinated  speech.  The  result  is  a  disturbance  in  the 
co-ordination  of  the  speech,  analogous  to  the  ataxia  of  the  extremities. in  partial 
paralyses  (see  p.  753  et  seq.),  so  that  a  patient  with  anarthria  pronounces  the 
word  with  approximately  correct  cadence  of  syllables  and  intonation,  but  with 
some  of  the  letters  of  the  word  lacking  or  else  incorrectly  pronounced.  Anarthria 
is,  therefore,  a  disturbance  of  pronunciation,  which  is  further  characterized  by  the 
fact  that  the  more  or  less  marked  paralysis  of  the  muscles  of  speech  also  affects 
the  other  functions  of  these  muscles. 

It  is  evident  that  quite  an  analogous  disturbance  of  speech  will  arise,  when 
not  the  terminal  fibers  of  the  speech  tract  in  the  neighborhood  of  the  nuclei, 
but  the  nuclei  themselves  or  the  peripheral  speech  nerves— e.  g. ,  facial  and  hypo- 
glossus — are  affected.     In  such  cases  speech  will  be  mutilated  and  pronunciation 


CortcenXet 
of  Facial 


CofVcenti/' 

yf/Zyfioflossus. 


^r oca's 

(motorj 

ISheeek  cenZer 


Fig.  345.— Diagram  of  the  motor  speech  tract.  For  simplicity,  of  the  nerves  which  subserve 
the  function  of  speech,  only  the  facial  (  F7/)  and  hypoglossus  (XII),  are  shown.  For  the 
center  for  spontaneous  breathing,  as  well  as  that  for  the  larynx,  see  Fig.  340 ;  and  for  the  motor 
trigeminus,  especially  for  the  part  that  presides  over  the  movement  of  the  jaws,  see  "  Chewing, 
Fig.  340.  Aside  from  this,  there  are  left  out  in  the  figure  the  commissural  fibers  coursing  in  the 
corpus  callosum,  which  unite  the  two  lateral  cortical  centers. 

will  suffer.  These  nuclear  and  peripheral  disturbances  of  speech  parallel  those 
of  supranuclear  anarthria,  insomuch  as  they  are  associated  with  paralyses  of 
other  movements. 

The  clinical  picture  of  anarthria  may  under  some  circumstances  result  even 
from  an  incomplete  interruption  of  the  speech  center  or  of  the  actual  speech  tract. 
This  can  be  explained  only  by  assuming  that  the  separate  fibers  or  cells  are  to  a 
certain  extent  individually  diseased,  because  the  fibers  of  the  central  speech  tract 
are  so  compact  that  larger  lesions  would  generally  affect  them  in  ioto.  Anatomic 
proof  of  the  existence  of  pure  anarthria  depending  upon  such  individual  disease 
of  separate  fibers  or  cells  has  not  yet  been  ftxrnished.  Anarthritic  disturbances 
of  pronunciation,  which  often  persist  for  a  long  time  after  recovery  from  aphasia, 
may  without  doubt  be  explained  by  the  fact  that  certain  individual  fibers  or 
cells  of  the  central  speech  apparatus,  which  is  at  first  widely  involved,  later  on 


890  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

recover,  while  certain  others  do  not.  In  the  same  way  manifold  combinations  of 
anarthria  and  aphasia,  which  have  been  sometimes  observed,  may  perhaps  be 
attributed  to  an  unequal  involvement  of  the  central  speech  apparatus.  As  has 
previously  been  stated,  the  characteristic  of  all  these  cases  of  central  "anarthria" 
is  that  the  muscles  perform  all  their  movements  except  those  necessary  for  the 
production  of  speech. 

The  simplest  method  of  examining  for  anarthria  is  to  have  the  patients  pro- 
nounce the  letters  of  the  alphabet  in  their  order,  and  then  combinations  of 
letters — i.  e.,  simpler  and  then  more  complicated  words.  Theoretically,  it  is  evi- 
dent that  anarthria  will  occur  veiy  frequently  in  all  lesions  in  the  neighborhood 
of  the  nuclei  of  the  Speech  muscles — i.  e.,  in  hemorrhagic  and  softened  areas  and- 
in  tumors  of  the  jions  and  of  the  oblongata,  but  especially  in  progressive  bulbar 
paralysis. 

(h)   Aphasia    (Agraphia ;  Alexia). 

As  contrasted  with  anarthria,  we  may  define  aphasia  as  embracing  those  dis- 
turbances of  speech  which  arise  from  diffuse  lesions  of  the  actual  speech  tract  or 
of  the  motor  speech  center  itself.  If  we  could  represent  the  latter  as  merely  a 
simple  center,  the  process  would  be  comparatively  simple;  a  loss  of  speech  would 
then  depend  upon  a  destruction  of  the  center  (Fig.  345,  a),  or  upon  a  destruction 
of  the  speech  tract  (heavy  line,  Fig.  345). 

The  conditions  of  aphasia  are,  however,  more  complicated,  because  the  speech 


n 

Fig.  316.— Primitive  speech  apparatus  of  the  child  for  mechanical  repetition  of  words  :  a,  Sen- 
sory speech  center ;  6,  motor  speech  center  (Broca's  center) ;  x,  acoustic  center,  center  of  simple 
sound  perception;  mz,  tract  of  the  auditory  nerve;  bn,  motor  speech  tract. 

center  is,  in  a  broader  sense  of  the  word,  not  a  simple  motor  center.  We  may 
consider  the  entire  apparatus  of  central  speech  formation,  which  has  been  estab- 
lished psychophysiologically  by  the  researches  of  Wernicke  and  Lichtheim,  as 
proceeding  centrally  from  the  point  a  of  Fig.  345,  and  this  latter  point  as  repre- 
senting merely  the  motor  terminus  of  the  central  speech  mechanism,  the  so-called 
motor  center  of  speech.  Lesions  of  these  portions  of  the  speech  apparatus,  which 
have  not  yet  been  studied,  can  also  give  rise  to  disturbances  properly  designated 
as  aphasias.  To  understand  these  different  forms  of  aphasia,  a  knowledge  of  the 
physiologic  mechanism  of  central  speech  formation  is,  therefore,  required.  ^  A 
discussion,  essentially  following  Wernicke  and  Lichtheim,  will  now  be  given,  going 
somewhat  more  minutely  into  detail. 

When  a  child  learns  to  speak,  the  sound  of  the  word  heard  is  sent  by  way  of 
the  acoustic  nerve  to  his  left  first  temporal  convolution  in  the  cortex  (sensory 
speech  center.  Fig.  346,  a).  The  child  then  attempts  to  imitate  this  word.  This 
latter  procedure  may  be  explained  by  assuming  that,  by  means  of  association, 
the  auditory  images  exert  a  conception  of  movement  corresponding  to  the  spoken 
words.  This  representation  of  movement,  as  Broca  proved,  is  situated  in  the  left 
inferior  frontal  convolution  (motor  or  Broca's  speech  center.  Fig.  339,  10).  The 
child's  primitive  speech  apparatus  (Fig.  346)  is  formed  in  this  way,  and  he  thus 
repeats  mechanically  the  word  spoken  beforehand,  a  represents  the  center  for 
auditory  images  of  the  word  heard — /.  e.,  the  sensory  speech  center  in  the  first  tem- 
poral convolution.    The  auditory  images  are  received  here  after  they  have  properly 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


891 


stimulated  the  correspo7iding  acoustic  center  (x),  the  center  of  simple  hearing  or 
sound  perception.  The  association  tract  (ab)  by  which,  by  mechanica  Ibabbling  of 
the  child,  the  center  b  is  incited  by  way  of  mab,  runs,  according  to  Wernicke,  along 
the  convolutions  of  the  Island  of  Reil  from  behind  forward.  The  arrow  pointing 
upward  to  x  represents  the  tract  of  the  auditory  nerve;  the  arrow  pointing  down- 
ward from  b  represents  the  motor  speech  tract  represented  in  detail  in  Fig.  345. 

The  child's  advance  to  that  stage  of  development  which  is  characterized  by 
voluntary  speech  is  attained  through  the  association  of  centers  (a)  and  (6)  with 
ideas.  The  idea  of  an  object  is  the  aggregate  of  its  partial  representations. 
After  the  partial  representations  are  acquired  by  experience,  they  are  stored  in 
the  different  sensory  areas  of  the  cerebral  cortex,  and  are  then  associated  as 
memories. 

The  conception  of  an  object  can,  therefore,  never  be  localized  at  a  single 
point  in  the  cerebral  cortex — e.  g.,  the  conception  "bell"  requires  association 
tracts  to  quite  different  parts  of  the  brain — to  the  acoustic,  optic,  and  tactile 
centers.  This  is  represented  in  the  more  complicated  diagram  (Fig.  347).  The 
partial  representations  c  +  c^  +  (/^  first  produce  the  conception  of  bell.^ 

To  simplify  the  speech  scheme,  we  reduce  the  conception  c  +  c^  +  (/^  to  a 


Acoustic 
division 


Fig.  347.— Apparatus  for  conscious  speech  and  speech  comprehension,  with  the  relationship 
to  the  primitive  speech  center  to  conceptions,  especially  the  sensory  division  of  the  latter.  For 
simplicity  merely,  three  divisions  of  the  cortical  sensory  areas  have  beeia  represented.  The 
letters  a,  b,  x,  m,  and  n  have  the  same  meaning  as  in  Fig.  345. 

single  jjoint  (c),  using  the  diagram  that  Wei'nicke  first  made  for  voluntary  con- 
scious speech  (Fig.  348).  For  the  sake  of  simplicity,  the  acoustic  center  (.r)  is 
omitted  here  and  in  the  following  diagrams,  because,  as  is  shown  upon  p.  892, 
note,  from  a  gross  anatomic  standpoint  it  practically  coincides  with  the  center  a. 
The  significance  of  the  double  arrows  will  be  explained  in  what  follows. 

With  the  aid  of  this  diagram  we  can  readily  explain  many  types  of  aphasia 
by  supposing  interruption  of  conduction  at  different  places.  We  differentiate 
between  motor  and  sensory  aphasia  according  to  whether  the  interruption  affects 
the   sensory   centripetal    {maC),  or    the    motor    centrifugal    conducting   2)ortion 

^  To  avoid  misundei-standing,  the  author  should  add  that  the  conception  wliicli  a 
child  has  of  a  bell  and  associates  with  the  word  "  bell "  is  a  natural  but  not  the  complete 
conception  of  a  "bell"  which  an  adult  possesses.  A  complete  conception  will  only  be 
developed  gradually,  in  the  course  of  mental  development,  by  adding  one  partial  repre- 
sentation to  another.  Thus,  in  small  children,  the  conception  of  a  "  bell "  may  be 
exclusively  the  partial  representation  of  the  tone  of  a  "bell"  and  jierhaps  of  some  of  its 
metallic  luster;  tlien,  in  the  course  of  development,  are  superadded  the  representations 
of  the  form  of  the  "  bell,"  of  the  sensation  of  cold  by  touching  it,  of  its  use,  and  of  many 
other  features  to  complete  the  conception. 


892 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


(Cbn).  Aphasia  arising  from  interruption  of  conduction  in  the  line  ab  is 
spoken  of  as  "conduction"  or,  perhaps  better,  "associated  aphasia."  Disturb- 
ances between  ab,  on  the  one  hand,  and  C,  on  the  other,  are  called  transcortical, 
those  in  a  or  6  cortical,  and  those  peripheral  to  a  or  6  subcortical.  These  names 
have  not  been  fittingly  chosen,  since  the  entire  area  of  innervation  {abc)  is 
situated  in  the  cerebral  cortex,^  and  should,  consequently,  be  designated  as 
cortical.  If  the  terms  had  not  become  so  fixed,  the  author  would  suggest  repla- 
cing them  by  he  expressions  transcentral,  central,  and  subcentral,  the  word 
"central"  naturally  referring  to  the  speech  center. 

To  explain  these  different  symptom-complexes,  we  must  now  call  attention  to 
the  fact  that,  for  correct  speaking,  the  tract  Cab  must  be  intact,  as  well  as  the 
tract  Cbn,  although  this  does  not  directly  appear  in  the  diagram.  If  the  tract 
Cab  is  interrupted  at  any  point,  word  production  is  still  possible  by  way  of  the 
tract  Cbn  ;  the  fund  of  words  is  sufficient,  but  we  observe  a  symptom  called 
paraphasia — i.  e.,  a  confusion  of  words — because  the  control  of  motor  innervation 
by  way  of  the  path  Cab  is  essential  for  correct  speaking.  Since  this  paraphasia 
may  also  be  caused  by  lesions  between  C  and  a,  it  must  be  assumed  that  not  only 
centripetal  but  also  centrifugal  conduction,  requisite  for  the  control  mentioned 
above,   is  situated  in  the  association  fibers  aC.     Words  are  sounded  inwardly. 


Fig.  348.— Simplification  of  the  diagram  of  conscious  speech  fFig.  346)  by  restriction  of  the 
conception  to  point  c  and  the  omission  of  the  acoustic  center  x.  The  letters  have  the  same  mean- 
ing as  in  both  preceding  diagrams.    The  figures  correspond  to  the  list  of  aphasias  in  the  text. 


The  double  arrows  in  Fig.  348,  between  a  and  C,  represent  this  idea;  but  it  must 
be  confessed  that  the  innervation  from  C  to  a  is  not  sufficient  to  speak  anything 
by  way  of  Cab,  as  otherwise  no  loss  of  speech  would  occur  with  a  lesion  between 
b  and  C,  and  experience  proves  that  this  is  not  the  case. 

The  following  main  types  of  aphasic  disturbances  should  now  be  easily  under- 
stood. The  numbers  represent  the  point  of  interruption  as  indicated  in  the  dia- 
gram (Fig.  346): 

1.  Cortical  sensory  aphasia.  Comprehension  of  speech  and  repetition  of 
speech  are  prevented.     Paraphasia  is  present. 

2.  Subcortical  sensory  aphasia"^  {^ViXQ  "word-deafness").  The  same  functions 
are  interfered  with  as  in  1,  except  that  there  is  no  paraphasia. 

^  This  is  demonstrated  by  the  fact  that  the  lesions  producing  aphasia  are  always 
situated  in  tlie  cortex  or  in  its  immediate  vicinity.  At  most  the  tract  am  (the  heavy 
line  in  Fig.  345)  describes  but  a  slight  curve  in  the  white  matter  in  the  vicinity  of  the 
cortex. 

^  The  anatomic  findings  in  this  form  of  aphasia  have  always  shown,  in  contradic- 
tion to  the  term  subcortical,  foci  of  disease  in  Wernicke's  sensory  speech  center.  (D^ 
jerine,  Veraguth).  For  this  reason  the  entire  Wernicke-Lichtbeim  conception  of  the 
speech  apparatus  has  been  said,  erroneously,  to  disagree  with  the  facts.     In  the  author's 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  893 

3.  Transcortical  sensory  aphasia.  Comprehension  of  speech  is  lost;  repetition 
of  speech,  as  contrasted  with  1,  is  retained.     Paraphasia  is  present. 

4.  Cortical  motor  aphasia.  Spontaneous  speech  and  capacity  to  repeat  are 
lost.     Comprehension  of  speech  is  preserved. 

5.  Subcortical  motor  aplia.na  (lesion  of  the  speech  tract).  Clinical  picture  as 
in  4.     Differentiation  between  4  and  5  is  discussed  below. 

6.  Transcortical  motor  apjhasia.  Spontaneous  speech  is  lost.  Repetition  and 
comprehension  of  speech  are  preserved. 

7.  Conduction  or  association  aphasia.  Spontaneous  speech  is  paraphasic. 
Repetition  by  way  of  aCb  is  possible,  but  also  paraphasic. 

A  differentiation  between  4  and  5  can  be  determined  by  noticing  the  written 
speech.  In  cortical  motor  aphasia  (4)  waiting  is  impossible ;  in  subcortical  (5)  it 
is  preserved.  Further  discussion  of  this  point  will  be  taken  up  later.  Lichtheim 
has  demonstrated  that  a  patient  with  subcortical  motor  aphasia  (5)  can  show  by 
signs  how  many  syllables  there  are  in  the  name  of  an  object  held  in  front  of  him  ; 
whereas,  with  cortical  motor  aphasia  (4),  destruction  of  the  center  (6),  this  is 
impossible. 

The  varied  disturbances  of  writing  and  reading  which  occur  in  aphasia  show 
that  the  centers  a  and  b  have  an  almost  reciprocal  relation,  expressed  in  Fig.  348 
by  the  double  arrows,  and  that  the  sensory  representation  and  the  motor  together 
produce  a  complete  so-called  word  conception  (Wernicke)  (see  p.  895).  In  this 
collective  word  conception,  and  not  merely  in  the  individual  representations  (a 
and  b),  are  to  be  found  not  only  the  letters,  as  we  shall  see,  but  also  to  a  certain 
extent  the  number  of  the  syllables,  presupposing  an  internal  speech.  Therefore, 
in  case  there  is  an  injury  in  a  and  b  or  between  the  two,  the  patient  can  no  longer 
determine  the  number  of  syllables  in  a  word  corresponding  to  some  conceived 
object.  Thus  far  the  author  believes  this  phenomenon  has  been  attributed  only  to 
lesions  in  b  ;  that  is,  to  cortical  motor  aphasia.  However,  if  this  exijlanation  is 
correct,  it  must  also  occur  in  cortical  sensory  and  in  association  aphasia. 

In  determining  the  characteristics  of  an  aphasia,  we  must  inquire  into  written 
speech — i.  e.,  the  ability  to  write  and  to  read — for  this  is  closely  connected  with 
articulate  speech. 

To  explain  the  psychical  mechanism  of  reading  and  writing,  one  cannot  do 
better  than  to  start  again  with  the  development  of  this  function  in  children. 

The  child  learns  to  read  and  write  by  having  the  optical  pictures  imprinted 
upon  a  center  (a.  Fig.  349),  and  by  learning  at  the  same  time  to  associate  with 
them  the  corresponding  auditory  images.  This  association  results  from  the  for- 
mation of  a  tract  (a  a),  in  which  a,  as  in  Fig.  348,  represents  the  sensory  (acoustic) 
speech  center.  By  means  of  such  an  association,  printed  or  written  letters 
acquire  a  certain  significance  to  the  child.  In  learning  to  write,  a  child  forms  an 
association  between  the  optic  center  (a)  and  a  motor  center  (/3),  and  making  use 
of  ;3,  learns  mechanically  to  copy  the  letters.  There  first  occurs  an  impression  of 
sensory  memory  pictures   (here   by  way  of  the  optic),  an  almost  simultaneous 

opinion,  the  only  conclusion  to  be  drawn  from  these  findings  is  that  the  path  am,  which 
in  the  diagram  is  represented  as  subcortical,  in  reality  lies  in  the  cortex  itself — i.  e.,  that 
a  and  x  in  Fig.  3i6,  from  the  gross  anatomic  standpoint,  coincide,  and  that,  from  reasons 
which  will  be  understood  from  what  follows,  the  subcortical  fibers  in  the  cortex  must  be 
injured  themselves  in  order  to  produce  a  sensory  aphasia.  The  separation  of  a  and  x  in 
the  diagram  should  merely  express  the  fact  that  sensory  disturbances  of  speech  and  of 
hearing  are  independent  of  each  other ;  provided  that,  from  the  gross  anatomic  stand- 
point, we  identify  the  left  sensory  speech  center  and  the  left  auditory  center.  This 
is  explained  by  the  fact  that  each  auditory  nerve  is  supplied  by  both  hemispheres 
(p.  8(>5).  As  a  result  of  the  arrangement,  lesions  of  the  left  temporal  lobe  can  be 
nullified,  so  far  as  the  auditory  function  is  concerned,  by  tlie  activity  of  the  right 
temporal  lobe;  and  lesions  of  the  white  substance  of  the  left  temporal"  lobe  need  not 
cause  sensory  aphasia,  because  the  sensory  speech  center  is  united  with  both  auditory 
nerves,  and  the  collective  auditory  stimulation  of  the  sensory  speech  center  cannot 
readily  be  eliminated,  as  would  much  more  probably  be  the  case  if  the  lesion  were  situ- 
ated in  the  left  temporal  cortex  itself  where  bilateral  subcortical  fibers  intermingle. 


894 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


association  of  these  witli  acoustic  memory  pictures,  and  then  a  production  of 
movement  representations  for  writing  the  separate  letters.  Therefore,  we  assume 
that  copying  letters  by  a  child  occurs  by  way  of  the  tract  {^afiv). 

Thus  far  we  have  included  in  the  child's  learning  written  speech  only  the 
mechanical  copying  of  letters.  Very  soon,  however,  he  learns  to  write  letters  when 
merely  their  auditory  images  have  impressed  him,  either  from  dictation  or  from 
resounding  spontaneously  in  his  mind  of  his  own  accord.  To  explain  the  process 
of  writing  letters  voluntarily  or  from  dictation,  we  must  introduce  into  our  dia- 
gram still  another  centrifugal  tract,  which  unites  the  diagram  of  writing  with  that 
of  speaking.  We  have  already  in  the  tract  a  a  (Fig.  349)  a  centripetal  connec- 
tion of  the  writing  mechanism  with  a  sensory  speech  center;  the  line  ba  may 
represent  the  centrifugal  connection  between  the  motor  speech  center  {b)  and  the 
psychical  writing  mechanism.  Wernicke  believes  that  he  has  proved  that  this 
connection  runs  from  b  to  a,  and  not  more  directly  from  b  to  /?.     Writing  letters 


Fig.  349.— Diagram  for  the  mechanism  of  written  speech  :  a,  Center  for  the  optic  representa- 
tion of  written  or  printed  letters;  y,  center  of  optic  perception  (cortical  optic  center);  iJ.y,  optic 
tract:  n,  sensory  speech  center  ;  6,  motor  speech  center  ;  C,  conception  ;  0,  |8',  3",  motor  centers 
for  writing  movements  O  for  writing  with  the  right  hand;  ^'  and  p"  for  writing  with  other 
parts  of  the  body) ;  fiu,  p'v',  ^'v",  motor  tracts  for  writing  movements.  The  numbers  8  to  14  repre- 
sent the  locations  of  lesions  in  the  so-called  isolated  alexias  and  agraphias  (see  p.  897  et  seq.). 
For  simplicity  only,  the  heavy  lines  should  be  noticed  at  first  in  reading  the  text. 

voluntarily  or  from  dictation  takes  place,  then,  in  this  way :  a  is  stimulated  by  the 
auditory  images  of  the  letter  emerging  from  the  mind,  and  excites  in  b  the  repre- 
sentation of  movements  of  the  spoken  letter,  then  the  optical  picture  in  a,  and 
from  there  finally  the  representation  of  movement  of  the  written  letter  in  fi. 
Where  do  we  find  the.  points  a  and  ft  in  the  brain  ?  The  center  a  is  apparently 
to  be  found  in  the  cortical  visual  area  (Fig.  339,  16),  according  to  pathologic 
findings  probably  chiefly  in  the  left  hemisphere  ;  this  seems  quite  comprehen- 
sible, if  we  take  into  consideration  the  connection  between  written  speech  and 
spoken  speech.  The  point  /3  has  oftentimes  been  supposed  to  exist  as  an  actual 
writing  center;  and  Charcot  located  it  in  the  frontal  lobes,  near  the  middle  of  the 
anterior  central  convolution  (see  Fig.  439,  8).  Simple  reflection  shows  that  such 
an  individual  writing  center  does  not  exist.  The  movement  of  writing  is,  as  a 
matter  of  fact,  like  any  other  movement,  in  case  the  form  of  the  letter  is  known; 
one  can  write  it  with  any  part  of  the  body — for  example,  the  nose  or  the  foot. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


895 


We  can  go  even  so  far  as  to  place  the  supposed  writing  center  in  the  brain  of  the 
horse  when  we  describe  the  form  of  a  letter  by  riding.  As  a  matter  of  fact,  we 
write  by  copying  approximately  the  optical  memory  pictures  of  letters,  using  any 
sort  of  movements.  Ordinarily,  ^  represents  the  cortical  center  of  the  right 
hand;  it  could,  however,  just  as  well  represent  another  motor  center.  The 
dotted  tracts  afVv',  aiy^v'\  etc.  (Fig.  349),  are  intended  to  express  this  multiplic- 
ity. Including  only  the  essentials  of  Figs.  348  and  349,  a  diagram  of  the  cen- 
tral speech  mechanism,  including  reading  and  writing,  may  be  represented  as  in 
Fig.  350. 

The  following  explanation  should  be  added  to  explain  reading  and  writing 
entire  words.  Experience  teaches  that  written  speech  is  always  disordered  in 
aphasias  if  there  is  an  injury  anywhere  upon  the  line  ab,  whether  it  be  at  a  or 
at  b,  or  between  the  two;  for,  as  mentioned  upon  p.  893,  a  and  b  seem  like  a 
unity,  which  Wernicke  has  designated  as  the  "substratum  of  the  word  concep- 
tion." Now,  it  is  ordinarily  assumed  that  the  word  conception  is  produced  from 
separate  letters,  that  the  tract  aab  is  traveled  by  each  letter,  and  that  in  writing 
entire  words  the  conception  will  be  dis- 
sected, so  that  an  innervation  impulse  pro- 
ceeds from  b  to  a  for  each  letter.  Broad- 
bent  and  Wernicke  believe  that  they  have 
proven  beyond  question  the  correctness  of 
this  assumption  that  reading  and  writing 
are  always  accomplished  letter  by  letter, 
but  the  point  is  closely  contested.  In  this 
connection  these  authors'  original  articles 
should  be  consulted.  We  need  add  only 
that  the  great  speed  with  which  a  practised 
person  runs  over  the  words  in  reading,  and 
the  rapid  writing  of  people  who  write  a  good 
deal,  argue  in  these  cases  against  writing 
and  reading  letter  by  letter. 

Even  if  the  beginner  and  the  unskilled, 
as  is  well  known,  always  read  by  letters, 
it  is  conceivable  and  perhaps  probable 
that  there  may  be  certain  men  in  \vhose 
daily  routine  writing  and  reading  play  a 
large  part  and  whose  brains  are  therefore 
so  especially  accustomed  to  these  pro- 
cesses that  they  no  longer  read  and 
write  by  letters,  but  perceive  the  optical 
writing  conceive   it  so. 


Fig.  350.— Diagram  of  all  the  central 
speech  apparatus  including  reading  and 
writing.  The  letters  and  figures  have  the 
same  meaning  as  in  the  two  preceding 
illustrations. 


word  picture  as  a  w^hole,  and  in 
Illegible  handwriting  in  which  individual  letters  can 
scarcely  be  recognized  is  possibly  always  read  in  this  fashion  of  grasping  the 
word  as  a  whole.  This  coincides  with  the  experience  that  the  illegible  hand- 
writing of  people  who  are  unaccustomed  to  write  and  who  therefore  write  and 
read  by  letters,  is  much  more  difficult  to  decipher  than  the  illegible  handwriting 
of  those  who  write  without  plain  individual  letters — i.  e.,  to  a  certain  extent  in 
hieroglyi^hics.  Wherever  writing  and  reading  no  longer  have  to  do  with  letters 
but  with  hieroglyphics,  the  centi'al  mechanism  for  Avriting  and  reading  in  the  brain 
naturally  becomes  to  a  certain  degree  independent.  The  center  a,  then,  instead  of 
being  an  optical  center  for  letters,  becomes  really  an  optical  center  for  words.  It  is 
conceivable  that,  as  it  is  developed  and  becomes  self-dependent,  the  centers  a  and  b, 
as  well  as  the  a.ssociation  tracts  {aa)  and  {ba),  become  less  necessary  for  writing 
and  reading,  and  the  word  center  («)  is  associated  more  and  more  directly  with 
the  conception  {C).  Quick  writing  is,  therefore,  very  much  facilitated.  But  this 
self-dependence  of  the  writing  apparatus  never  becomes  complete,  and  even  when 
at  a  not  only  letters  but  entire  optical  word  pictures  are  stored,  still  in  writing 
and  i-eading  the  territory  aab  continues  to  be  very  important.  This  is  proved  by 
the  fact  that  the  aphasias  1,  4,  and  7  always  produce  a  decided  disturbance  of 
writing  and  reading.     It  does  not  seem  absolutely  essential  that  the  territory  ab, 


896  EXAMINATION  OF  THE  NERVOUS  SYSTE3I. 

accredited  by  Wernicke  with  being  the  anatomic  substratum  of  the  word  concept, 
should  be  limited  to  rendering  spelling  possible;  but  we  can  imagine  that  to  a 
man  who  has  gradually  abandoned  spelling  in  reading  and  writing,  and  who 
merely  make  suse  of  entire  words,  the  centers  a  and  b  and  then-  connecting  tract 
are,  nevertheless,  essential  for  centripetal  as  well  as  for  centrifugal  impressions  of 
the  optical  word  picture.  With  this  conception,  it  is  clear  that  written  speech 
will  always  be  very  decidedly  affected  with  the  aphasias  situated  at  1,  4,  or  7. 
The  greater  or  less  development  of  independence  of  the  optical  word  center  should 
easily  explain  the  variations  in  the  grade  of  writing  and  reading  disturbances  in 
aphasias. 

After  what  has  been  said,  it  is  plain  that  written  speech  (including  both  the 
reading  and  writing  of  words)  will  always  be  affected  if  the  word  concept  (a  and 
b)  is  injured  in  any  way — that  is,  if  the  lesion  is  situated  at  a,  at  b,  or  between  a 
and  b.  This  applies,  on  the  one  hand,  just  as  much  to  reading  aloud  as  to  the 
comprehension  of  written  sjjeech  ;  and,  on  the  other  hand,  just  as  much  to  spon- 
taneous writing  as  to  writing  from  dictation.  An  interference  in  mechanical 
copying,  in  which  one  letter  is  pictured  after  the  other,  always  depends  upon  a 
lesion  in  the  territory  of  the  Avriting  arc  {fiajii).  It  is  worthy  of  note  that, 
because  a  lesion  between  a  and  b  destroys  the  word  concept,  it  makes  writing 
quite  impossible,  or  occasions  a  very  marked  defect  in  it,  but  never  leads  to  para- 
graphia. The  latter  is  analogous  to  paraphasia,  and  produces  only  a  confusion 
of  words  in  writing.  Paragraphia  occurs  only  in  transcortical  sensory  aphasia 
(see  below). 

The  effects  of  the  different  kinds  of  aphasias  on  written  speech  (see  p.  892)  are 
as  follows  :  ^ 

1.  Cortical  Sensory  Aphasia.  Lost:  voluntary  writing  to  dictation,  compre- 
hension of  writing,  reading  aloud.      Eetained  :  mechanical  copying. 

2.  Subcortical  Sensory  Ajihasia^.    Written  sj^eech  is  quite  unaffected. 

3.  Transcortical  Sensory  Aphasia.  Lost :  comprehension  of  writing.  Re- 
tained :  reading  aloud  without  comj^rehension,  and  writing  in  all  its  forms.  Para- 
graphia is,  however,  present  in  sjjontaneous  writing — i.  e.,  the  words  are  confused, 
just  as  in  speaking. 

4.  Cortical  Motor  Aphasia.  Lost  :  all  forms  of  writing  and  reading,  with  the 
single  exception  of  mechanical  copying. 

5.  Subcortical  Motor  Aphasia.  Lost :  reading  aloud.  Eetained  :  writing  in 
all  its  forms,  and  the  comprehension  of  writing. 

6.  Transcortical  Motor  Aphasia.  Lost  :  spontaneous  writing.  Eetained  : 
writing  to  dictation,  copying,  reading  aloud,  and  the  comprehension  of  writing. 

7.  Conduction  or  Association  Aphasia.  Lost :  all  kinds  of  reading  and  of 
writing,  wath  the  exception  of  mechanical  copying. 

In  these  disturbances  dependent  upon  aphasias,  the  writing  and  reading  of 
individual  letters  is  generally  quite  the  same  as  the  writing  and  reading  of  entire 
words.  All  aphasias  cannot  be  tabulated  under  one  of  the  above  divisions,  for 
reasons  which  will  follow. 

Besides  disturbances  in  writing  and  reading  dependent  upon  aphasias,  there 
may  also  occur  disturbances  of  written  speech  which  are  independent  of  the 
aphasias.  This  will  be  the  case  when  a  lesion  occurs  in  the  lower  part  of  the 
diagram  (Fig.  350) — i.  e. ,  in  the  writing  arc  and  in  its  connections  with  the  cen- 
tral speech  api^aratus. 

These  disturbances,  as  contrasted  with  those  depending  upon  aphasias,  may 
be  termed  isolated  alexias  and  ar/raphias.  According  to  the  diagram  seven  such 
disturbances  are  possible,  for  which  a  similar  terminology  may  be  employed  as  for 
the  aphasias  (Fig.  350). '^ 

8.  Subcortical  alexia  (injury  between  «  and  a).  Eeading  of  letters  and  words 
impossible  ;  writing  of  letters  and  words,  with  the  exception  of  copying,  possible. 

'  The  numbers  correspond  to  those  in  Fig.  350  (see  p.  891). 

'^  In  regard  to  the  actual  anatomic  localization  of  the  lesion,  see  p.  892,  note. 

^  The  numbers  correspond  to  those  in  Fig.  350. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  897 

9.  Subcortical  agraphia  (injury  between  /?  and  v).  Reading  of  letters  and 
words  retained,  but  words  can  neither  be  written  nor  copied.  (See  below  for  the 
significance  of  this  form.) 

10.  Cortical  alexia  (injury  at  a).  Letters  and  words  can  neither  be  written 
nor  read,  and  even  copying  is  impossble. 

11.  Cortical  agraphia  (injury  at  ft).  Letters  and  words  can  be  read  but  not 
written  nor  copied  (as  in  9).      (See  below  for  the  significance  of  this  form.) 

12.  Conduction  or  association  agrapihia  (injuiy  between  a  and  ft).  Letters  and 
words  can  be  read  but  not  written  nor  coi^ied  (again  as  in  9  and  11).    (See  below.) 

13.  Transcortical  alcvia  (injuiy  between  a  and  a).  Reading  of  letters  and 
words  impossible.     Writing  of  letters  and  words,  including  copying,  possible. 

14.  Transcortical  agraphia  (injuiy  between  b  and  a).  Reading  of  letters  and 
words  possible.  Writing  of  letters  and  words,  except  mechanical  copying,  impossible. 

In  the  narrow  sense  of  the  word,  lesions  9  and  11  do  not  actually  come  under 
the  head  of  the  agraphias,  because  the  agraphias  here  depend  only  upon  a  paralysis 
of  the  arm. 

Therefore  only  lesions  12  and  14  are  to  be  considered  as  isolated,  pure  agraphias, 
and  they  can  be  distinguished  one  from  the  other  by  the  retention  of  the  power 
of  copying  in  14,  and  its  loss  in  12. 

The  three  alexias,  8,  10,  and  13,  can  be  differentiated  one  from  the  other  by 
the  fact  that  in  13,  as  opposed  to  8  and  10,  copying  is  retained,  and  that  in  8,  as 
opposed  to  10,  spontaneous  writing  is  retained. 

Form  13,  which  we  have  called  transcortical  alexia,  is  the  only  well-known 
form  of  isolated  alexia.  It  is  also  called  word-blindness.  The  characteristic 
localization  of  the  lesion  in  these  cases  is  in  the  gyrus  angularis  (pli  courbe). 
There  is  evidently  an  interruption  in  the  association  between  the  optical  pictures 
of  written  characters  stored  in  the  occipital  lobe  and  the  sensory  speech  center  in  the 
temporal  lobe.  The  term  transcortical  or,  better,  transcentral  (in  the  sense  indi- 
cated upon  p.  891),  is  consequently  justified. 

The  forms  of  isolated  alexias  and  agraphias,  considered  here  theoretically, 
have  thus  far  rarely  been  observed  as  pure  cases,  but  much  more  frequently  there 
occur  mixed  forms  arising  from  diffuse  injuries  to  the  cortical  mechanism  of 
speech  writing  or  from  the  general  injury  of  two  or  even  more  of  the  opposite 
convergent  tracts  in  the  neighborhood  of  the  decussation  angle.  For  this  reason, 
and  on  account  of  incomplete  interruptions  of  conduction,  a  local  diagnosis  of 
alexia  and  agraphia  disturbances  often  becomes  very  difficult  or  even  impossible. 

It  should  also  be  noted  that  the  significance  of  individual  cases  is  often  made 
very  ditficult  in  aphasias  also  by  the  occurrence  of  such  mixed  forms  from  lesions 
of  the  converging  tracts,  as  well  as  by  the  occurrence  of  incomplete  lesions  of 
individual  tracts  and  centers  and  of  diffuse  lesions.  Hence,  every  case  of  aphasia 
cannot  be  tabulated  under  one  or  the  other  of  the  above  types  ;  at  all  events,  not 
without  much  difficulty.  There  is  still  another  reason  why,  practically,  aphasias 
are  often  more  difficult  to  explain  than  one  would  judge  from  our  simple  diagram. 
For  in  addition  to  the  above-described  type,  where  the  disturbances  depend  upon 
injuries  to  tracts  and  destruction  of  centers,  there  is  still  another  group  of  aphasias 
in  which  the  difficulty  is  merely  functional  in  nature  and  the  tracts  and  centers  in 
question  are  not  actually  destroyed  or  even  injured.  Such  aphasias  depend  upon 
a  very  difficult  or  an  imperfect  innervation  of  the  center  and  tracts  upon  the  part 
of  the  patient.  From  the  nature  of  the  trouble,  the  clinical  picture  not  only 
varies  so  conspicuously  as  to  make  a  local  diagnosis  difficult,  but  also  presents 
many  other  peculiarities.  Under  this  head  come  the  aphasias  which  are  attrib- 
uted to  a  disturbance  of  the  memory,  as  the  following  case  of  Grashey  will  illus- 
trate. This  patient  could  give  the  name  to  an  object  held  in  front  of  him  only 
so  long  as  he  was  looking  at  it,  and  even  then  only  while  he  was  Avriting  down 
its  name  and  thus  aiding  his  memory.  These  aphasias  from  disturbances  of 
memory  have  been  considered  fundamentally  different  from  the  other  aphasias, 
but  the  author  cannot  agree  with  this  view.  For  what  do  we  actually  understand 
by  a  disturbance  of  memory?  Apparently,  on  the  one  hand,  only  a  difficulty  in 
voluntarily  recalling  certain  latent  memory  pictures — i.  e.,  a  difficulty  in  associa- 
57 


898  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

tions — and,  on  the  otlier  hand,  an  abnormally  rapid  loss  of  representations  soon 
after  their  origin.  Between  these  conditions  and  a  complete  destruction  of  the 
association  fibers  or  of  the  representation  centers  there  is  only  a  diiference  in 
degree.  Such  destructions  depend  upon  appreciable  anatomic  lesions,  while  dis- 
turbances in  memorj'  are  to  be  attributed  only  to  slight  functional  damage  to  the 
same  centers  and  tracts. 

By  sticking  to  this  definition  of  disturbances  of  memory,  we  can  term  these 
functional  aphasias  memory  aphasias  (in  Grashey's  sense),  in  contrast  to  aphasias 
from  destructive  lesions.  But  the  former  include  not  only  Grashey's  and  similar 
cases,  but,  as  will  be  easily  understood,  most  of  the  transcortical  and  especially 
the  complete  transcortical  aphasias.  In  a  complete  transcortical  motor  aphasia, 
which  is  the  direct  consequence  of  a  gross  anatomic  lesion,  all  tracts  which  lead 
from  b  in  Fig.  347  to  the  partial  representations  of  the  idea  must  be  interrupted. 
But  since  these  partial  representations  of  the  idea  are  spread  out  in  the  entire 
cortex,  we  must  assume  that  the  fibers  be,  b&',  bcf' ",  etc.,  in  reality  extend  in 
all  directions  from  the  motor  speech  center.  A  complete  interruption  of  conduc- 
tion of  these  collected  tracts  could  then  be  imagined  only  if  the  center  b  were 
to  a  certain  extent  isolated,  as  by  a  ring-shaped  lesion.  However,  in  assuming  a 
gross  anatomic  lesion,  it  is  quite  impossible  that  the  center  h  could  itself  remain 
intact,  so  that  symptoms  of  a  cortical  instead  of  a  transcortical  aphasia  must 
result.  It  is,  therefore,  evident  that  complete  transcortical  motor  aphasia  and,  for 
similar  reasons,  even  a  transcortical  sensory  aphasia  cannot  arise  trom  direct  gross 
anatomic  destruction  of  all  the  transcortical  tracts.  A  complete  anatomic  destruc- 
tion of  the  latter  is  absolutely  impossible  -svithout  a  lesion  of  the  center  b  or  of 
the  centre  a}  But  from  what  has  been  said,  it  is  easy  to  understand  that  these 
transcortical  disturbances  may  result  from  those  functional  lesions  defined  above 
as  disturbances  of  memory. 

Such  a  functional  disturbance  may,  of  course,  be  diffused  not  only  to  the 
tracts  of  the  speech  mechanism,  but  also  over  the  entire  brain.  In  the  former 
case  merely  a  memory  disturbance  of  speech  will  result ;  in  the  latter,  a  general 
mental  weakness. 

Most  of  the  disturbances  of  speech  called  indefiniie  or  diffuse  aphasias,  as  con- 
trasted with  the  definite,  accompany  functional  lesions.  They  include  aphasias 
which  can  be  explained,  not  by  a  lesion  at  definite  places  in  the  scheme,  but  only 
by  the  assumption  of  a  disturbance  diffused  over  the  territory  of  the  speech 
apparatus.  Such  aphasias  usually  present  an  exceptionally  variable  character, 
and  so  cannot  be  attributed  to  the  direct  action  of  gross  anatomic  disturbances. 

It  should,  however,  be  noted  that  in  designating  certain  aphasic  disturbances 
as  functional,  we  do  not  mean  that  they  cannot  occur  from  the  remote  action  of 
gross  anatomic  lesions.  On  the  contrary,  indefinite  and  transcortical  aphasias, 
which,  according  to  the  above  definition,  must  be  considered  as  functional,  gener- 
ally exhibit  lesions  in  the  neighborhood  of  the  speech  centers.  There  is  no 
actual  destruction  of  brain  substance  in  a  gross  mechanical  sense,  but  the  lesion 
indirectly  causes  a  functional  disturbance  of  the  speech  apparatus  from  remote 
action,  or  reaction  at  a  distance.  This  remote  action,  playing  so  important  a  part 
in  other  parts  of  the  cerebral  pathology,  is,  as  is  well  known,  to  be  attributed 
partly  to  the  results  of  circulatory  disturbances,  partly  to  inhibition. 

Although  most  transcortical  aphasias  can  thus  be  considered  as  functional, 
or,  in  the  sense  above,  as  of  an  amnesic  nature  (arising  from  weakness  of  memory 
or  of  association),  such  a  grouping  does  not  necessarily  include  those  transcortical 
aphasias  in  which  not  all  the  transcortical  tracts  uniting  the  conceptual  part  of 
the  brain  with  the  speech  center,  but  merely  a  certain  number  of  transcortical 
tracts  of  separate  ftinction,  are  affected.  To  this  class  belong  Freund's  so-called 
optic  aphasias,  in  which  the  patient  cannot  name  objects  after  he  has  received 
their  optical  impression.  Here  we  must  assume  an  isolated  lesion  of  the  fibers 
running  fi-om  the  visual  center  to  the  motor  speech  centre.     Such  a  lesion  may 

^  As  we  shall  see  below,  it  must  be  acknowledged  that  transcortical  aphasias  may 
arise  indirectly  from  gross  anatomic  lesions  by  so-called  remote  action. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  899 

be  anatomic  as  well  as  functional.  Acoustic  and  tactile  aphasias  are  analogously- 
explained. 

Finally,  it  may  be  mentioned  that  in  aphasia  the  numbers  are  eflfected  like 
other  words  only  when  they  are  spoken,  not  written.  Numbers  expressed  in 
figures  occupy  a  peculiar  place  in  written  speech,  because  no  real  word  concept 
of  them  occurs  either  in  writing  or  reading.  The  figure  is  a  direct  symbol  of  the 
notion  of  counting  ;  to  a  certain  extent,  a  hieroglyphic.  Its  optical  representa- 
tion probably  may  be  considered  as  directly  associated  with  the  conception 
(Fig.  350).  Hence,  even  when  the  word  concept  in  aphasia  is  destroyed,  the 
patient  can  write  figures  quite  well  and  can  understand  written  figures. 

For  the  explanation  of  anarthria  as  a  result  of  incomplete  aphasia — i.  e.,  of 
incomplete  lesions  of  the  central  speech  apparatus — p.  888  et  seq.  may  be  con- 
sulted. In  another  type  of  incomplete  aphasia  the  difficulty  is  limited  to  certain 
definite  words.  These  are  forms  in  which  ordinarily  no  definite  location  in  the 
speech  mechanism  is  possible,  and  which  usually  come  under  the  head  of  the 
functional  or  diffuse  disturbances  (p.  898). 

(c)  Other  Speech  Disturbances  from  Paralytic  Phenomena. 

Anarthria  and  aphasia  are  the  best  known  and  the  best  studied  of  the  disturb- 
ances of  speech  resulting  from  paralytic  phenomena.  There  are,  however,  a 
number  of  other  speech  disturbances  to  be  regarded  as  paralytic  phenomena  which 
are  not  yet  exactly  explained  and,  in  fact,  cannot  be  definitely  localized. 

The  disturbance  of  speech  in  progressive  paralysis  which  is  characterized  by 
syllable- stumbling  belongs  to  this  class.  From  its  peculiarities  it  belongs  rather 
to  the  anarthrias  than  to  the  aphasias,  and  is  ordinarily  so  classed ;  but  it  is  ques- 
tionable whether  such  a  classification  is  correct.  The  well-known  anatomic 
localization  of  j^rogressive  paralysis  in  the  cerebral  cortex  makes  it  most  probable 
that  the  speech  disturbance  is  also  cortical.  Such  a  conception  of  its  origin  would 
suggest  a  closer  relation  to  the  aphasias,  despite  its  external  resemblance  to  the 
anarthrias.  As  a  matter  of  fact,  such  a  disturbance  of  speech  may  perfectly  well 
be  conceived  to  arise  from  minute  lesions  in  the  area  of  the  speech  center,  by 
which  speech  co-ordination  is  destroyed,  although  a  complete  paralysis  of  the 
center  does  not  result.  Perhaps  the  disturbances  of  speech  in  intoxicated  persons 
may  be  similarly  explained.  Without  doubt  the  hysteric  speech  disturbances — 
hysteric  aphonia  (improperly  called  hysteric  vocal-cord  paralysis)  and  hysteric 
mutism — should  be  localized  in  the  cortex,  and,  therefore,  despite  clinical  differ- 
ences, are  closely  related  to  aphasia.  Congenital  dumbness  is  nothing  more  than 
motor  aphasia,  and  deaf-mutism  is  sensory  aphasia  plus  motor  aphasia  plus  deaf- 
ness. The  monotonous  and  imperfect  speech  which  deaf-mutes  can  be  taught  may 
be  considered  as  a  form  of  speech  arising,  with  sensory  aphasia,  by  arduous  and 
unusual  paths,  in  which,  instead  of  the  entire  word  concept  a  -{-  b,  there  is  only 
available  a  motor  word  representation.  The  diflferent  disturbances  of  speech  of 
those  who  are  seriously  ill  (the  vibrating,  tremulous,  slowed,  and  abnormally  faint 
speech)  have  not  as  yet  been  definitely  localized.  They  may  be  central  as  well 
as  peripheral.  The  characteristic  scanning  speech  of  multiple  sclerosis  and  the 
speech  defect  of  Friedreich' s  ataxia  do  not  yet  possess  a  definite  significance. 
The  former,  perhaps,  may  be  regarded  as  a  sort  of  spastic  gait  of  the  speech. 
As  a  result  of  the  increased  muscle  and  tendon  refiexes,  which  may  frequently  be 
demonstrated  in  the  muscles  of  speech  in  this  disease  (jaw-clonus,  etc.),  the 
speech  movements  are  mechanically  hindered  by  the  occurrence  of  spasms  of  the 
muscles,  which  the  patient  instinctively  tries  to  overcome  by  slowing  his  speech 
and  accentuating  its  movements.  The  monotone  and  the  lack  of  the  ability  to 
modulate  the  voice  may  also  be  explained  by  such  spastic  phenomena.  Ordi- 
narily the  speech  does  not  become  tremulous,  as  do  the  other  spastic  movements, 
although  a  tremor  may  sometimes  be  observed  as  a  result  of  quivering  contrac- 
tions of  the  vocal  cords.  This  is  probably  due  to  the  fact  that  the  muscles  of 
speech  run  in  all  the  directions  of  space,  and  that  tremors  can  be  produced  only 


900  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

by  the  alternate  activity  of  antagonistic  muscles,  tlie  lines  of  whose  action  are 
situated  in  the  same  plane. 

3.  AFFECTIONS  OF  SPEECH  FROM  IRRITATION  PHENOMENA, 

These  irritation  or  spasmodic  phenomena  in  the  territory  of  the  speech  appa- 
ratus are  considered  as  exceptional,  and  have  been  much  less  studied  than  the 
speech  disturbances  thus  far  described. 

They  include  the  commonest  varieties  of  stuttering  (labiochorea  and  guttural 
tetanic  stuttering),  which  names  characterize  them  sufficiently.  They  also 
include  the  affections  of  speech  in  chorea.  It  is  not  yet  clear  how  these  disturb- 
ances arise,  nor  is  it  known  from  what  point  the  impulses  spring,  although  they 
probably  have  a  cortical  localization.  For,  as  the  speech  muscles  are  not  utilized 
exclusively  for  speech  and  are  not  innervated  exclusively  by  the  speech  center,  it 
is  easy  to  understand  that  choreic  movements  of  the  speech  muscles  might  arise 
from  other  parts  of  the  cortex  and  still  affect  the  speech. 

4.  PLAN  FOR  TESTING  THE  FUNCTIONS  OF  SPEECH. 

The  following  procedure  for  examining  patients  with  speech  disturbances  has 
been  devised  from  what  has  been  said  above  : 

1,  Disturbances  of  pronunciation  of  letters  and  then  of  simpler  and  more 
complicated  words.  Anarthritic  disturbances  of  bulbar  paralysis;  speech  disturb- 
ances of  progressive  paralysis ;  of  multiple  sclerosis ;  stuttering,  etc.  For  the 
differential  diagnosis  between  pure  anarthria  and  what  is  called  on  p.  889  "  central 
anarthria,"  it  must  be  noticed  whether  disturbances  other  than  those  of  speech 
(swallowing,  masticating)  occur  in  the  region  of  the  speech  muscles. 

2.  In  the  actual  aphasic  disturbances  the  following  functions  should  always 
be  examined 

(a)  Test  foe  Words. 

1.  Voluntary  speech 

2.  Repetition. 

3.  Eeading  aloud. 

4.  Voluntary  writing  (figures  to  be  tested  especially). 

5.  Writing  from  dictation  (figures  to  be  tested  especially) 

6.  Copying. 

7.  Speech  comprehension. 

8.  Script  comprehension  (figures  to  be  tested  especially). 

9.  Counting  syllables  (see  p.  893  ef.  seq.). 

One  should  note  whether  paraphasic  disturbances — that  is,  confusion  of  words 
— occur  in  speaking  or  writing. 

{b)  Test  for  Letters 

1.  Speaking  the  letters  of  the  alphabet  spontaneously  with  special  attention 
to  the  quality  of  the  pronunciation. 

2.  Repetition  of  letters. 

3.  Reading  letters  aloud. 

4.  Writing  the  alphabet  spontaneously. 

5.  Writing  letters  from  dictation. 

6.  Copying  letters. 

7.  Recognition  of  spoken  letters — i.  e.,  association  of  the  letters  pronounced 
with  the  pictures  of  letters  (picking  out  the  corresponding  printed  letters). 

8.  Recognition  of  written  letters — i.  e.,  association  of  the  letter  pictures  with 
the  spoken  letters  (where  the  letters  cannot  be  named,  suggestive  questions  should 
be  used  in  the  test). 

Since  paralysis  of  the  right  arm  is  very  commonly  associated  with  aphasia, 
the  patient's  ability  to  write  with  the  left  hand  should  be  tested  (many  aphasias 
produce  mirror-writing).     If   the  patient  cannot  write  with  the  left  hand,  he 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  901 

should  attempt  to  construct  the  words  with  letters  such  as  are  used  in  the  ordi- 
nary game  of  anagrams. 

If  every  case  of  aphasia  is  examined  according  to  this  plan,  it  is  easy  either 
to  localize  the  aphasia  at  one  or  more  definite  points  of  the  speech  mechanism, 
or  to  determine  that  it  is  caused  by  an  indefinite — i.  e. ,  a  functional  or  diifuse — 
injury  of  the  speech  mechanism. 

Vn.   DISTURBANCES  RELATED  TO  APHASIA:  ASYMBOLIA;  AMIMIA; 
APRAXIA;  AMUSIA;  PSYCHIC  DEAFNESS;  PSYCHIC  BLINDNESS. 

Asymbolia  is  a  condition  of  the  mind  in  which  the  ability  to  make  one's  self 
understood  by  signs  and  gestures  (as  well  as  by  speech)  is  impaired  or  lost.  A  dif- 
ferentiation may  be  made  between  active  or  motor  and  passive  or  sensory  asymbolia, 
dependent  upon  whether  pantomimic  speech  or  the  ability  to  understand  it  is 
afiected. 

Amimia  is  a  disturbance  or  loss  of  the  power  of  imitation,  whether  it  be 
simply  the  mimicry  associated  with  speech  or  the  mimicry  expressing  psychic 
processes. 

Apraxia  is  the  inability  to  employ  objects  in  the  proper  way,  the  patient  taking 
a  spoon  or  fork  in  his  hand,  for  example,  and  being  unable  to  use  it  correctly. 

The  disturbances  just  described  are  also  characterized  by  the  fact  that  they 
are  not  associated  with  actual  motor  paralysis — i.  e. ,  with  motor  disturbances  of 
the  affected  muscles  for  other  muscular  functions.  The  intimate  relation  between 
the  functions  above  mentioned  and  the  function  of  speech  sufficiently  explains  the 
fact  that  these  disturbances  are  found  almost  exclusively  with  aphasias,  and  that 
their  localization  is  practically  the  same  as  that  of  aphasia. 

The  loss  of  the  ability  to  produce  or  comprehend  music  or  musical  sounds  has 
laeen  designated  as  amusia.  From  the  definition,  it  will  be  seen  that  amusia 
may  be  either  motor  or  sensory.  Motor  amusia  is  related  to  motor  aphasia;  it 
lias  a  similar  localization  and  is  sometimes  associated  with  it.  Sensory  amusia  is 
related  to  sensory  aphasia,  with  which  it  is  not  infrequently  combined.  Its 
presence  is  indicative  of  a  lesion  in  the  left  temporal  lobe.  A  special  form  of 
amusia,  the  loss  of  the  ability  to  recognize  the  musical  significance  of  notes  or  to 
sing  or  play  from  notes,  has  been  designated  as  ' '  note-blindness, ' '  and  another 
form,  in  which  the  power  to  comprehend  music  has  been  abolished,  has  been 
rather  inappropriately  called  ' '  tone-deafness. " 

Psychic  deafness  is  a  condition  in  which  not  only  words,  but  all  sounds, 
though  heard  and  perceived  as  such,  awaken  no  intelligent  conception.  This 
disturbance  evidently  includes  sensory  aphasia,  and  the  relationship  of  the  two 
conditions  is  shown  by  the  fact  that  sensory  aphasia  or  word -deafness  is  some- 
times combined  with  psychic  deafness  or  passes  into  the  latter  condition. 

Psychic  blindness  requires  a  more  detailed  description.  By  this  term  is 
meant  that  peculiar  condition  in  which  objects  are  seen  but  not  recognized.  In 
other  words,  in  spite  of  maintained  optic  perception,  the  association  of  optic 
impressions  is  no  longer  possible.  It  holds  the  same  relation  to  blindness  as  does 
psychic  deafness  to  deafness.  Psychic  blindness  can  be  produced  only  by  a 
lesion  in  the  transcortical  tracts  of  the  visual  apparatus — i.  e.,  by  a  lesion  in  the 
association  fibers  of  the  visual  center  (see  p.  891) — and  is  associated  with  lesions 
in  the  occipital  lobes. 

As  the  retinal  impression  of  one  eye,  on  account  of  the  semidecussation  of 
the  optic  nerve,  affects  both  hemispheres,  it  is  probable  that  the  visual  representa- 
tions, upon  whose  associations  with  other  representations  depends  the  recognition 
of  objects,  are,  unlike  speech  or  word  representation,  localized  in  both  hemispheres. 
This  will  explain  the  fact  that  psychic  blindness  is  never  observed  in  a  unilateral 
lesion  of  the  brain.  If  one  hemisphere  is  completely  preserved,  visual  perception 
and  representation  are  not  only  pictured  but  also  associated.  The  following 
figure  explains  diagrammatically  the  occurrence  of  psychic  blindness  from  bilat- 
eral lesions  of  the  occipital  brain.     It  is  supposed  to  represent  a  horizontal  section 


902 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


of  the  brain:  a  the  left,  b  the  right  retina  ;  c  the  left,  d  the  right  visual  center  ; 
ad  and  bd  the  fibers  of  the  right,  ac  and  be  those  of  the  left  optical  tract ;  ec 
and  fd  represent  diagrammatically  examples  of  association  fibers  between  the 
optic  centers  and  other  parts  of  the  brain  upon  the  same  side.  These  are,  of 
course,  not  single,  but  run  in  countless  directions  to  all  regions  of  the  cortex  not 
associated  with  vision.  Now,  according  to  the  above,  psychic  blindness  may 
arise  from  lesions  of  the  bilateral  association  tracts  (ec  and  fd) — for  example, 
from  lesions  g  and  h  ;  but  it  is  highly  improbable  that  in  both  posterior  lobes- 
only  the  association  tracts  should  be  affected  in  this  way.  As  a  matter  of  fact, 
heretofore  it  has  been  found  that  the  fibers  of  the  optic  tract  or  even  the  visual 
center  itself  are  injured  coincidently  with  the  association  tracts  upon  the  one 
side  by  a  large  lesion  like  i ;  whereas  upon  the  other  side  a  smaller  lesion  (A)  may 
affect  only  the  association  tracts  and  not  include  the  visual  tracts  or  even  the 
visual  center. 

A  patient  with  such  a  bilateral  lesion  (/  and  h)  presents  clinically  homonymous 


Cliiasma. 

---  Nucleus  caudalus. 
-  Nucleus  lenticularis. 
-  Thalamus  opticus. 


■Ftg  S51  -Diaeram  to  explain  the  simultaneous  occurrence  of  psychic  blindness  and  hemi- 
opia'^^Sm  a  bi^KuedonlS  the  occipital  lobe.    Horizontal  cross-se^^^^^^^^ 

6  right  retina;  c,  left  sight  center;  d,  right  sight  center  (see  Fig.  od9j  ;  ad  and  ba,  noert,  oi  me 
right ;  ac  and  &c,  fibers  of  the  left  optic  tract ;  g,  h,  and  i,  lesions. 

hemianopsia— i.  e.,  he  is  absolutely  blind  to  objects  whose  pictures  fall  upon  the 
left  retina.  He  perceives  objects  with  the  right  retinal  half,  but  he  cannot  recog- 
nize them,  because  the  association  of  the  right  visual  center  with  the  remainder 
of  the  brain  is  interrupted.  It  need  scarcely  be  emphasized  that  all  the  associa- 
tions of  optical  representations  need  not  be  destroyed  m  every  case  ot  ps>  chic 
blindness,  but  that  in  many  cases  only  certain  of  them  fail,  while  others  are 
retained.  Thus,  it  is  conceivable  that  a  patient  can  associate  the  optical  repre- 
sentation of  a  rose  with  the  word  representation  of  a  rose,  but  not  with  the 
representation  of  the  smell  of  the  rose.  Such  examples  of  partial  psychic  blind- 
ness are  undoubtedlv  not  so  verv  rare  in  the  psychoses.  But  we  ordinarily  speak  ot 
psychic  blindness  in  the  narrow  sense  of  the  word,  or  of  a  total  psychicjjlmdness 
only  when  so  many  associations  of  the  optical  representations  are  affected  that 
the  conception  of  the  latter  (see  p.  890  et  seq.)  can  no  longer  be  elicited— i.  e 
the  object  can  no  longer  be  recognized.  An  interference  with  the  association  ot 
the  optical  representation  with  the  speech  mechanism,  which  is  a  kind  ot  partial 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  903 

psychic  blindness,  has  been  studied  as  a  partial  transcortical  aphasia  upon  p.  898, 
under  the  title  of  Optic  Aphasia. 

Complete  psychic  blindness  frequently  presents  the  clinical  picture  of  mental 
confusion  or  insanity.  Patients  do  not  recognize  objects  at  all,  and  name  them  in 
a  most  jjeculiar  fashion.  In  certain  characteristics  they  may  behave  like  the 
blind,  stumbling,  for  example,  over  objects  which  they  may  jaerhaps  see  but  do 
not  recognize.  The  condition  is,  therefore,  often  not  very  easy  to  diagnose,  and  in 
examining  such  a  case  the  following  plan  may  be  adopted  : 

1.  Examination  of  the  perception  in  order  to  differentiate  from  a  simple  visual 
disturbance  or  from  blindness.  To  be  tested  are  :  refraction,  visual  field  (deter- 
mination of  hemiopia),  acuteness  of  vision  (this  may  be  attempted  with  corrected 
refraction).  Testing  the  visual  acuteness  in  psychic  blindness  naturally  presents 
very  serious  obstacles,  as  the  ordinary  test  objects,  such  as  letters,  etc.,  cannot  be 
recognized.  We  are  therefore  usually  obliged  to  make  use  of  some  artificial  device, 
such  as  requiring  the  patient  to  name  the  number  of  black  points  upon  a  sheet  of 
paper. 

2.  Examinations  to  determine  whether  visual  representations  exist.  In  this 
connection  only  the  patients'  statements  about  optical  memory,  etc.,  can  furnish 
any  information. 

3.  Examination  of  association  of  visual  imjjressions.  Recognition  of  objects 
by  statement  of  the  name  or  by  demonstration  of  their  use,  reading  (aloud  and 
with  comprehension),  copying,  drawing,  voluntary  reactions  to  optical  ii-ritation, 
power  of  orientation. 

4.  Examination  of  the  association  of  visual  representations.  Drawing  from 
memory,  writing  spontaneously,  writing  from  dictation. 

5.  In  differentiating  j^sychic  blindness  from  general  confusion  or  insanity,  it  is 
necessary  to  determine  whether  the  other  senses — viz.,  those  of  hearing,  smell, 
taste,  as  well  as  the  sensory  skin  sensation — are  properly  associated,  and  to  observe 
whether  the  patients  deport  themselves  sensibly  so  far  as  their  behavior  toward 
visual  sensations  is  concerned. 

The  diagnosis  of  actual  psychic  blindness  is  frequently  very  difficult,  and  is 
often  impossible  when  comi^licated  with  marked  diminution  in  vision,  because 
conditions  occur  in  all  forms  of  diminished  visual  acuteness  which  have  this  in 
common  Avith  real  psychic  blindness,  that  the  significance  of  what  is  seen  is  dis- 
turbed merely  because  the  visual  impressions  are  not  sharp  enough. 

Psychic  blindness  is  not  to  be  confused  with  cortical  blindness.  The  latter 
affection  is  an  actual  blindness,  a  loss  of  the  A'isual  power,  produced  by  lesions  of 
the  cortex,  and,  owing  to  the  hemiopic  distribution  of  the  visual  function  in  both 
hemispheres,  must  be  bilateral. 

Vni.  SPINAL  HEMIPLEGIA. 

•  Unilateral  lesions  of  the  spinal  cord  produce  a  symptom-complex  which  is 
known  as  "spinal  hemiplegia,"  in  the  broadest  sense  of  the  word.  This  hemi- 
plegia varies  in  character  according  to  the  location  and  extent  of  the  lesion. 

The  motor  disturbances  appear  in  the  extremity  upon  the  same  side  as  the 
lesion  and  in  only  the  lower,  or  both  the  lower  and  the  upper,  extremities,  accord- 
ing to  the  level  of  the  lesion.  The  motor  paralysis  dependent  upon  an  interrup- 
tion of  the  long  tracts,  parti culary  of  the  pyramidal  tract,  is  spastic  in  character, 
as  in  a  complete  transverse  lesion  of  the  cord,  is  associated  with  increased  tendon 
reflexes,  and  Ls  not  accompanied  by  degenerative  atrophy  of  the  paralyzed  muscles. 
If  the  lesion  have  a  considerable  vertical  dimension,  this  spastic  paralysis  may  be 
associated  with  a  degenerative  atrophic  relaxed  paralysis  due  to  involvement  of 
the  nuclei  in  the  anterior  cornua.  "With  an  extensive  vertical  lesion  in  the  cer- 
vical enlargement,  for  example,  the  spastic  paralysis  will  be  bounded  above  by  a 
degenerative  relaxed  paralysis  of  the  upper  extremity;  if  the  extensive  vertical 
lesion  be  situated  in  the  lumbar  cord,  the  paralysis  of  the  muscles  supplied  by  the 
injured  segments  will  be  atrophic  and  relaxed.  Should  the  lesion  involve  the 
entire  length  of  the  lumbar  swelling,   the  spastic  paralysis  of   the  leg  will  be 


904  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

entirely  replaced  by  a  relaxed  degenerative  paralysis.  In  reference  to  tlie  spastic 
components  of  the  paralysis  dependent  upon  the  involvement  of  the  long  tracts,  it 
may  be  said  that  the  laws  given  for  cerebral  hemiplegia  on  p.  876  et  seg.  in  refer- 
ence to  the  more  or  less  marked  involvement  of  the  individual  muscle  groups  also 
obtain  in  spinal  hemiplegia. 

The  vasomotor  tracts  are  involved  upon  the  side  of  the  lesion,  so  that  the 
extremity  at  first  seems  warmer  than  its  fellow  of  the  opposite  side.  This  differ- 
ence subsequently  becomes  equalized  by  the  decreased  heat  production  in  the 
paralyzed  muscles,  and  also  by  the  disappearance  of  the  vasomotor  palsy  as  the 
result  of  the  vicarious  action  of  deeper  centers.  The  paralyzed  side  may  then 
even  be  colder  to  the  touch  than  its  opposite  fellow. 

The  sensory  disturbances  in  unilateral  spinal  lesions  are  of  special  interest 
and  somewhat  more  complicated.  We  have  just  seen  that  the  motor  symptoms, 
corresponding  to  the  uncrossed  exit  of  the  motor  tracts  from  the  spinal  cord, 
occur  only  upon  the  same  side  as  the  lesion;  but  the  sensory  disturbances  are 
partly  bilateral,  although  most  of  them  are  present  only  upon  the  side  opposite  to 
the  lesion.  The  observation  of  the  sensory  phenomena  in  such  cases  has  re- 
sulted in  the  establishment  of  the  three  following  types :  ^ 

Type  1  (Fig.  352).  Upon  the  same  side  as  the  lesion:  Cutaneous  hyper- 
esthesia of  the  skin  to  touch,  bounded  above  by  a  zone  of  cutaneous  anesthesia  for 
all  sensory  qualities;  above  the  latter  area  there  is  sometimes  still  another  narrow 
zone  of  hyperalgesia  to  touch.  Disturbances  of  sensation  of  the  deep  viscera 
(disturbance  of  the  percej^tion  of  passive  changes  of  the  position  of  the  extremities 
and  of  bone  sensation). 

Upon  the  opposite  side :  Cutaneous  analgesia  and  thermanesthesia,  sometimes 
(though  more  rarely  than  upon  the  same  side  as  the  lesion)  bounded  above  by  a 
zone  of  cutaneous  hyperalgesia  to  touch.     Intact  sensation  to  touch. 

Type  2  (Fig.  353).  As  in  Type  1,  except  that  the  analgesic  and  therman- 
esthetic  regions  upon  the  side  oj^posite  to  the  lesion  also  exhibit  hyperesthesia  or 
anesthesia  to  touch. 

Type  3  (Fig.  354).  As  in  Type  1,  but,  with  the  exception  of  the  zones  at 
the  level  of  the  lesion,  there  is  no  hyperalgesia  to  touch  uj^on  the  side  of  the 
lesion;  on  both  sides  below  the  lesion  or  below  the  small  zones  of  hyperalgesia 
there  is  hyperesthesia  to  touch  (Gowers). 

These  different  symptoms  may  be  explained  by  the  following  assumptions: 
The  majority  of  the  fibers  conducting  the  sensations  of  pain  and  temperature 
decussate  immediately  upon  their  entrance  into  the  spinal  cord  and  pass  uj^ward 
to  the  brain  upon  the  other  side  of  the  median  line.  About  half  of  the  fibers 
conducting  the  sensation  of  touch  decussate  immediately  and  half  remain  upon 
the  same  side.  The  fibers  for  the  perception  of  passive  movements  of  the  extremi- 
ties and  for  bone  sensation  run  upward  in  the  sjiinal  cord  without  decussation. 
The  uncrossed  fibers  probably  i^ass  upward  in  the  posterior  columns,  while  the 
crossed  fibers,  after  their  decussation,  run  upward  in  the  anterolateral  columns. 
The  decussation  of  the  fibers  in  the  latter  group,  if  it  occur  at  all  (see  above), 
takes  place  in  the  gray  matter,  since  an  impulse  from  a  collateral  in  the  posterior 
horn  of  one  side  is  taken  up  by  an  offshoot  of  the  anterolateral  column  of  the 
other  side  (see  Fig.  362).  It  should  be  noted  that,  as  the  decussation  never 
affects  the  entire  fibers  of  the  posterior  roots  but  always  only  their  collaterals," 
we  might  indicate  the  relation  between  the  crossed  and  uncrossed  sensory  fibers 
diagrammatically  by  representing  the  posterior  root  as  consisting  of  a  crossed  and 
an  uncrossed  portion.  This  conception  is  of  importance  for  the  explanation  of 
the  hyperalgesia  upon  the  side  of  the  lesion. 

^  See  Mann,  Zeits.  f.  Nervenkrankh.,  1896,  vol.  x.,  and  Gmvers's  Handbook  of  Nervous 


^  As  is  well  known,  every  fiber  of  the  posterior  root  immediately  upon  entering  the 
spinal  cord  divides  into  an  ascending  and  a  descending  branch,  both  of  which  give  off 
transverse  ramifications  known  as  collaterals.  These  collaterals  run  approximately 
transversely  in  the  cord,  and  send  on  the  sensory  impulses  through  their  terminal 
arborizations. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


905 


The  most  important  of  these  assumptions  are  diagrammatically  indicated  in 
the  accompanying  illustration  (Fig.   355).     In  order  to  render  it  more  compre- 


FiG.  352. 


Fig.  353. 


Fig  352— Spinal  hemiplegia.    Lesion  upon  the  right  side  of  the  patient.    Typel: 
r^////////.'/y.        Motor  and  vasomotor  paralysis.    Varying  degree  of  disturbance  ol  sensation  ot 
^^^P        the  deep  viscera  (perception  of  position),  including  the  bones. 

o  o  o  o  o     Analgesia  and  thermanesthesia  of  the  skin.    Intact  sensation  to  touch. 
o   o    o   o 

•'.'.'..       Cutaneous  hyperalgesia  to  touch  (also  in  the  red  shaded  area). 

3?||||*|        Complete  cutaneous  anesthesia. 

Upon  the  white  side  there  is  neither  motor  nor  vasomotor  paralysis. 

Fig.  353.-Spinal  hemiplegia.    Lesion  upon  the  right  side  of  the  patient.    Type  2 : 

Motor  and  vasomotor  paralysis.    Varying  degree  of  disturbance  of  sensation  of 
^^^P       the  deep  viscera  (perception  of  position),  including  the  bones. 

''.'  •'.•  •  ',     Cutaneous  hyperalgesia  to  touch  (also  in  the  red  shaded  area). 
|$$$|JII        Complete  anesthesia. 

?^f^    Diminished  sensation  to  touch  and  abolished  sensations  of  pain  and  temperature. 
Upon  the  white  side  there  is  neither  motor  nor  vasomotor  paralysis. 

hensible,  the   sensory  fibers   for   the   perception   of  passive   movements   of  the 
extremities  and  for  bone  sensation,  as  well  as  the  motor  and  vasomotor  fibers, 


906 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


have  been  omitted.     By  the  use  of  this  diagram  the  differences  between  the 
sensory  symptom-complexes  of  unilateral  lesions  may  be  readily  understood. 

The  red  lines  represent  the  fibers  for  the  conduction  of  the  sensations  of  pain 
and  temperature;  although  these  sensations  are  not  transmitted  by  the  same 
fibers,  they  both  pursue  a  similar  course.  The  black  lines  represent  the  fibers  for 
the  conduction  of  the  sensation  of  touch.     It  will  be  observed  that  each  of  these 


Fig.  354.— Spinal  hemiplegia.    Lesion  upon  the  right  side  of  the  patient.    Type  3 : 
'^^M       ?i    2'  ^°^  vasomotor  paralysis.    Varying  degree  of  disturbance  of  sensation  of 
WmM.       the  deep  viscera  (perception  of  position),  including  the  bones. 


•.•:•.■."•'.•'.•.•;  Hyperalgesia  to  touch. 

JiJIJj;*       Complete  anesthesia. 

_s_?_£.  !L°     Diminished  sensation  to  touch  and  abolished  sensations  of  pain  and  temperature. 

—'Z:^z::z     Diminished  sensation  to  touch  (also  in  the  red  shaded  area). 

Upon  the  white  side  there  is  neither  motor  nor  vasomotor  paralysis. 

fibers,  after  its  entrance  into  the  spinal  cord,  divides  into  a  crossed  and  a  direct 
portion.  The  direct  portions  of  the  (red)  fibers  for  the  conduction  of  the  impulses 
of  pain  and  temperature  are  indicated  by  light  lines,  in  order  to  give  the  impres- 
sion that  they  are  few  in  number  and  that  they  play  an  unimportant  role  in 
comparison  with  the  much  greater  number  of  crossed  fibers.  The  direct  and  the 
crossed  portions  of  the  (black)  fibers  for  the  sensation  of  touch  are,  on  the  con- 
trary, indicated  by  exactly  similar  lines.     For  the  sake  of  clearness,  no  attention 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


907 


has  been  paid  to  the  topographic  arrangement  of  the  fibers  in  the  cross-section 
of  the  spinal  cord,  nor  to  the  composition  of  the  crossed  tracts  from  two  neurons. 
The  shaded  area  represents  the  substance  of  the  spinal  cord  which  is  involved  by 
a  unilateral  lesion. 

With  the  aid  of  this  figure  the  sensory  phenomena  of  Type  1  (Fig.  352) 
may  now  be  explained.  The  fact  that  the  perceptions  of  passive  motion  of  the 
extremities  and  of  bone  sensation  will  be  disturbed  upon  the  side  of  the  lesion 
clearly  follows  from  the  fact  that  these  fibers  (not  indicated  in  Fig.  355)  pass 
upward  uncrossed  in  the  spinal  cord.  We  can  also  understand  that  a  complete 
transverse  section  of  one-half  of  the  cord  will  be  followed  by  an  almost  complete 
absence  of  the  sensations  of  pain  and  temperature  upon  the  opposite  side  below 
the  lesion  (due  to  involvement  of  the  heavy  red  lines  in  Fig.  355).  The  direct 
fibers  for  these  sensations  (indicated  by  the  light  red  lines)  are  so  few  in 
number  that  they  are  unable  to  produce  symptoms  upon  the  same  side  as  the 
lesion,  and  are  equally  powerless  to  prevent  a  marked  disturbance  of  the  sensa- 
tions for  pain  and  temperature  upon  the  opposite  side.     The  figure  also  explains 


cec 


Fig.  355.— Diagram  of  the  sensory  fibers  for  the  explanation  of  the  phenomena  of  spinal 

hemiplegia. 


why  in  many  cases  there  is  no  diminution  of  the  sensation  to  touch  below  the 
lesion,  with  the  exception  of  the  zone  corresponding  to  the  involved  segment, 
since  the  equal  division  of  these  fibers  into  crossed  and  uncrossed  tracts  is  evi- 
dently suflBcient  to  maintain  the  normal  sensory  conditions.  Many  theories  have 
been  advanced  to  explain  the  hyperalgesia  to  touch  which  is  usually  observed 
upon  the  same  side  and  below  the  lesion.  The  author  believes  that  this  symptom 
can  be  rendered  intelligible  by  assuming  that  the  crossed  and  direct  tracts  for 
tactile  sensation  are  mutually  complementary  ramifications  of  the  sensory  roots. 
When  the  direct  tracts  bbb  aaa  are  interrupted,  the  crossed  tracts  bbb  ccc 
receive  a  nervous  impulse  of  double  intensity,  and  this  intensity  is  sufficient  to 
cause  the  impulse  to  radiate  into  the  dendritic  network  of  the  gray  matter  and 
excite  the  tract  for  the  sensation  of  pain.  Upon  the  opposite  side  the  crossed 
fibers  for  tactile  sensation  are  involved,  and  this  would  be  followed  by  hyper- 
algesia from  analogous  reasons  were  it  not  that  the  increased  intensity  of  tactile 
sensation  cannot  be  converted  into  pain  on  account  of  the  interruption  of  the 
tract  for  its  transmission.  The  anesthetic  zone  observed  upon  the  side  of  the 
lesion  is  explained  simply  by  the  involvement  of  the  spinal  segment  by  the 


908  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

lesion,  since  all  of  the  sensory  root  fibers  are  interrupted.  The  hyperalgesic 
zone,  sometimes  observed  above  this  anesthetic  zone  upon  the  same  side  as  the 
lesion,  and  occasionally  upon  the  opposite  side,  can  hardly  be  explained  other- 
wise than  by  the  supposition  that  the  roots  in  the  vicinity  of  the  lesion  may 
easily  be  rendered  hyperirritable  by  inflammatory  hyperemia,  possibly  from  the 
meninges. 

The  involvement  of  tactile  sensation  in  the  hemianesthesia  opposite  to  the 
lesion  in  Type  2  (Fig.  353),  is  explained  by  presuming  that  in  these  cases  the 
crossed  fibers  for  tactile  sensation  preponderate  greatly  over  the  direct.  Such 
individual  peculiarities  are  frequently  encountered  in  neuropathology. 

The  cases  of  Type  3  (Fig.  354),  in  which,  instead  of  hyperalgesia  to  touch 
on  the  same  side  below  the  lesion,  we  have  hyperesthesia  on  both  sides  below  the 
lesion,  are  explained  by  the  supposition  that  the  excitability  of  the  tract  for 
tactile  sensation  is  so  diminished  that  the  loss  of  one-half  of  its  innervation 
results  in  a  decrease  of  sensibility,  and,  since  the  fibers  run  to  both  sides,  this 
symptom  is  bilateral.  Hyperalgesia  is  not  produced  below  and  upon  the  same  side 
as  the  lesion  on  account  of  the  diminution  of  the  sensory  impulses. 

It  should  also  be  noted  that,  according  to  the  condition  of  irritability  of  the 
sensory  tracts  and  according  to  the  remote  effects  of  the  unilateral  lesion  upon 
the  opposite  side,  the  symptom  complex  of  spinal  hemiplegia  is  subject  to  still 
further  variation. 

IX.  PATHOLOGIC  GAITS  AND  POSTURES. 

In  many  diseases,  and  especially  in  nervous  diseases,  the  way  patients 
stand  and  walk  shows  something  very  characteristic,  permitting  a  con- 
clusion not  only  in  regard  to  the  type  of  the  functional  disturbance,  but 
frequently  even  in  regard  to  the  anatomic  nature  of  the  disease.  The 
following  are  the  best-known  pathologic  gaits  : 

(a)  The  Paraparetic  or  Paraplegic  Gait. — In  paresis  of  both 
lower  extremities.  Both  legs  are  brought  forward  slowly,  dragging  and 
trailing  upon  the  floor. 

(6)  The  Hemiparetic  or  Hemiplegic  Gait. — In  unilateral 
paralysis  of  the  legs  or  hemiplegia.  The  aifected  leg  drags  after  the 
other,  or  is  first  circumducted  by  a  twisting  movement  of  the  pelvis  and 
so  brought  forward.  An  explanation  of  this  gait  is  to  be  found  upon 
p.  877  etseq.  The  predominance  of  the  paralysis  of  the  flexors  is  con- 
sidered responsible  for  the  hemiplegic  disturbances  of  motility. 

(c)  The  Atactic  Gait. — Characterized  by  the  incoordinate  atactic 
nature  of  the  movements.  Sometimes  the  foot  feels  uncertainly  for  the 
ground,  sometimes  it  is  thrown  outward  at  random  or  stamps,  and  again 
is  lifted  high  from  the  ground,  making  the  gait  resemble  that  of  a  fowl. 
(See  Ataxia,  p.752  et  seg.) 

(d)  The  Spastic  Gait. — In  spastic  paresis  of  the  lower  extremi- 
ties (spastic  spinal  paralysis,  multiple  sclerosis,  etc.),  the  legs,  being 
very  slightly  flexible,  are  put  forward  very  stiflly.  In  putting  the  foot 
down  the  tendon  reflexes  (especially  the  Achilles-tendon  reflex)  are  some- 
times excited  and  the  gait  becomes  characteristically  jumping.  The 
difficulty  in  the  spastic  gait  depends  at  one  time  more  upon  the  stiffness  of 
the  knee-joints,  at  another  more  upon  the  knees  being  pressed  together 
by  the  forcible  action  of  the  adductors. 

(e)  The  Spastic  Paretic  Gait. — Mixture  of  a  and  c. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  909 

(/)  The  Gait  of  Hip-joint  Disease. — This  is  characterized  by 
a  rigidity  of  the  hip  joint,  so  that  the  pelvis  is  largely  responsible  for 
any  forward  motion  of  the  limb.  Under  some  conditions  the  gait  in 
hysteric  coxalgia  may  be  identical. 

[g)  The  gait  in  sciatica  may  resemble  that  in  hip-joint  disease. 
The  patient  favors  the  affected  leg  by  fixing  it  to  the  pelvis,  almost  as 
regularly  as  in  hip-joint  disease.  In  so-called  sciatic  scoliosis  the  ver- 
tebral column  is  curved  while  the  patient  is  walking  or  standing.  There 
are  usually  two  characteristic  curves ;  the  lower  curve  is  convex,  the 
upper  concave  toward  the  affected  side.  The  trunk  is,  therefore,  as  a 
rule,  bent  toward  the  healthy  side  (heterologous  sciatic  scoliosis), although 
the  curves  may  be  reversed  (homologous  sciatic  scoliosis). 

Attempts  have  been  made  to  explain  these  differences  in  sciatic 
scoliosis,  but  it  seems  quite  plain  that  no  explanation  is  possible  for 
them  all.  Albert  described  heterologous  sciatic  scoliosis,  but  did  not 
venture  an  explanation.  Lorenz  assumes  that  this  form  of  scoliosis  is 
brought  about  simply  by  shifting  the  point  of  gravity  to  the  healthy 
leg.  Kocher  explains  it  by  an  associated  neuralgic  affection  of  the 
sensory  nerves  supplying  the  territory  of  those  muscles  which  hold  the 
trunk  straight.  When  the  contraction  of  these  muscles  results  in  pain 
it  is  no  longer  attempted.  The  spinal  column  bends,  therefore,  its 
direction  depending  upon  what  nerves  are  thus  affected. 

{h)  The  Choreic  Gait. — In  chorea.  (See  Chronic  Movements^ 
p.  750.) 

(i)  The  Staggering  Gait. — In  affections  which  are  associated 
with  vertigo  and  disturbances  of  equilibrium  (drunkenness,  cerebellar 
tumor,  paralyses  of  the  eye  muscles,  diseases  of  the  internal  or  middle 
ear,  lead  encephalopathy). 

{k)  The  Gait  of  Propulsion  and  Retropulsion. — In  affec- 
tions with  stiffness  and  weakness  of  the  muscles,  especially  in  'paralysis 
agitans.  This  gait  is  peculiar  in  that  patients  once  started  forward  or 
backward  are  not  able  to  stop  quickly,  but  must  go  on  a  little  farther 
in  the  direction  in  which  they  are  headed,  because  they  cannot  correct 
quickly  the  point  of  gravity  which  impels  them  in  that  direction.  It  is, 
however,  not  really  specific  for  paralysis  agitans,  as  is  sometimes 
thought,  for  one  often  notices  the  same  peculiarity  in  pedestrians  who 
have  been  tired  by  a  long  tramp. 

The  attitude  or  mode  of  standing  is  very  characteristic  in  many  of 
the  affections  cited  above.  In  hip-joint  disease  and  in  imilateral  leg 
paralysis  the  patient  supports  himself  entirely  upon  the  healthy  \e^. 

In  sciatica  the  scoliotic  appearances  described  above  are  very  promi- 
nent. In  paralysis  agitans  the  position  of  the  trunk,  bent  over  forward, 
with  slightly  flexed  knees  and  elbow  joints,  is  highly  characteristic. 
(See  the  picture  in  StrilmpeWs  Lehrbiich  der  Pathologic.)  Romberg's 
symptom  consists  of  more  or  less  noticeable  swaying  in  patients  who 
stand  with  closed  eyes  (in  severe  cases  even  with  open  eyes).  It  occurs 
in  anesthesia  of  the  lower  extremities,  also  in  ataxia  with  or  without 
anesthesia  (especially  in  tabes),  in  affections  of  the  cerebellum,  and  in 


910  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

some  other  affections  which  lead  to  a  staggering  gait.     The  sign  depends 
upon  a  disturbance  of  the  equilibrium. 

X.    SPECIAL   POINTS   IN    REFERENCE   TO   THE   EXAMINATION   OF 
THE  SPINAL  NERVOUS  SYSTEM. 

I.    PLANS  FOR  THE  EXAMINATION  OF  MUSCLE  ATROPHIES  AND 
PERIPHERAL  MOTOR  PARALYSIS.^ 

Upper  Extremity. 

(For  motor  points  compare  p.  802  et  seq.) 

Shoulder-blade  Movements. 

1.  Elevation  of  the  Shoulder  Blade. 

Middle  portion  of  the  trapezius  (spinal  accessory). 
Rhomboids  (branch  from  V.  cervical). 

Levator  anguli  scapulae  (II.  to  III.  cervical  and  branch  from  V.  cervical). 
Superior  portion  of  the  pectoralis  major  (thoracic  anterior  from  V.  and 
VI.  cervical). 

2.  Depression  of  the  Shoulder  Blade. 

Pectoralis  minor  (thoracic  anterior). 

Inferior  portion  of  the  latissimus  dorsi  (subscapular). 

Inferior  portion  of  the  pectoralis  major  (thoracic  anterior). 

3.  Adduction  of  the  Shoulder  Blade. 

Inferior  portion  of  the  trapezius  (spinal  accessory). 
Superior  portion  of  the  latissimus  dorsi  (subscapular). 
Ehomboids.     (Branch  from  V.  cervical). 

4.  Abduction  of  the  Shoulder  Blade. 

Superior  third  of  the  pectoralis  major  (thoracic  anterior). 
Serratus  anticus  major  (thoracic  longus  from  sixth,  seventh,  and  eighth 
cervical  nerve). 

Shoulder-joint  Movements. 

1.   Elevation  of  the  Upper  Arm. 

(a)  To  the  side  : 

Up  to  the  horizontal :  deltoid  (circumflex). 

Up  to  the  vertical :  deltoid  and  serratus  anticus  major  (thoracic 
longus). 
With  straining,  the  upper  part  of  the  trapezius  in  addition 
(spinal  accessory). 

(b)  Forward  : 

Anterior  portion  of  the  deltoid  (circumflex). 
Coracobrachialis  (musculocutaneous). 
Biceps  (musculocutaneous). 

In  elevation  to  the  vertical,  the  serratus  anticus  major  also 
aids. 

(c)  Backward  : 

Posterior  portion  of  the  deltoid  (circumflex). 

^  The  anatomic  statements  in  these  schemes  have  been  collected  from  Scheube  and 
Duchenne,  and  then  compared  with  Gegenbauer's  Anatomy  (4th  edition,  1890).  For  the 
sake  of  simplicity,  the  origin  of  a  nerve  from  its  motor  root  is  stated  in  the  plan  only 
where  the  nerve  "is  mentioned  for  the  first  time.  In  this  way  it  is  easy  enough  to  find 
the  root  origin  of  a  certain  nei-ve  for  a  certain  muscle  by  searching  for  the  name  of  this 
nerve  in  the  first  place  it  is  mentioned  in  the  scheme.  For  those  nerves  whose  origin  is 
not  stated  in  the  scheme,  the  reader  should  consult  the  diagrams  of  the  extremity  plex- 
uses, pp.  935,  936,  and  Koclier's  plates  of  the  spinal  motor  segmental  innervation.  Fur- 
ther clinical  experience  is  necessary  to  clear  up  individual  points  still  under  contention. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  911 

2.  Depression  of  the  Upper  Arm. 

The  united  adductors  of  the  upper  arm. 

3.  Adduction  of  the  Upper  Arm. 

Pectoralis  major  (thoracic  anterior  from  V.  and  VI.  cervical). 
Latissimus  dorsi  and  teres  major  (subscapular). 
Infraspinatus  (suprascapular  from  V.  and  VI.  cervical). 
Teres  minor  (circumflex).  » 

4.  Inward  Rotation  of  the  Upper  Arm. 

Subscapularis  (subscapular). 
Teres  major  (subscapular). 
6.    Outward  Rotation  of  the  Upper  Arm. 
Infraspinatus  (suprascapular). 
Teres  minor  (circumflex). 

Elbow-joint  Movements. 

1.  Flexion  of  the  Forearm. 

Biceps  [flexor  and  supinator]  (musculocutaneous). 
Brachialis  anticus  (musculocutaneous). 

Supinator  longus  [supinates  or  pronates  according  to  the  position  ;  it  is, 
however,  chiefly  a  flexor  in  the  median  position]  (musculospiral), 

2.  Extension  of  the  Forearm. 

Triceps  (musculospiral). 

3.  Supination  of  the  Forearm. 

Supinator  brevis  (musculospiral). 
Supinator  longus  (see  flexion). 

4.  Pronation  of  the  Forearm. 

Pronator  quadratus  (median). 

Pronator  teres  [pronation  and  flexion]  (median). 

Supinator  longus  [in  an  extreme  position  of  supination]  (musculospiral). 

Wrist  Movements. 

1.  Flexion  of  the  Hand. 

Flexor  carpi  radialis  [flexion  to  the  radial  side]  (median). 
Flexor  carpi  ulnaris  [flexion  to  the  ulnar  side]  (ulnar). 
Palmaris  longus  (ulnar). 

2.  Extension  of  the  Hand. 

Extensor  carpi  radialis  longior  and  brevior   [extension  to  the  radial 

side]  (musculospiral). 
Extensor  carpi  ulnaris  [extension  to  the  ulnar  side]  (musculospiral). 

3.  Abduction  {Radial  Flexion)  of  the  Hand. 

Flexor  carpi  radialis  and  extensor  carpi  radialis  longior  and  brevior 
(median  and  musculospiral). 

4.  Adduction  (Ulnar  Flexion)  of  the  Hand. 

Extensor  carpi  ulnaris  and  flexor  carpi  ulnaris  (musculospiral  and  ulnar). 

Finger  Movements. 
1.  Flexion  of  the  Fingers. 

Flexor  digitorum  sublimis  [flexing  the  second  phalanx]  (median). 

Flexor  digitorum  profundus  [flexing  the  finger  from  the  distal  phalanx] 
(median  and  ulnar.  The  former  supplies  the  radial  sides  ;  the 
latter,   the  ulnar  sides  of  the  several  fingers). 

The  interossei  and  lumbricales  (flexing  the  proximal  phalanx  and  extend- 
ing the  two  distal  phalanges).  Nerve  supj^ly  principally  the  ulnar  ; 
in  the  innervation  of  the  lumbricales,  the  ulnar  nerve  is  aided  liy  the 
median  nerve  to  the  extent  that  the  latter  is  distributed  to  the  two 
radial  and  a  portion  of  the  next  lumbrical  while  the  ulnar  supplies 
the  rest. 


912  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

2.  Extension  of  the  Fingers. 

Extensor  digitonim  communis,  extensor  indicis,  extensor  minimi  digiti 
[extending  the  proximal  phalanx]  (musculospiral). 

Interossei  and  lumbricales  [extending  the  two  distal  phalanges]  (ulnar 
and  median ;  see  above). 

3.  Adduction  of  the  Fingers. 

Palmar  interossei  [flexing  the  proximal  phalanx  simultaneously]  (ulnar). 

4.  Abduction  of  the  Fingers. 

Dorsal  interossei  [flexing  the  proximal  phalanx  simultaneously]  (ulnar). 

Thumb  Motemexts. 

1.  Flexion  of  the  Thumb. 

Flexor  longus  pollicis  [flexing  the  distal  phalanx]  (median). 
Flexor  brevis  pollicis  [flexing  the  proximal  phalanx]  (median). 

2.  Extension  of  the  Thumb. 

Extensor  brevis  pollicis  (musculospiral). 
Extensor  longus  pollicis  (musculospiral). 

3.  Abduction  of  the  Tliumb. 

Abductor  longus  pollicis  (musculospiral). 

Abductor  brevis  pollicis  [more  opponens  than  abductor]  (median). 

4.  Adduction  of  the  Thumb. 

Adductor  pollicis  (ulnar). 

5.  Opposition  of  the  Thumb. 

Opponens  pollicis  (median). 

Abductor  brevis  pollicis  [more  opponens  than  abductor]  (median). 

LiTTLE-FIXGEE   MOYEMEXTS. 

1.  Flexion  of  the  Little  Finger. 

Flexor  digitorum  communis  profundus  and  sublimis  (median  and  ulnar).. 
Flexor  brevis  minimi  digiti  (ulnar). 

2.  Extension  of  the  Little  Finger. 

Extensor  minimi  digiti  proprius  (musculospiral). 

3.  Abduction  of  the  Little  Finger. 

Abductor  minimi  digiti  (ulnar). 

4.  Opposition  of  the  Little  Finger. 

Opponens  minimi  digiti  (ulnar). 

Lower   Extremities. 

(For  motor  points,  see  p.  804  et  seq.) 

Hip- JOINT  Movements. 

1.  Elevation  of  the  Thigh. 

Ileopsoas  [outward  rotation  simultaneously]   (lumbar  plexus). 
Eectus  femoris   |  ,      ^^^  ^^^^  ^^^  j   ^^  jy    lumbar). 
Sartorius  j  ^ 

2.  Depression  of  the  TJiigh . 

Gluteus  maximus  [outward  rotation  simultaneously]  (gluteal  inferior 
from  ischiadic  plexus). 

\  (ischiadic,  lY.  lumbar  to  HI.  sacral)  [at  the  same 
Biceps  ^-j^^^g  flexing  the  leg,  but  onlv  with  extension  of 

Semitendmosus        S      ^^^  ^^..    ^^^  -^  walking— Wernicke-Mann  (see 
Semimembranosus  877V1 

3.  Immrd  Rotation  of  the  Thigh. 

Gluteus  medius  et  minimus  (gluteal  superior  from  ischiadic  plexus). 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  913 

Outward  Rotation  of  the  Thigh. 

Quadratus  femoris  "I  ,    •  +•  \ 

Obturator  internus  and  Gemelli  j  V^ciatic;. 

Obturator  externus  (obturator  from  II.  to  IV.  lumbar). 

Pyriformis  (ischiadic  plexus). 

Ileopsoas  (lumbar  plexus). 

Gluteus  maximus  (gluteal  inferior  from  ischiadic  plexus). 
Adduction  of  the  Thigh. 

Adductors  [simultaneous  outward  rotation]  (obturator). 

Pectineus  [simultaneous  flexion]  (crural  and  obturator). 

Gracilis  (obturator). 
Abduction  of  the  Thigh. 

Gluteus  medius  et  minimus  (gluteal  superior). 


Principal  flexor  (shortener  of  the 
leg)  in  walking — Wernicke-Mann 
(see  p.  877). 


Semitendinosus       1  [simultaneous  inward  ro- 
Semimembranosus  j        tation]  (sciatic). 
Biceps  '  [simultaneous      outward 

rotation]  (sciatic). 


Knee-joint  Movements. 

1.  Flexion  of  the  Leg. 

Sartorius    [simultaneous   inward 
rotation    of    the    flexed    leg] 
(crural). 
Gracilis  [simultaneous  inward  ro- 
tation] (obturator). 

Not  as  flexion  of  the 
leg,  but  as  extensor 
of  the  thigh  in  walk- 
ing (elongator  of 
the  leg) — Wernicke- 
Mann  (see  p.  877). 
Popliteus  [simultaneous  inward  rotation]  (internal  popliteal  from  sciatic). 

2.  Extension  of  the  Leg. 

Quadriceps  (anterior  crural). 

3.  Inward  Rotation  of  the  Leg. 

Popliteus  (internal  popliteal). 
Sartorius  (anterior  crural). 
Gracilis  (obturator). 
Semitendinosus  1  ('-  •  f  \ 

Semimembranosus     j  ^*'  -'■ 

4.  Outward  Rotation  of  the  Leg. 

Biceps  (sciatic). 


Foot-joint  Movements  (Sciatic).     . 

1.  Dorsal  Flexion  of  the  Foot. 

Tibialis  anticus  [innervating  at  the  same  time  the  inner  foot  surface] 

(anterior  tibial  nerve  from  sciatic). 
Extensor  digitorum  communis  longus  (simultaneous  abduction). 

2.  Extension  {plantar  flexion)  of  the  Foot. 

Gastrocnemii )  ,.   ,         ,         t-     i  ^  •  .•  n 

SoIpus'  1  O^^ternal  popliteal  from  sciatic). 

Peroneus  longus  [simultaneous  abductor  and  elevator  of  the  outer  foot 
surface]  (musculocutaneous  nerve  from  sciatic). 

3.  Adduction  of  the  Foot. 

Tibialis  posticus  [simultaneous  raising  of  the  inner  foot  surfaces  and 

plantar  flexion  of  the  foot]  (posterior  tibial  nerve). 
Tibialis  anticus  [simultaneous  dorsal  flexion  of  the  foot  and  raising  of 
the  inner  foot  surfaces]  (anterior  tibial  nerve). 
58 


914  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

4.  Abduction  of  the  Foot. 

Peroneus  longus   [simultaneous  plantar  flexion  with  elevation  of  the 

outer  foot  surfaces]  (musculocutaneous). 
Peroneus  brevis   [pure  (?)  abductor  with  elevation  of  the  outer  foot 

surfaces]  (musculocutaneous). 
Extensor  digitorum  communis  longus  (anterior  tibial). 

5.  Elevation  of  the  Inner  Foot  Surfaces. 

Tibialis  anticus  [simultaneous  dorsal  flexion  and  adduction]  (anterior 

tibial). 
Tibialis  posticus  [simultaneous  adduction  and  plantar  flexion]  (internal 

popliteal). 

6.  Elevation  of  the  Outer  Foot  Surfaces. 

Peroneus  longus  and  peroneus  brevis  (musculocutaneous). 
Peroneus  tertius  (anterior  tibial). 


Toe  Movements  (Sciatic). 

1.  Flexion  of  the  Toes. 

Flexor  digitorum  communis  longus  and  brevis  [second  and  third  phal- 
anges] (tibial). 
Interossei  and  lumbricales  [first  phalanx]   (tibial). 

2.  Extension  of  the  Toes. 

Extensor  digitorum  communis  longus  and  brevis  (anterior  tibial). 

3.  Adduction  of  the  Toes. 

Interossei  plan  tares  (tibial). 

4.  Abduction  of  the  Toes. 

Interossei  dorsales  (tibial). 

Great-toe  Movements     (Sciatic). 

1.  Flexion  of  the  Great  Toe. 

Flexor  hallucis  longus  [second  phalanx]  (tibial). 
Flexor  hallucis  brevis  [first  phalanx]  (tibial). 

2.  Extension  of  the  Great  Toe. 

Extensor  hallucis  longus  [second  phalanx]  (anterior  tibial). 
Extensor  hallucis  brevis  [first  phalanx]  (anterior  tibial). 

3.  Adduction  of  the  Great  Toe. 

Adductor  hallucis.  \  ....  .  -.. 

Inner  belly  of  the  flexor  hallucis  brevis  J  ^      ^    ''* 

4.  Abduction  of  the  Great  Toe. 

Abductor  hallucis  1  I'fl  "  n 

Outer  belly  of  the  flexus  hallucis  brevis  J  ^ 

Little-toe  Movements     (Tibial). 

1.  Flexion  of  the  Little  Toe. 

Flexor  digiti  quinti  (tibial). 

2.  Abduction  of  the  Little  Toe. 

Abductor  digiti  quinti  (tibial). 

3.  Opposition  of  the  Little  Toe. 

Opponens  digiti  quinti  (tibial). 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


915 


2.  THE  PERIPHERAL  DISTRIBUTION  OF  THE  SENSORY  CUTANEOUS  NERVES. 
For  the  localization  of  peripheral  sensory  disturbances  consult  Figs.  356-361. 


N.  eiliaris  (Vi). 


N.  supratrochl. 

N.  infratrochl. 

( Fi). 

N.  nasal  ext.  (Fi). 


N.  lacrym.  ( Fi). 


Anterior  branches  of  the       Posterior  branches  of  the 
cervical  plexus.  cervical  nerves. 

Fig.  356.— Cutaneous  nerves  of  the  head.    The  back  of  the  ear.  and  the  skin  of  the  back  wall  of 
the  external  auditory  meatus  are  supplied  by  the  auricularis  vagi. 


916 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


Fig.  357.— Cutaneous  nerves  of  the  anterior  surface  of  the  trunk  (see  also  Fig.  364.). 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


917 


Kiuulial. 


Fig.  358.— Cutaneous  nerves  of  the  flexor  surface  of  the  upper  extremity  (see  also  Fig.  354)^ 


918 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


—  N.  cut.  brach.  ext.(from 
N.  musculocutaneus). 


N.  median. 
Fig.  359.— Cutaneous  nerves  of  the  extensor  surface  of  the  upper  extremity  (see  also  Fig.  364). 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


919 


<fs^ 


External  cutaneous  nerve. 


Anterior  crural  nerve. 


^^ 


yi^tn  la  I 
xltimb) 


^'f fimh  '  I  T Pudie  nerve  (sacral  plexus). 


External  popliteal  nerve. 


Musculocutaneous  nerve. 

Short  saphenous  nerve  (from 
external  and  internal  popliteal 
nerves). 

External  plantar   nerve    (from 

posterior  tibial  nerve). 


Obturator  nerve  (lumbar 
plexus). 


Long  saphenous  nerve  (from 
anterior  crural). 


...  Anterior  tibial  nerve. 


Internal  plantar  nerve  (from 

"     posterior  tibial  nerve). 


Fig.  360.— Cutaneous  nerves  of  the  anterior  surface  of  the  lower  extremity  (see  also  Fig.  364). 


920 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


/  a'*' 

pleM-fuwh  etscta 


W.ileaimf.  U. 
ileohijpocf. 
(^cmi  fatplex. 
Imn'b.efsacnJ 


Obturator  nerve 


Long  saphenous  nerve  (from 
anterior  crural  nerve). 


Plantar  cutaneous  nerve  (from 
posterior  tibial  nerve. 

Internal  plantar  nerve  (from 
posterior  tibial  nerve). 


External  cutaneous  nerve 
(from  lumbar  plexus). 


External  popliteal  nerve. 


Short  saphenous  nerve  (from 
internal    and  external  poj)- 

liteal  nerves). 


Musculocutaneous  nerve. 

,  Short  saphenous  nerve. 
External  plantar  nerve  (from 
posterior  tibial  nerve). 


Fig.  361.— Cutaneous  nerves  of  the  posterior  surface  of  the  lower  extremity  (see  also  Fig.  364). 


3.  SPINAL  LOCALIZATIONS. 

(a)  Cross-section  Localization  of  the  Spinal  Cord. 

In  regard  to  this  point  the  reader  is  referred  to  the  text-books  upon 
Spinal  Anatomy,  which  discuss  the  anatomic  significance  and  the  physio- 
logic functions  of  the  individual  areas  of  the  cross-section.  We  must 
be  content  here  with  inserting  the  two  plates  taken  from  Edinger  and 
Obersteiner  for  orientation  of  the  sensory  tracts. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  921 

Type  of  the  crossed  sensory  tract  (principally  for  temperature  and  pain). 
Type  of  sensory  tracts  supplying  reflexes. 

Type  of  the  direct  sensory  tracts. 


Direct  pyramidal  tract. 


Anterior  roots; 


Fig.  362.— Crossed  section  of  the  cord  (Edinger).    The  interpretation  for  the  posterior  roots 
not  according  to  Edinger. 


B,  Burdach's  column ;  Ca,  anterior  commis- 
sure ;  Coa,  anterior  cornu  ;  Cop,  posterior  cornu  ; 
GS,  column  of  GoU  ;  GSZ,  mixed  lateral  tract ;  Ha, 
postero-external  field ;  iS,  intermediate  lateral 
tract;  KS,  direct  cerebellar  tract;  L,  Lissauer's 
marginal  zone ;  PyS,  lateral  pyramidal  tract  in 
marginal  zone  ;  PyV,  anterior  pyramidal  tract; 
R,  substantia  gelatinosa  Rolandi;  Ka,  anterior 
roots;  SC,  Schultze's  comma ;  SG,  lateral  bound- 
ary zone  ;  Sgc,  substantia  gelatinosa  centralis  ; 
VG,  anterior  ground  bundle :  vH,  central  sub- 
stance behind  the  columns ;  vm,  fasciculus  sub- 
comarginalis ;  Rp,  and  W,  posterior  roots  (after 
Obersteinerj. 


Fig.  363.— Cross-section  of  the  cervical  cord. 


922  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

(6)  Segmental  Localization  of  the  Spinal  Cord. — Longitudinal  Localization. 

Recent  Views. 
Segmental  l/ocali^ation  of  Cutaneous  Sensibility. — The 

behavior  of  the  cutaneous  sensibility  in  lesions  of  separate  sensory 
roots — i.  e.,  of  separate  segments  of  the  spinal  cord — has  been  very 
minutely  studied  recently  by  Sherrington,  ^  Thoburn,  ^  and  Kocher.  ^ 
Sherrington  has  shown  experimentally  that  individual  sensory  roots — 
i.  e.,  segments  of  the  dorsal  cord — supply  a  circular  girdle-shaped  area 
of  the  skin  upon  the  trunk,  and  that  the  individual  segments  overlap 
each  other  in  both  directions.  Hence  the  upper  boundary  of  the  dis- 
turbance of  sensibility,  in  cross-lesions  of  the  spinal  cord,  does  not  fol- 
low the  descending  direction  of  the  ribs,  but  presents  a  girdle-shaped 
line  perpendicular  to  the  body  axis.  (See  Fig.  364.)  On  account  of 
the  overlapping  of  the  separate  zones  of  sensibility,  we  find  that  in 
cross-sections  of  the  spinal  cord  a  zone  of  relatively  disturbed  sensi- 
bility can  always  be  distinguished  above,  between  the  boundary  of  the 
absolute  loss  of  sensibility  and  the  higher  zone  of  hyperesthesia.  This 
zone  of  relatively  disturbed  sensibility  corresponds  to  the  area  which  is 
supplied  also  by  the  segment  lying  above  the  lesion,  and  which  is  deprived 
of  the  lower  part  of  its  double  innervation.  As  is  shown  by  the  figure, 
the  rules  for  the  segmentary  arrangements  of  disturbance  of  sensibility 
do  not  hold  good  for  the  extremities  or  the  neck  and  head.  However, 
if  the  arms  are  horizontally  abducted,  these  rules  still  apply  (Fig.  364). 
In  almost  complete  conformity  with  the  experiments  of  Sherrington 
and  with  the  clinical  observations  of  Thobum,  Kocher,  from  minute 
investigation  of  traumatic  lesions  of  the  spinal  cord,  has  represented  in 
Fig.  364  the  cutaneous  areas  corresponding  to  the  separate  spinal  cord 
segments — i.  e.,  the  sensory  roots.  We  should  supplement  this  figure 
by  including  the  overlapping  of  the  zones,  as  determined  by  Sherring- 
ton. In  Fig.  364  the  boundary  between  each  segment  and  the  one 
next  below  corresponds,  according  to  Kocher,  to  the  upper  limits  of  the 
absolute  disturbance  of  sensibility  M'hich  he  found  in  individual  cases 
of  transverse  lesions  of  the  spinal  cord — /.  e.,  to  the  lower  limits  of  the 
innervation  area  of  the  upper  segment.  Therefore  all  these  boundaries 
should  be  understood  as  representing  the  lower  limits  of  the  upper  zone 
— e.  g.,  the  boundary  between  the  seventh  and  eighth  dorsal  zones  cor- 
responds to  the  lower  boundary  of  the  seventh  zone — i.  e.,  to  a  level  to 
which  the  seventh  zone  still  sends  its  prolongations  in  lesions  of  the 
eighth  segment,  as  a  result  of  the  double  innervation  ;  but  the  upper 
boundary  of  the  eighth  innervation  area  should  be  sought  somewhat 
farther  upward.  The  upper  sensibility  girdle  must  therefore  be  under- 
stood to  overlap  the  lower,  like  shingles  on  a  roof,  although  in  the  figure 
only  the  uncovered  parts  are  represented. 

^  Philosophical  Transactions  of  the  Royal  Society,  vol.  clxxxiv.,  London,  1893. 

^  A  Contribution  to  the  Surgci-y  of  the  Spinal  Cord,  London,  1889,  Griffin  &  Co. ;  again, 
Brain,  1893  and  1894. 

^ "  Die  Verletzungen  der  Wirbelsaule,  zugleich  als  Beitrag  zur  Physiologie  des 
menschlichen  Riickenmarks,"  Mittheilung  aus  den  Grenzgebieten  der  Medicin  und  Chir- 
urgie,  vol.  i.,  part  4. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


923 


The  relation  of  the  plane  of  the  sensibility  zones  of  the  skin — i.  e., 
of  the  anesthesia  in  lesions  of  the  sensory  roots  or  focal  lesions  of  the 
cord — to  the  plane  of  the  corresponding  spinal  cord  segments,  spinal 
roots,  and  vertebrae  is  of  the  greatest  importance.     Fig.  364  and  the 


c.e-7 


Fig.  364.— The  sensory  innervation  of  the  body  by  the  spinal  segments  according  to  Kocher. 
Red :  Cervical  segments.    ] 


The  intensity  of  the  color  depends  upon  the  level  of  the  seg- 
ment. 


Brown:  Dorsal 

Violet:  Lumbar 

Blue :  Sacral 

C2,  D2.  L2.  So,  etc.=Second  cervical,  dorsal,  lumbar,  sacral  segment,  etc. 


following  pages  demonstrate  plainly  enough  that  the  injured  spinal  cord 
segment,  the  place  of  exit  of  the  corresponding  sensory  root,  or  the  ver- 
tebra corresponding  numerically  to  the  injured  segment,  and,  finally,  the 
cutaneous  sensibility  border  do  not  lie  in  a  horizontal  plane,  but  that  the 


924  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

cutaneous  sensibility  is  pushed  considerably  downward  in  relation  to  the 
vertebra  or  the  exit  of  the  nerve,  and  this  again  in  relation  to  the  seg- 
ment of  the  cord.  In  the  operative  treatment  of  certain  spinal  cord 
affections,  a  neglect  of  this  peculiarity  has  occasioned  many  unfortunate 
results.  The  plainest  rules  for  use  in  such  conditions  have  been  recently 
formulated  by  Kocher.     They  will  be  given  later. 

One  reason  for  such  caudal  dislocation  of  the  limits  of  cutaneous  sen- 
sibility, as  compared  with  the  affected  segment,  depends  upon  the  fact 
that  the  spinal  cord  is  so  much  shorter  than  the  vertebral  column  that 
the  nerve  roots  within  the  vertebral  canal  must  take  a  descending 
course.  As  a  result  (see  Fig.  365)  each  segment  up  to  the  fourth  or 
fifth  upper  dorsal  vertebra  is  situated  at  the  level  of  the  next  higher 
vertebra.  Thus,  the  first  dorsal  root  arises  from  its  segment  in  the 
spinal  cord  behind  the  seventh  cervical  vertebra,  the  sixth  dorsal  root 
behind  the  fifth  dorsal  vertebra,  etc.  From  the  fourth  or  fifth  vertebra 
downward  the  segments  lie  still  higher  in  relation  to  the  corresponding 
vertebra,  so  that  the  eighth  dorsal  segment  lies  behind  the  upper  part 
of  the  seventh  dorsal  vertebra ;  the  ninth  segment,  behind  the  cartilage 
between  the  seventh  and  the  eighth  vertebra  ;  the  tenth  segment,  behind 
the  lower  part  of  the  eighth  ;  the  eleventh,  behind  the  ninth ;  the 
twelfth,  behind  the  tenth  vertebra.  Thus,  in  the  upper  half  of  the 
dorsal  column  the  difference  of  level  between  the  segment  and  the  cor- 
responding vertebra  is  equal  to  the  height  of  one  vertebra ;  whereas  in 
the  lower  dorsal  column  it  approaches  more  and  more  the  height  of  two 
vertebrae. 

This  variation  of  level  between  the  segment  and  the  corresponding 
vertebra  naturally  shows  at  the  same  time  the  difference  in  height 
betw^een  the  segment  and  the  exit  of  the  corresponding  roots. 

Now,  the  upper  boundaries  of  the  absolute  sensibility  disturbance 
which  correspond  to  a  lesion  of  a  certain  nerve  root-^f.  e.,  of  its  corre- 
sponding segment — are  again  lower  than  the  point  of  exit  of  the  nerve 
root,  because  the  intercostal  nerves  take  a  still  further  descending  course 
to  reach  the  skin,  and  because  the  unaffected  root  which  lies  above  over- 
laps about  one  finger's  breadth  the  area  supplied  by  the  affected  root. 
In  consequence  of  this  in  lesions  of  a  sensory  root,  or  in  transverse 
lesions  of  the  dorsal  cord,  the  limitations  of  sensibility  (upper  border 
of  absolute  anesthesia)  are  in  the  upper  dorsal  region  about  three,  in  the 
lower  dorsal  from  four  to  five,  vertebral  heights  below  the  points  of 
exit  of  the  affected  roots — i.  e.,  the  uppermost  segments  affected.  Since 
the  spinal  cord  segments  in  the  upper  dorsal  column  are  situated  about 
one  vertebral  height,  and  in  the  lower  dorsal  two  vertebral  heights, 
above  the  exit  of  the  corresponding  nerve  root,  the  affected  segment 
in  cross-lesions  of  the  upper  part  of  the  dorsal  cord  is  situated 
about  four  (3  +  1),  and  of  the  lower  part  of  the  dorsal  cord  from 
six  to  seven,  vertebral  heights  above  the  upper  boundaries  of  absolute 
anesthesia. 

These  relations  are  represented  diagrammatically  in  Fig.  365. 

This  diagram  corresponds  with  the  rules  empirically  established  by^ 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


925 


Kocher — viz.,  that  in  cross-lesions  of  the  dorsal  cord — i.  e.,  in  lesions 
of  its  sensory  roots — the  upper  boundaries  of  absolute  sensibility  dis- 
turbance correspond  to  the  deepest  (nearest  the  end  of  the  spine),  and 
to  the  most  anterior  point  (for  the  upper  ribs)  of  the  intercostal  space 
in  which  the  intercostal  nerve  belonging  to  the  affected  root  runs. 
From  this  level  the  limitations  of  sensibility  run  horizontally  back- 
ward— i.  e.,  perpendicular  to  the  vertebral  column,  and  not  obliquely 
like  the  ribs.  For  those  roots  whose  intercostal  spaces  do  not  reach 
the  sternum,  we  must  determine  the  boundaries  anteriorly,  correspond- 
ing to  the  supply  of  the  abdominal  wall,  by  following  the  intercostal 


1 

\ 

z 

v\ 

3 

\\^ 

t 

x^ 

5 

v\ 

6 

\5 
\\ 

7 

w 
:\x 

\x 

8 

9 
10 

11 

12 

\x 

\l2 

{Boundary  of  absolute  disturbance  of  sensibility 
in  lesions  of  a  segment  or  of  a  sensory  root,  on 
the  skin  of  the  back  about  3  vertebral  heights 
lower  than  the  place  of  exit  of  the  alFected 
root. 


C  Boundary  of  absolute  disturbance  of  sensibility 
J  in  lesions  of  a  segment  or  of  a  root,  on  the  skin 
■  I  of  the  back  about  4  to  5  vertebral  heights  lower 
[than  the  place  of  exit  of  the  affected  root. 


Fig.  365. — Diagram  of  the  level  of  the  dorsal  segments  in  relation  to  the  dorsal  vertebrae  and 
to  the  corresponding  boundaries  of  the  zones  of  insensibility  on  the  back.  Drawn  from  Kocher's 
rules.    The  oblique  lines  represent  the  emerging  roots. 


nerve  downward  in  an  outward  convex  curve — e.  g.,  the  boundaries 
corresponding  to  the  twelfth  intercostal  nerve  will  reach  down  to  the 
symphysis.  In  reality,  Kocher's  rules  hold  good  even  here,  because  the 
borders  run  j^ractically  horizontally  backward  from  the  deepest  point 
of  the  intercostal  space. 

From  what  has  been  said  about  the  variations  in  levels  between  the 
exit  of  the  root  and  the  corresponding  segment,  it  is  clear  that  one  and 
the  same  upper  boundary  of  anesthesia  may  signify  lesions  at  diiferent 
planes,  depending  upon  whether  the  spinal  cord  or  a  root  is  involved. 
This  point  is  of  some  importance  in  operative  cases,  as  it  adds  an  ele- 
ment  of    uncertainty    in    determining   the   appropriate    point   for   an 


926 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


attempted  incision.  Of  course,  additional  surgical  evidence,  such  as  a 
fracture  of  a  vertebra,  dislocation,  or  spondylitis,  frequently  indicates  the 
proper  place  for  the  incision.  When  in  doubt,  it  is  advisable  to  begin 
the  incision  midway  between  the  vertebra  and  its  corresponding  seg- 
ment, and  from  there  to  enlarge  the  field  of  operation  according  to  the 
findings. 

There  is  still  another  difficulty  in  local  diagnosis  that  is  worth  men- 
tioning. In  incomplete  spinal  cord  lesions,  which  involve  the  central 
parts  of  the  section  of  the  spinal  cord  more  than  the  periphery,  the  dis- 
turbance of  sensibility  begins  considerably  deeper  than  we  should 
expect  from  the  above  rules,  because  some  of  the  sensory  fibers  of  the 
central  parts  of  the  white  substance  take  their  exit  lower  down  than 
those  from  the  periphery.     Such  a  preponderance  of  involvement  of 


ML 


o      71  ir      7       ^  n     7   /  Ti      ■  Blue :  I.,  IV.,  and  VII.  Cerv.  Segment. 

binau  Muscles  o;}  Back  {Recti  et  obliqul  capitisjFtBlnck:  II.,  Iv.,  and  VIII.  Cerv  Segment. 


.  { Siemo -Tii/oideas 


AAxwicularis  superior  (3^^J^^ 
J  Branch  to  accessoriusyCucuHaris 

^Plafys7na(Fl.) 


Ked:  III.,  VI.  Cerv.  and  I.  Dorsal-segment. 


The  word  N.  radialis  is  somewhat  too  low 
on  the  fiigure.  It  belongs  to  the  entire 
group  of  black,  red,  and  blue  lines  run- 
ning parallel  with  it. 


'Scalenus 

yhreniaus  ^Iliaphraff7na,\ 

«j\>V  Phomhoiclei 
'"^^  Supra  etittfrttspinatiis 

I   Coracol>rachialis\Fl.) 

^.m^v^  \  (^"^^^rachialis  internus 

■Deltoideus 


^ORSiUSSt' 


■Siqiimi/or  loTtgus&brevis^^  Extensors    f  Eadiales  Mterni  ) 
ofWrist     \  Ulnaris  extemus } 
Flexors    [Badialis  int.) 
iof  Wrist 


Long  finger  extensors 
^■;z  Long  finger  flexors 


.}iL£uhs.cafmlaris 
•^ectortdis  Truijor  ^■miiwr' 
PrOTUdorigr^s  • 

—  Teres  nuTfd: 
'i^»  Triceps  — 

mthtlie  Ganglion     "        -<:-;o^^___^^^^^ '^^mn '■^.^^fimall  Muscles 

^iellafum  ioculopupiUary  '"*.a/,.^-  ."     of  Hand  and 

fibers)  *^""'==-. =-.=._.-,,^-.^-i  Fingers 

Fig.  366.— Spinal  motor  nerves  from  cervical  plexus  (Kocher). 


\communicating 


the  central  parts  of  the  spinal  cord  is  observed  not  only  in  lesions  which 
actually  proceed  from  the  interior  of  the  cord  (central  myelitis  and 
hemorrhage),  but  even  in  traumatic  and  spondylitic  pressure  lesions, 
probably  because  the  central  portions  are  more  susceptible  to  injury  than 
the  periphery.  So  that  it  scarcely  needs  to  be  emphasized  that  the 
rules  for  localization  are  to  be  applied  strictly  only  when  we  are  con- 
vinced that  the  transverse  lesion  affects  the  entire  cross-section  equally. 
This  is  practically  very  difficult.  Among  other  aids,  the  condition  of 
the  reflexes  may  be  utilized  to  decide  the  question.  The  more  complete 
the  involvement  of  the  spinal  cord  cross-section  the  more  decidedly  the 
reflexes  are  affected.     (See  p.  784  et  seq.) 

Segmental  I<ocali^ation  of  Motility. — Kocher  has  represented 
the  motor  segmental  localization  in  the  two  plates  Figs.  366,  367).    They 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


927 


are  based  upon  his  own  observations  and  upon  the  well-known  atlas  of 
Flower  ^  and  the  works  of  Risien  Russel  ^  and  Thoburn.^  The  names 
of  the  great  nerve  trunks  composed  of  the  fibers  from  the  different 
roots  are  printed  in  black  capital  letters,  while  the  names  of  the  indi- 
vidual branches  are  printed  in  italics  and  agree  in  color  with  the  corre- 
sponding segments — i.  e.,  the  corresponding  motor  roots. 

According  to    Kocher,  these  plates    illustrate  the  following    facts 
aboijt  the  segmental  motor  innervation  of  the  dorsal  cord  :    I.-XII. 

Lowest  part  of  Abdominal  Muscles  {N.  iliohypogastricus) 
and  M.  quadratus  lumborum         [N.  ilio-inguinahs) 

Blue :  I.  and  IV.  Lumbar-  and  IV.  Sacral- 
segment. 
Black :  II.  and  V.  Lumbar-  and  II.  and  V. 
.•t^  Cremaster(Nspernui&:us  eitenmt)  Sacralsegment. 

_^_,«**"  'Hed  :  III.  Lumbar-  and  I.  and  III.  Sacral- 

:"l,Jiamus  a>mm/McansrvTnP/&xus,  Segment. 

■spennaiicua  (Kisde/erensj\Sh) 
tsoas 
Sartomis 
Jliacus  intemus 
■Pectineus  (S/i) 
Adductores 

Quadriceps fenwris 
Gracilis 

ObtairsUor  exBemus? 


Long  Extensors  of  Feet  and  Toes 
•Pemnens  loiigus  Sthreuis 

"sir"".^  *^'^.     ^-  -^OMjr  flexors  of  feet  and  toes 

Us    '"•-•-.»,5j_.,.£^^_-JlfMsdes  of  calf 
•5?/*«„,  ^  ,  ^  .  "-"^Small  muscles  of  feet 

""•■i. director  muscles  (Corpora  cavernosa) 

'  rmeal.  Ejaciniuonj  Muscles 

■SpMncterani  Sphincter eiBetmsor vesical 
LemUorani 

Fig.  367.— Spinal  motor  nerves  from  lumbar  and  sacral  plexus  (Kocher). 

dorsal  segments  supply  the  intercostal  muscles ;  VII.-XII.  dorsal  seg- 
ments supply  the  abdominal  muscles ;  I.-IV.  dorsal  segments  furnish 
the  sympathetic  nerves  to  the  head,  neck,  heart,  and  lungs ;  V.-IX. 
dorsal  segments  furnish  the  sympathetic  nerves  to  the  intestinal  canal  and 
to  the  abdominal  glands  (superior  splanchnic  nerve) ;  X.— XII,  dorsal 
segments  furnish  sympathetic  nerves  to  the  testicles,  bladder,  and 
rectum  (inferior  splanchnic  nerve,  internal  spermatic  plexus,  and  infe- 
rior mesenteric  plexus). 

Segmentary  I/Ocali^ation  of  the  Reflexes. — By  the  diagrams 

^  Atlas.  schemati<jue  de  systeme  nerveux ;  translated  by  Duprat  and  D^jdrine. 

^  "  Experimental  Investigation  of  the  Nerve  Roots  of  the  Lumbosacral  Plexus,"  etc., 
Proc.  of  the  Royal  Society,  vol.  liv. ;  and  "  Experimental  Investigations  of  the  Nerve 
Eoots  of  the  Brachial  Plexus  of  the  Dog,"  Pathological  Laboi-atory  of  University  Col- 
lege, 1892.  *  Lac.  dt. 


928 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


of  the  motor  and  sensory  segmental  innervation  of  the  spinal  cord 
(Figs.  364,  366,  and  367,  etc.),  the  reflexes  may  be  localized  at  the 
appropriate  segments.  Their  value  for  the  local  diagnosis  of  the  level 
of  a  cross-lesion  is  evident.  The  shortest  reflex  tracts  in  the  spinal 
cord  must  be  contained  in  that  portion  situated  between  the  entrance  of 
the  sensory  and  the  motor  roots  which  conduct  the  reflex  in  question. 
If  one  knows  the  segment  which  perceives  the  sensory  irritation  exciting 
the  reflex  and  the  segment  which  sends  out  the  motor  fibers  inner- 


7  Lenlrtd  Intkmi^tioiu 
"v  of  the  bnj  Reflex  traetSj 


Fig.  368.— Diagram  of  a  cerebronuclear 
(cutaneous)  reflex  to  illustrate  the  connec- 
tion between  short  (segmental)  and  long  re- 
flex tracts. 

In  this  diagram  only  the  cerebral  reflex 
arc  is  represented  completely.  But  the  nu- 
mero^is  collaterals  (supplied  with  terminal 
twigs)  show  that,  in  addition  to  the  shortest 
(segmental)  circuit  and  to  the  cerebral  arc, 
numerous  spinal  lateral  circuits  must  be 
taken  into  account.  This  shows  how  incor- 
rect it  is  to  speak  of  reflex  centers. 

This  figure  should  explain  at  the  same 
time  the  doctrine  of  reflex  stasis  in  trans- 
verse lesions  of  the  cord  which  was  dis- 
cussed upon  p.  783.  It  explains  why  beneath 
the  lesion  a  reflex  stasis— i.  e.,  increase,  and, 
later,  abnormality  of  the  reflexes,  and,  fi- 
nally, pathologic  reflexes — would  result  from 
a  transverse  lesion  (c  d) :  whereas,  if  the  le- 
sion is  at  a  6  in  the  brain,  there  will  be  no 
reason  for  any  reflex  stasis,  because  of  the 
countless  paths  of  escape  for  the  sensory  irri- 
tation. Therefore,  a  destruction  of  the  cere- 
bral arc  is  much  more  apt  to  enfeeble  the  re- 
flexes. For  the  sake  of  simplicity  we  have 
omitted  any  representation  of  the  bilateral 
course  of  the  tracts. 


_cl  Spinal  Interruption 
of  Ike  lory  Reflex  tracti. 


Motor 
Root 


vating  the  reflex  movement,  then  between  the  two  must  be  situated  the 
shortest  intraspinal  reflex  tract.  This  was  formerly  spoken  of  as  the 
"  reflex  center."  There  is,  of  course,  no  question  of  any  actual  reflex 
center,  for  we  have  learned  that  there  is  no  actual  transformation  of 
the  sensory  reflex  impulses  in  one  group  of  ganglion  cells  directly  to 
the  motor  limb  of  the  so-called  reflex  arc.  At  most,  such  an  idea  can 
assist  our  conception  only  as  a  diagram  does.  In  reality,  the  reflex 
tracts  comprise  numerous  ganglion  cells  intercalated  one  after  the  other, 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  929 

as  well  as  manifold  lateral  connections.  (Compare  p.  779  et  seq.  for  the 
modern  idea  of  the  origin  of  the  reflexes.)  The  shortest  path  of  a 
reflex  lies  between  the  entrance  of  the  sensory  and  the  exit  of  the  motor 
root  of  the  reflex  arc  ;  but  this  does  not  mean  that  in  normal  cases  the 
reflex  always  proceeds  only  by  this  shortest  path.  On  the  contrary, 
we  have  already  seen  upon  p.  783  et  seq.  that  an  upper  reflex  arc  reach- 
ing to  the  brain  must  ordinarily  be  innervated  at  the  same  time,  and 
that  the  shortest  path  can  be  exclusively  afiected  only  in  interruptions 
of  spinal  cord  conduction,  as  a  result  of  reflex  stasis.  Fig.  368  may 
recall  this  conception  to  the  reader.  It  has  been  more  minutely  explained 
upon  p.  783.  Without  any  further  explanation,  it  is  evident  that  only 
for  the  tendon  reflexes  does  the  interference  in  the  reflex  arc  normally 
occur  exclusively  by  the  shortest  way  (between  the  entrance  of  the  sensory 
and  the  exit  of  the  motor  roots).  Clinically  these  shortest  reflex  paths 
are  important,  for,  as  shown  in  Fig.  368,  in  a  complete  cross-lesion  of 
their  segment  of  the  spinal  cord  the  reflexes  in  question  must  be  lost, 
because  naturally  all  longitudinal  accompanying  circuits  are  interrupted 
as  well.  On  the  contrary,  we  must  emphasize  the  fact  that  if  the  shortest 
path  is  anatomically  intact,  the  reflex  in  question  may  be  either  preserved 
or  lost,  depending  upon  whether  the  reflex  normally  proceeds  by  the  short- 
est path  or  by  a  longer  path,  whether  the  latter  is  free  or  interrupted,  and 
whether  the  reflexes  are  diminished  by  the  indirect  action  of  an  area 
lying  farther  above,  which  causes  inhibition  or  circulatory  disturbances, 
or  (p.  779),  conversely,  reflex  stasis.  In  other  words,  preservation  of  a 
certain  reflex  shows  that  the  segment  of  the  spinal  cord  uniting  its 
motor  and  sensory  nerve  roots  must  still  possess,  at  least,  partial  conduc- 
tivity ;  whereas  the  loss  of  such  a  reflex  suggests  an  interruption  of  the 
corresponding  segment  of  the  spinal  cord,  although  it  does  not  in  any 
way  prove  such  interruption  with  certainty. 

Older  Views. 

In  concluding  this  presentation  of  the  segmental  localization  of  the  spinal 
cord,  derived  from  the  most  recent  sources,  it  seems  necessary  to  include  in  the 
following  pages  the  most  essential  of  the  older  views  upon  this  topic.  The  fre- 
quent, contradictions  which  exist  between  individual  views  prove  how  unsettled 
this  question,  still  remains,  and  show  that  accurate  clinical  and  pathologico- 
anatomic  examinations  will  not  only  supply  numerous  corrections,  but  will 
extend  our  knowledge  as  well.  These  findings,  especially  where  they  concern 
the  reflexes  and  their  relation  to  the  segments,  must  be  critically  examined  for 
light  upon  the  genesis  of  the  reflexes  (see  pp.  779  and  783).  Thus  far  the  com- 
parison of  the  conformity  and  non-conformity  of  individual  views  has  been  the 
only  method  of  judging  the  accuracy  of  the  data.  In  the  discussion  certain 
experiments  performed  upon  animals  are  not  included,  because  they  are  less 
suitable  for  criticism.  In  this  connection  the  observations  made  by  Ferrier  and 
Yeo  upon  apes  by  irritating  the  motor-nerve  roots  are  especially  valuable,  par- 
ticularly because  many  other  experiments,  especially  the  well-known  researches 
of  Horsley  and  Beevor  upon  the  cerebral  cortex,  show  the  most  intimate  analogy 
between  the  nervous  system  of  apes  and  that  of  man.  Even  the  gross  anatomy 
of  the  plexuses  of  the  extremities  must  be  taken  into  account,  and  therefore  finds 
a  place  in  the  following : 
59 


930 


EXAMINATION   OF  THE  NERVOUS  SYSTEM. 


CLINICAL   DATA. 


Localization    of  the  Functions    in  the  Different   Spinal-corcl  Segments 
(from  Starr-Edinger-Bruns).' 


Segments. 

Motor  roots  for— 

"Reflex  centers "2 
for— 

Sensory  roots  (cutane- 
ous innervation)  for — 

I. 

Small  muscles  of  the  neck, 

Cervical  nerve. 

Sternocleidomastoid  and  -tiu- 
pezius. 

II.-III. 

Sternocleidomastoid, 

Neck  and  occiput. 

Cervical  nerves. 

Trapezius, 

Scaleni  and  neck  muscles 
(complexus,  splenius,  lon- 
gus  colli). 

IV. 

Complexus, 

Dilatation    of    the 

Neck, 

Cervical  nerve. 

Splenius,  longus  colli. 

pupils  from  a  sen- 

Upper-shoulder  re- 

Levator scapulas, 

sory   stimulation 

gion. 

Diaphragm, 

of      the       neck 

Outside  of  the  arm 

Supra-  and  infra-spinati. 

(IV.-VII.  Cervi- 

to the  second  rib. 

Deltoid, 

cal  nerve). 

Biceps  and  coracobrachialis, 

Supinator  longus. 

Rhomboidei. 

V. 

Diaphragm, 

Scapular  reflex  (V. 

Posterior  aspect  of 

Cervical  nerve. 

Deltoid, 

Cervical  nerve  to 

the  shoulder  and 

Biceps,  brachialis  anticus, 

I.  Dorsal  nerve). 

arm. 

Coracobi-achialis, 

Sup.  longus  and  brevis. 

Tendon  reflexes  of 

Outside  of  the  arm 

Pect.  major  (pars  clavicuL), 

the  muscles  and 

and  forearm. 

Serratus  magnus. 

tendons  about  the 

Rhomboidei, 

elbow-joint    (V.- 

Teres  minor, 

VI.    Cervical 

Latissimus  dorsi. 

nerve). 

VI. 

Biceps, 

Extensor     reflexes 

Outside  of  the  fore- 

Cervical nerve. 

Brachialis  anticus. 

of  the  arm   and 

arm. 

Pectoralis  major  (pare  clav- 

forearm. 

icuL), 

Serratus  anticus  major. 

Triceps, 

Extensors  of   the  hand   and 

fingei-s, 

Pronatoi-s. 

yii. 

Long  head  of  the  triceps. 

Flexor  reflexes. 

Radial  area  of  the 

Cervical  nerve. 

Extensors   of  the  hand   and 

hand  and  part  of 

finger. 

the  median  area. 

Flexors  and  pronators  of  the 

hand. 

Pectoralis  major  (pars  cost.), 

Subscapularis, 

Latissimus  dorei, 

Teres  major. 

1  Starr  collected  the  older  data  from  the  clinical  examinations  of  localized  spinal-cord 
lesions,  which  are  recorded  as  late  as  1888. 

■■'  This  expression  (see  p.  928  et  seq.  and  Fig.  368)  is  incorrect,  and  signifies  here 
merely  the  shortest  reflex  arc,  and  therefore  that  segment  of  the  cord  which  includes  the 
sensory  and  motor  roots  of  the  reflex  in  question. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 
Localization  of  the  Functions,  etc.  (Continued). 


931 


Segments. 


yiii. 

Cervical  nerve. 


I. 
Dorsal  nerve. 


II.-XII. 
Dorsal  nerve. 


I. 
Lumbar  nerve. 


II. 

Lumbar  nerve. 


III. 
Lumbar  nerve. 


IV. 

Lumbar  nerve. 


V. 

Lumbar  nerve. 


I.-II. 
Sacml  nerves. 


III.-IV. 
Sacral  nerves. 


Motor  roots  for- 


Flexors    of    the    band    and 

fingers, 
Small  muscles  of  the  hand. 


Extensors-of  the  thumb, 
Small  muscles  of  hand, 
Muscles  of  ball  of  thumb  and 
little  finger. 


Back  muscles. 
Abdominal  muscles. 


Abdominal  muscles, 

Psoas, 

Sartorius. 


Psoas, 

Sartorius, 

Flexors  of  the  knee 

(Eemak?) 
Quadriceps  femoris. 

Quadriceps  femoris. 
Psoas  and  pectineus, 
Inward  rotators  of  the  thigh. 
Abductors  of  the  thigh. 

Adductors  and  abductors  of 

the  thigh, 
Tibialis  anticus  femoris, 
Peroneus  longus. 
Flexors  of  the  knees  (Ferrier?). 

External  rotators  of  the  hip. 
Flexors  of  the  knees 

(Ferrier?), 
Flexors  of  the  foot. 
Extensors  of  the  toes, 
Peronei. 

Flexors  of  toes  and  foot, 
Small  muscles  of  feet, 
Peronei. 

Perineal  muscles. 


'  Reflex  centers ' 
for — 


Dilator  of  the  pupil 
and  smooth  mus- 
cles of  the  orbit, 
with  I.  Dorsal 
nerve. 

Dilator  of  the  pupil 
and  smooth  mus- 
cles of  the  orbit 
in  junction  with 
VIII.      Cervical 


Abdominal  reflexes 
in  the  IV.-XI. 
dorsal  segments ; 
according  to 
Dinkier,  in  the 
IX.-XII.  Dorsal 
segments. 

Cremaster  reflex. 


Cremaster  reflex. 

Patellar  tendon  re- 
flex (IL -IV. 
Lumbar  nerve). 


Patellar  tendon  re- 
flex (II.  -  IV. 
Lumbar  nerve). 


Patellar  tendon  re- 
flex (II.  -  IV. 
Lumbar  nerve). 

Gluteal  reflex  (IV.- 
V.  Lumb.  nerve). 

Gluteal  reflex  (IV.- 
V.  Lumb.  nerve). 


Plantar  reflex. 
Bladder  and  rectal 
center  (Sarbo). 

Achilles  tendon  re- 
flex. Bladderand 
rectal  center. 


Sensory  roots  (cutane- 
ous innervation)  for— 


Median  area, 
Ulnar  area. 


Ulnar  area. 


Skin  of  the  breast, 
back,  abdomen, 
and  upper  gluteal 
region. 


Skin  of  the  pubic 
region,  anterior 
surface  of  the 
scrotum. 

Outside  of  the  hip 
region. 


Anterior  and  inner 
side  of  the  hip  re- 
gion. 


Inner  side  of  the  hip 
and  leg  as  far  as 
the  ankle.  Inner 
side  of  the  foot. 


Posterior  side  of  tlie 
hip,  of  the  thigh, 
and  external  part 
of  the  foot. 


Posterior  side  of  the 
thigh,  outside  of 
the  leg  and  foot. 

Posterior  side  of  t  he 

scrotum, 
Perineum,  anus,  sac- 

i-al  region. 


932  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

W.  Thoburn  ^  has  obtained  similar  results  to  Kocher. 


Cervical  nerves : 
IV. 
V. 
VI. 

VII. 
VIII. 

Dorsal  nerve : 
I. 


Brachial  Plexus  (Motor  Innervation). 

Supra-  and  infraspinatus,  teres  minor  (?). 

Biceps,  brachialis  anticus,  deltoid,  supinator  longus,  supinator  brevis. 

Subscapularis,  pronatores,  teres  major,  latissimus  dorsi,  pec toralis  major, 

triceps,  serratus  major. 
Extensors  of  the  wrist. 
Flexors  of  the  wrist. 

Small  muscles  of  the  hand. 


Lumbar  nerves : 
I. 

II. 

in. 

IV. 
V. 


Sacral  nerves : 
I. 


n. 


LuMBOSACRAIi  PlEXUS. 

Motor  distribution. 
(?) 


III. 
IV. 


(?) 

Sartorius, 

Adductoi-s, 

Flexors  of  the  thigh. 

Extensors  of  the  knee, 

Abductors  of  the  thigh. 

Flexors  of  the  leg. 


rCalf  muscles, 
-j  Gluteal  muscles. 

Perineal  muscles. 

Dorsal  flexoi-s  of  the  ankle- 
jomt, 
L  Small  muscles  of  the  foot. 

Nervi  erigentes. 

Perineal  muscles. 

Bladder  and  rectum. 


Sensorj'  distribution. 
The  iliohypogastric  and  ilio-inguinal 

nerves. 
External  (?)  and  upper  region  of  the 

thigh. 
Anterior  surface  of  the  thigh,  below 

the    region    supplied   by   the   II. 

Lumbar  nerve. 
Anterior  and   inner   surface  of  the 

thigh. 
Posterior  side  of  the  thigh,  except 

the  territory  supplied  by  the  saciul 

roots. 


Narrow  strip  on  the  posterior  surface 

of  the  thigh  and  leg,  sole  of  foot, 
A  part  of  the  dorsum  of  the  foot. 


V     Perineum,  external  genitals. 
Posterior  surface  of  the  thigh. 

Dinkier' s'-i  observations,  made  in  Erb's  Clinic,  upon  the  localization  of  the 
abdominal  reflexes,  should  be  mentioned.  He  found  that  the  abdominal  reflexes 
have  their  shortest  circuit  in  the  lowest  part  of  the  dorsal  cord,  that  the  middle 
and  lower  abdominal  reflexes  (p.  777)  belong  to  the  X.,  XL,  and  XII.  inter- 
costal nerves  and  their  corresponding  spinal  segments,  while  the  upper  abdominal 
reflex  is  limited  to  the  tract  of  the  IX.  and  possibly,  also,  of  the  VIII.  dorsal 
nerves.  This  tallies  with  the  segment  localization  of  the  corresponding  cuta- 
neous areas  (see  Fig.  364,  p.  923).  Still,  these  statements  apply  only  to  the 
shortest  circuit  of  the  reflex  arc  and  do  not  exclude  the  longer  reflex  arcs  reach- 
ing further  up  through  the  affected  sections. 

For  the  local  diagnosis  of  lesions  of  the  cervical  cord  the  reader  should  consult 
Kraus's  article  (from  Kahler's  Clinic),  Zeits.  f.  klin.  Med.,  1891,  vol.  xviii.,  p.  343. 
In  conformity  with  Fraulein  Klumpke's  experiments  on  animals,  he  found 
that  in  man  the  sympathetic  oculopupillary  fibers,  whose  paralysis  causes  myosis 
and  retraction  of  the  globe  with  sympathetic  ptosis  (Paralysis  of  Miiller's  Smooth 
Orbital  Muscle,  see  p.  833),  leave  the  spinal  cord  with  the  motor  root  of  the  first 
dorsal  nerve.  These  are  the  fibers  which  connect  the  principal  trunk  of  the 
sympathetic  with  the  so-called  ciliospinal  center  of  the  spinal  cord.  The  latter 
was  localized  by  Budge  between  the  sixth  cervical  and  the  second  dorsal  seg- 
ments.    Kraus's  statements  coincide  with  L.  Jakobsohn's  ^  anatomicopathologic 

^  A  Contnbufion  to  the  Surgery  of  the  Spinal  Cord,  London,  1889. 
^  Deutsch.  Zeits.  f.  NervenheilL,  1892,  vol.  ii.,  p.  325. 
^  Zeits.  /.  klin.  Med.,  1899,  vol.  xxxvii. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 
Gowers  gives  the  following  table  :  ^ 


933 


Motor  functions.    Nerves.       Motor  functions.       Nerves.     Sensory  functions.  Reflex. 


Sternomastoid, 
upper    neck 
muscles,  up--" 
per   part  of 
trapezius. 


C'l 
2 
3 


Lower       neck 
muscles,  mid- 
dle   part    of  \ 
ti-apezius. 


Lower  part  of 
trapezius  and 
doi"sal  mus 
cles. 


Lumbar     mus 
cles.  -} 


Peroneus    I. 
Flexors  of 
ankle,   ex- 
tensore  of 
ankle. 


n 

oj 


Small   rotators    of 

head, 
Depressoi-s  of  hyoid. 

Levator  anguli  scap- 
ulae. 

Diaphragm. 


Sen-atus,         1   «  k" 
Flexors  of       I  2  -| 

o  S 


elbow, 
Supinators,     j  oq  = 


D 


lo- 
ll 
12 

L  1 


Extensors  of  wrist 
and  fingei-s. 

Extensors  of  elbow. 
Flexors  of  wrist  and 

lingers, 
Pronatoi-s. 


Muscles  of  hand. 


Intercostal  muscles. 


Abdominal    mus- 
cles. 


Cremaster, 
Flexors  of  hip. 
Extensors  of  knee, 
Adductore  of  hip, 
Extensoi-s   and   ab- 
ductore  of  hip. 

Flexors  of  knee. 


S  1 


Small    muscles    of 
2  ^  I      foot. 

4} 

5 


Co. 


muscles. 


11 
I 

sj 

4 
5^ 


9 
10 
11 
12 


Scalp, 

]  Neck  and   upper 

I      part  of  chest. 

>  Shoulder. 

Arm,  outer  side. 
Radial     side    of 
forearm      and 
hand,  thumb. 
Arm,     inner     side, 
ulnar  side  of  fore- 
arm   and    hand, 
tips  of  fingers. 


Front  of  thorax. 


(Ensiform 
ai'ea. 

Abdomen 
(Umbilicus  10). 


(  Buttock,  upper 
j      part. 

Groin    and    scro- 
tum. 

f  Outer  side. 

I 
Thigh  -{  Front. 

I 

[  Inner  side. 
Leg,  inner  side. 
Buttock,  lower  part. 

Back  of  thigh. 
Leg    ( except 
and    <  inner 
foot     (.  part. 

Perineum  and  anus. 

Skin  of  coccyx  and 
anus. 


Scapular. 


IJ 
2 
3 

41 
5 
6 
7 
8 
9 
10      Abdom- 


Epi- 
gastric. 


11 
12 

1:^ 


inal. 


Cre- 
master. 

I  Knee- 
I    jerk. 


Co. 


1.  J  " 

2  I-  Plantar. 

3^ 

4 

5 

Go. 


^  Handbook  of  Nervous  Diseases,  vol.  1,  p.  222. 


934  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

findings  in  man.     This  author  found  the  lateral  horn  corresponding  to  the  first 
dorsal  segment  diseased  in  a  lesion  of  the  oculopupillary  sympathetic  fibers. 

EXPERIMENTAL  DATA. 
Ferrier  and  Yeo/  in  irritation  experiments  upon  apes,  obtained  the  follow- 
ing results  in  reference  to  the  assignment  of  individual  muscles  to  the  motor- 
nerve  roots  : 

Motor  Eoots  of  the  Brachial  Plexus  (after  Ferrier  and  Yeo). 

IV.  Cervical  Nerve. — Deltoid,  rhomboids,  supra-  and  infraspinatus,  teres 
minor,  brachialis  anticus,  supinator  longus,  extensors  of  the  hands  and  fingers, 
diaphragm. 

V.  Cervical  Nerve. — Deltoid  (clavicular  portion),  biceps,  brachialis  anticus, 
serratus  anticus  major,  supinator  longus,  extensors  of  the  hands  and  fingers. 

VI. — Cervical  Nerve. — Latissimus  dorsi,  pectoralis  major,  serratus  magnus, 
pronators,  flexors  of  the  wrist  (?),  triceps. 

VII.  Cervical  Nerve. — Teres  major,  latissimus  dorsi,  subscapularis,  pectoralis 
major,  flexors  of  the  hand  and  fingers  (median),  triceps. 

VIII.  Cervical  Nerve. — Long  flexors,  ulnaris  internus,  small  muscles  of  hand, 
extensors  of  the  hand  and  fingers,  long  head  of  the  triceps,  pectoralis  major  (?). 

I.   Dorsal  Nerve. — Small  muscles  of  the  hand. 

Motor  Eoots  of  the  Lumbosacral  Plexus  (after  Ferrier  and  Yeo). 

III.  Lumbar  Nerve. — Psoas,  sartorius,  adductors,  extensor  cruris. 

IV.  Lumbar  Nerve. — Extensors  of  the  thigh,  extensor  cruris,  peroneus 
longus,  adductors. 

V.  Lumbar  Nerve. — Flexors  and  extensors  of  the  toes,  tibial  muscles,  calf 
muscles,  peroneal  muscles,  external  rotators  of  the  thigh,  flexors  of  the  leg 
(biceps,  semitendinosus,  etc.). 

I.  Sacral  Nerve.— Cali  muscles,  flexors  of  the  leg,  flexor  hallucis  longus, 
small  muscles  of  the  foot. 

II.  Sacral  Nerve. — Small  muscles  of  the  foot. 

Dastre  and  Morat  found  in  experimenting  upon  animals  that  most  _  of  the 
vasomotor  and  sweat-secretoiy  fibers  for  the  face  first  leave  the  cord  with  the 
second  to  sixth  dorsal  nerves. 

Additional  experimental  results  worth  mentioning  are  those  obtained  by  Naw- 
rocki  and  Skabitschewsky  upon  the  origin  of  the  motor  and  sensory  fibers  for  the 
bladder  of  the  cat.  They  found  that  the  motor  nerves  of  the  bladder  leave  the 
spinal  cord  by  two  paths— an  upper  and  a  lower.  The  upper  leads  to  the  vesical 
plexus  from  the  fourth  and  fifth  anterior  lumbar  roots;  the  lower  from  the  second 
and  third  anterior  sacral  roots.  The  sensory  fibers  are  partly  sympathetic, 
partly  cerebrospinal,  in  origin;  the  former  are  contained  exclusively  in  the  hypo- 
gastric nerve,  the  latter  in  the  four  upper  posterior  sacral  roots.  (See,  also, 
L.  B.  Miiller's  data,  on  p.  944,  /.) 

Rossolimo  found  in  dogs  that  the  center  for  the  anal  reflex  (p.  778)  was 
situated  in  the  region  of  the  third  and  fourth  sacral  nerves. 

PURELY  ANATOMIC  DATA. 
Herringham  ^  obtained  the  following  results  in  regard  to  motor  innervation 
from  purely  anatomic  researches  upon  the  course  of  the  individual  motor-nerve 
roots  through  the  brachial  plexus  : 

V.  Cervical  Root. — Biceps,  brachialis  anticus,  subscapularis,  deltoid. 

VI.  Cervical  Root. — Pectoralis   major,   biceps,   brachialis   anticus,    pronator 
1  Brain,  1882,  vol.  iv.,  p.  226.  ^  Proc.  Royal  Soc,  1886,  No.  243,  p.  225. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


935 


teres,  radialis  internus,  thenar  muscles,  subscapularis,  teres  major,  deltoid,  supi- 
nator longus  and  brevis,  radialis  externus,  longus  and  brevis. 

VII.  Cervical  Hoof. — Pectoralis  major   and   minor,    coracobrachialis,    flexor 
sublimus,  latissimus  dorsi,  triceps,  radialis  externus,  longus  and  brevis. 

VIII.  Cervical  Boot. — Pectoralis  major  and  minor,  flexor  sublimus,  latissimus 
dorsi,  triceps. 

I.   Dorsal  Boot. — Pectoralis  major  and  minor. 

At  all  events,  we  have  anatomic  examinations  to  thank  for  the  knowledge 
that  the  phrenic  nerve,  to  a  large  extent,  derives  its  fibers  from  the  fourth  motor 


Suprascap.i 
Dorsalis  scapulse. 


Subclav. 

Subscap. 
Circumflex 


Musculocuta. 


IntercostoMim. 
Long  thoracic. 
Internal  cutaneous. 
Lesser  internal  cutan. 

FiGi  369.— Plexus  brachialis:  IV.,  V.,  VI.,  VII.,  VIII.,  I.,  Anterior  branches  of  the  five  lowest 
cervical  nerves,  and  of  the  I.  dorsal  nerve.  Of  the  branches  extending  anteriorly,  only  the  sub- 
clavius  nerve  is  represented  (after  Gegenbaur). 


cervical  nerve  root,  and  sometimes  a  part  from  the  third  and  fifth  ;  whereas,  the 
occipitalis  magnus  derives  its  fibers  from  the  second,  the  occipitalis  minor  from  the 
first,  second,  and  third,  and  the  auricularis  inagnus  from  the  third  and  fourth 
sensory  cervical  nerve  roots. 

The  annexed  figures  (369  and  370)  and  Gegenbaur' s  Lehrbuch  der  Anatomie 
may  be  consulted  for  a  general  idea  of  the  origin  of  the  plexuses  for  the  extremi- 
ties, and  their  subdivisions  into  the  peripheral  nerves. 


936 


EXAMISATIOX  OF  THE  XEEVOUS  SYSTEM. 


Subcostalis. 

Iliohypogastric  nerve. 
Ilio-inguinal  nerve. 

External  cutaneous. 


Genitocrural     i  lumbo-inguin- 
alis  +  spermatic,  ext.j. 


Anterior  crural. 


Obturator. 

Lumbosacral  cord. 
Superior  gluteal. 

Inferior  gluteal. 

Pyriformis. 

Quadrat  et  Gemell. 
Internal  popliteal. 


N.pud.comni. 
^Kcutfem.^osi. 


External  popliteal  Sciatic 

Fig.  370.— Lumbosacral  plexus  :  ps,  Branches  to  the  psoas  muscle ;  il,  branches  to  the  iliac  muscle 

(after  Gegenbaur). 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


937 


(c)  Topography  of  the  Lumbosacral  Cord,  of  the  Conus  Terminals,  and  of  the 

Cauda  Equina. 
In  order  to  make  a  diflferential  diagnosis  and  determine  the  definite  localiza- 
tion of  afiections  of  the  cauda  equina  and  of  the  lumbar  and  sacral  cord,  it  is 
very  essential  to  possess  an  exact  knowledge  of  the  topographic  relations  of  this 
region  and  especially  of  the  situation  of  the  points  of  origin  of  the  lumbar  and 
sacral  nerves  from  the  cord,  as  compared  with  the  vertebrae  or  the  points  of  exit 
of  the  nerve  roots  from  the  spinal-cord  canal.     The  following  plates  will  serve 

for  orientation.  i        i     i  ^     j 

The  limits  of  the  conus  terminalis  have  not  yet  been  very  sharply  defined. 


Fig.  371.-The  lower  end  of  the  vertebral  column  and  its  topographic  relation  to  the  lum- 
bar and  sacral  cord,  and  to  the  origins  and  exits  of  the  lumbar  and  sacral  ner>es  The  double 
lined  portion  represents  the  conus  terminalis,  according  to  Raymond  s  definition  (see  the  text) 
to  which  is  attached  the  fllium  terminale.  Between  it  and  the  wall  of  the  ,^,eytebral  canaMth^ 
part  in  white)  the  cauda  equina  passes.  The  upper  horizontal  lines  in^'cate  the  heights  at  which 
the  nerve  roots  spring  from  the  spinal  cord:  and  the  lower  horizontal  lines  c^onnected  with  Uie 
upper  ones  by  means  of  vertical  lines  indicate  the  exits  of  the  exjrresponding  roots  from  the^^er^ 
tical  column.  The  vertical  lines  thus  represent  the  lengths  of  the  separate  roots  of  the  cauda 
equina  (after  Raymond  i). 

Eaymond  puts  its  upper  borders  sufficiently  high  to  include  the  ceiiters,  or  the 
medullary  origins  of  the  last  three  sacral  nerves.  Such  delimitation  conforms 
both  with  the.  requirements  of  descriptive  anatomy — i.  e.,  with  the  boundiiries 
of  the  actual  wedge-shaped  terminal  portion  of  the  spinal  cord— and  with  those 
of  clinical  experience— i.  e.,  the  clinical  picture  of  a  lesion  of  the  second  lumbar 
vertebra. ■'     In  lesions  of  the  conus  terminalis,  both  motility  and  sensibility  ot 

1  Eaymond,  "  Sur  les  affections  de  la  queue  de  cheval,"  NouveUe  inconof/rapkie  de  la 
Salpelriere,  1895,  Nos.  1  and  2.  v       i-  .i,     r^  t„,. 

2  ASchiff  (from  Schrotter's  Clinic),  "A  case  of  Hematomyeha  of  the  Conus  ier- 
minalis,"  Zeits.  f.  klin.  Med.,  1896,  vol.  xxx.,  p.  87. 


938 


EXAMIXATION  OF  THE  NERVOUS  SYSTEM. 


the  lower  extremities  are  practically  intact,  but  the  functions  of  the  bladder  and 
rectum  are  disturbed,  and  there  is  an  anesthesia  of  the  perineum,  the  inferior 


DM 


LIV 


Fig.  372.— Topography  of  the  cauda  equina,  showing  its  relation  to  the  vertebral  column  and 
to  the  lower  end  of  the  spinal  cord  f%  natural  size).  Schultze  gives  the  following  explanation: 
"  The  lower  end  of  the  lumbar  enlaf.ffement  is  found  at  the  level  of  the  flr.-t  lumbar  vertebra  : 
the  third  lumbar  nerve  (heavy  black  linei.  with  its  crural  and  obturator  fibers,  arises  at  different 
levels,  as  indicated,  in  the  upper  part  of  the  lumbar  enlargement,  according  to  Gerlach  between 
the  spinal  processes  of  the  eleventh  and  twelfth  dorsal  vertebrae, a  height' which,  according  to 
the  original  investigations  of  SchieflFerdecker,  corresponds  to  the  lower  part  of  the  bodv  of  "tlie 
twelfth  dorsal  vertebra"  (after  Schultze  and  Schiefferdecker ').  The  position  of  the  couus 
terminalis  is  higher  here  than  in  Fig.  371. 

gluteal  region,  and  of  a  zone  upon  the  back  of  the  thigh,  which  is  supplied  by 
the  posterior  femoral  cutaneous  nerve.     This  does  not  entirely  coincide  with  the 

^  Schultze,  "  Zur  Differentialdiagnose  der  Yerletziingen   der  Cauda  equina  und  der 
Lendenanschwellung,"  D.  Zeitschr.  f.  Nenenheilk.,  1894,  vol.  v.,  p.  247. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  939 

topography  of  sensibility  disturbance  pictured  upon  p.  923.  A  lesion  of  the 
lower  part  of  the  cauda  equina  will,  of  course,  produce  a  similar  clinical  picture. 
Fig.  372  shows,  according  to  Schultze,  that  still  other  clinical  pictures  can 
be  produced  by  lesions  of  the  cauda  equina,  as  well  as  by  lesions  of  the  lowest 
part  of  the  spinal  cord.  It  is  quite  plain  from  the  drawing  that  the  lesion  A,  at 
the  most  inferior  portion  of  the  spinal  cord,  and  the  lesion  B,  at  the  height  of  the 
third  lumbar  vertebra,  which  injures  the  cauda  equina,  will  produce  the  same 
motor  and  sensory  disturbances  of  the  sciatic  region  and  will  not  involve  the 
crural  and  obturator  region  (II.-IV.).  A  hyperesthesia  of  the  crural  region,  or  a 
very  slight  initiatory  involvement  of  it,  may  occur  in  either  case,  because  the 
lesion  A  (represented  by  shading)  affects  the  spinal  cord  itself  above  the  origin 
of  the  crural  fibers,  whereas  the  lesion  B  involves  the  same  fibers  laterally  and 
lower  down  at  the  height  of  the  third  lumbar  vertebra. 

4.  THE  VESICAL  AND  RECTAL  FUNCTIONS. 

The  Mechanism  of  the  Vesical  and  Rectal  Fonctions  under  Physiologic  and 
Pathologic  Conditions. 

It  is  difficult  to  understand  the  vesical  and  rectal  disturbances 
occurring  in  diseases  of  the  nervous  system,  since  our  knowledge  of 
the  physiologic  evacuation  of  the  bladder  and  rectum  is  still  quite 
incomplete  and  contains  much  that  is  hypothetic.  In  studying  this 
subject  we  are  confronted  by  a  special  difficulty,  because  the  old  teach- 
ins:  that  the  central  mechanism  for  the  vesical  and  rectal  functions  is 
situated  in  the  spinal  cord  has  been  overthrown.  The  prevailing 
opinion  at  present,  based  upon  the  work  of  Goltz,  Freusberg,  Ewald,^ 
and  particularly  upon  the  recent  work  of  L.  R.  Miiller,^  inclines  to  the 
view  that  the  central  mechanism  for  the  vesical  and  rectal  functions  is 
situated  in  the  sympathetic  system.  Since  this  question  has  not  been 
absolutely  decided,  but  requires  further  investigation  (which  may  show 
that  both  conceptions  possibly  contain  a  portion  of  the  truth),  the  only 
thing  to  be  done  is  to  give,  first,  the  old,  and  then  the  newer,  teaching, 
and  to  conclude  with  a  few  remarks  as  to  the  possibility  of  combining 
the  two  theories  (see  p.  947). 

I.  The  Old  Conception  of  the  Vesical  and  Rectal  Func- 
tions, in  which  the  Central  Mechanism  was  Supposed  to 
be  in  the  Spinal  Cord. — The  Physiologic  3Iechanism  of  the  Vesical 
Functions. — The  following  diagram  of  the  innervation  of  the  bladder 
(Fig.  373)  should  be  of  assistance  in  comprehending  the  clinical  fea- 
tures of  the  question  : 

Bl  represents  the  bladder.  The  detrusor  muscle  is  represented  by  a 
thick  line,  the  mucous  membrane  by  a  dotted  line.  The  physiologic 
sphincter,  which  is  composed  of  the  different  voluntary  muscles  sur- 
rounding the  urethra  ^  (Krause's  musculus  urethralis)  is  represented  by 
two  circularcross-sections  at  both  sides  of  the  bladder  orifice,  6'. 

The  points  a,  b,  c,  correspond  to  the  so-called  bladder  centers,  as 
they  have  been  thus  far  usually  conceived. 

^  Pflugei''s  Arch.,  vols,  viii.,  is.,  Ixiii. 
^  Zeits.  J.  Nervenheilk.,  vol.  xxi.,  parts  1  and  2. 

^  The  so-called  "  smooth  sphincter "  probably  plays  no  important  physiologic  func- 
tion. 


940 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


a  corresponds  to  a  sensory  cell,  or,  better  expressed,  a  cell  in  con- 
nection with  the  sensory  terminal  arborizations  of  the  tract  a  to  a' ;  b 
represents  a  motor  cell  for  the  sphincter ;  c  represents  a  motor  cell  for 
the  detrusor,  a  should  be  considered  as  connected  with  the  mucous 
membrane  by  means  of  the  sensory  tract  a  to  a'  ;  h  with  the  sphincter 
by  the  motor  tract  h  to  h' ;  and  c  with  the  detrusor  by  the  motor  tract 
c  to  c'. 

The  normal  bladder  reflex  takes  place  in  this  way  :  When  the  blad- 
der fills,  the  mucous  membrane  stimulates  the  tract  a'  to  a.     From  a 


£rtUfi.  Cortex. 


J) 


GcuigUon  cells  <L 

ofthecuitiirier 
horn. 


■^bdommaZ 
fofessure 


Fig.  373.— Scheme  for  the  physiologic  mechanism  of  the  bladder  functions. 


the  stimulation  proceeds  to  the  sphincter  center,  6,  and  from  there,  in 
the  form  of  a  tonic  innervation,  to  the  sphincter,  h' ,  w^hich  then  shuts 
the  bladder  more  powerfully.  When  the  filling  increases  still  further, 
until  a  certain  degree  of  distention  is  reached,  a  more  intense  stimula- 
tion a'  to  a  proceeds  from  a  even  to  c,  and  finally  causes  a  contraction 
of  the  detrusor.     The  bladder  will  then  be  emptied.     The  normal  blad- 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  941 

der  reflex,  therefore,  consists  of  two  acts  :  the  closing  reflex  and  the 
emptying  reflex.  We  have  included  in  our  diagram  the  longitudinal 
tracts,  which  have  an  influence  upon  emptying  the  bladder ;  they  have 
been  demonstrated  both  physiologically  and  clinically,  ascending  and 
descending  within  the  spinal  cord.     They  are  : 

1.  The  tract  a  to  A,  a  sensory  tract  leading  to  the  brain,  which 
informs  us  how  full  the  bladder  is. 

2.  The  tract  B  b  b' ,  subserving  the  voluntary  innervation  of  the 
sphincter.  As  we  cannot  voluntarily  innervate  the  detrusor,  it  prob- 
ably does  not  possess  an  analogous  tract. 

3.  The  tract  /9  to  6,  which  inhibits  the  tonus  of  the  sphincter. 
Since  there  is  no  voluntary  detrusor  tract,  /?  6  presides  over  the  volun- 
tary emptying  of  the  bladder. 

4.  The  tract  D  to  d,  inserted  upon  the  left  of  the  annexed  diagram, 
comes  from  the  brain  and  innervates  the  abdominal  pressure,  therefore 
assisting  in  forced  voluntary  emptying. 

Voluntary  emptying  of  the  bladder  takes  place  normally  by  means 
of  these  longitudinal  tracts.  For,  after  we  have  become  cognizant  of 
the  bladder  distention  by  means  of  the  tract  a'  to  a,  we  voluntarily 
relax  the  sphincter  by  an  innervation  along  Bbb' .  This  gives  free  scope 
to  the  reflex  innervation  of  the  detrusor  by  the  path  a'  ace'.  Under 
some  circumstances,  when  emptying  the  bladder  is  urgent,  abdominal 
pressure  is  called  in  to  assist  by  way  of  the  tract  D  d. 

It  should,  of  course,  be  understood  that  the  longitudinal  tracts  are 
bilateral  ^  and  that  their  radiations  are  in  connection  with  both  hemi- 
spheres of  the  brain.  One  hemisphere  would,  therefore,  be  sufficient  to 
care  for  the  voluntary  function  of  the  bladder  (as  in  the  case  of  the 
muscles,  p.  829,  Fig.  318). 

Functions  of  the  Bladder  in  Cerebral  Affeciions. — Since  only  one 
hemisphere  is  involved  ordinarily  in  diseases  of  the  brain  and,  therefore, 
not  all  the  fibers  passing  from  the  brain  to  the  spinal  cord  are  injured, 
and  since  the  long  tracts  to  the  bladder  are  bilateral,  lesions  of  the 
long  tracts  do  not  usually  produce  disturbances  of  the  bladder  in  cere- 
bral diseases,  except  from  affections  of  the  medulla  and  the  pons.  In 
the  latter  case,  on  account  of  the  intimate  proximity  of  the  bilateral 
tracts,  results  are  like  those  produced  by  lesions  of  the  spinal  cord  (see 
below). 

Bilateral  cerebral  lesions,  on  the  contrary,  may  lead  to  disturbances 
in  the  bladder  function,  especially  if  they  are  diffused.  This  is  because 
the  bladder  tracts  are  not  arranged  in  the  brain  compactly  in  a  bundle, 
but  seem  to  spread  out  diffusely.  These  disturbances  are  ordinarily 
associated  with  disturbances  of  consciousness.  An  unconscious  pei'son 
allows  his  urine  to  escape  because  he  has  no  will-power  and  no  sensation. 
He  is  obliged  to  trust  everything  to  the  reflexes.  The  bladder  reflex  may 
be  entirely  unaff*ected,  so  that  from  time  to  time  the  bladder  is  emptied 
quite  normally,  even  though  unconsciously  and  involuntarily.     Quite 

^  For  the  sake  of  simplicity  our  diagram  shows  only  a  unilateral  arrangement  of  the 
tract. 


942  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

severe  conditions  of  unconsciousness  may  lead  to  retention  of  the  urine, 
with  an  eventual  overflow  of  the  overfilled  bladder  (paradoxic  inconti- 
nence). These  cases  are  most  readily  explained,  as  in  spinal-cord 
affections  (see  below),  by  assuming  loss  of  inhibition  of  the  sphincter 
reflexes.  The  bladder  may  be  similarly  affected  by  brain  injury  in  any 
serious  illness,  such  as  typhoid  fever,  etc. 

Functions  of  the  Bladder  in  Diseases  of  the  Spinal  Cord. — The  fol- 
lowing possibilities  are  conceivable  : 

1.  The  bladder  center  itself  is  injured.  Both  the  sphincter  and  the 
detrusor  reflexes  are  lost.  The  bladder  behaves  like  a  mere  bag.  The 
urine  trickles  continually,  of  course,  only  after  the  bladder  has  been  more 
or  less  moderately  distended,  as  a  certain  pressure  of  the  urine  is  required 
to  open  the  urethra.  This  is  a  condition  of  incontinence,  with  a  more 
or  less  marked  retention.  Sounding  by  means  of  a  catheter  proves  the 
existence  of  an  actual  bladder  paralysis.  The  opposition  of  the 
sphincter  is  lost,  and  the  contents  of  the  bladder  can  be  quite  easily 
expressed  by  manual  pressure  upon  the  lower  abdominal  region. 

2.  The  bladder  center  is  intact,  the  lesion  is  located  above  the 
center,  and  only  the  long  tracts  which  lead  to  the  brain  are  injured. 
The  influence  of  volition  upon  emptying  the  bladder  will  be  more 
or  less  completely  lost.  If  the  injury  to  the  long  tracts  is  complete 
(and  this  is  the  usual  effect  of  any  pronounced  focal  lesion  of  the  spinal 
cord,  everything  being  so  crowded  together  in  a  narrow  cross-section), 
the  patient  will  not  be  conscious  of  any  distention  of  the  bladder,  nor 
possess  any  voluntary  influence  over  it.  One  would  naturally  suppose 
that  at  least  the  reflex  activity  of  the  bladder  would  be  normal ;  but 
this  is  only  rarely  true.  To  be  sure,  in  exceptional  cases  of  a  cross- 
lesion  of  the  spinal  cord  above  the  so-called  bladder  center,  the  patient 
will  empty  the  full  bladder,  from  time  to  time,  in  a  perfectly  normal 
fashion,  but  entirely  involuntarily.  Perhaps  this  type  of  disturbance 
occurs  only  in  the  less  complete  interruptions  of  conduction.  But  much 
oftener  these  patients  suffer  from  urinary  retention ;  the  bladder  becomes 
more  and  more  distended ;  the  sphincter  finally  gives  way  ;  and  the 
urine  trickles  out.  Such  a  condition  of  incontinence  with  an  overfilled 
bladder  is  called  paradoxic  incontinence.  The  distinctive  appearance 
of  decided  retention,  which  is  always  much  more  pronounced  in  these 
cases  than  in  those  under  the  first  head,  is  to  be  explained  by  assuming 
that  in  severe  cross-lesions  of  the  spinal  cord  above  the  bladder  center, 
the  tract  inhibiting  the  sphincter  reflex  (/?  b,  Fig.  373,  p.  940)  is 
injured  as  well  as  the  other  long  tracts.  Analogous  to  the  increase  of 
tendon  reflexes  usually  accompanying  these  cases,  the  tonus  of  the 
sphincter  is  naturally  accentuated  enough  to  overcome  the  power  of  the 
detrusor,  and  retention  consequently  ensues. 

3.  The  lesion  is  situated  below  the  bladder  center.  Since  both  sen- 
sory and  motor  fibers  for  the  bladder  run  down  from  the  bladder  center 
within  the  spinal  cord  for  a  short  distance  before  they  pass  out,  such  a 
focal  lesion  will  partially  interrupt  the  reflex  arc  of  the  bladder.  The 
eff'ect  must,  therefore,  be  similar  to  that  of  a  lesion  of  the  bladder 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  943 

center  itself  (see  1,  p.  942).  As  we  do  not  know  just  where  the 
motor  and  sensory  bladder  nerves  leave  the  spinal  cord,  it  might  be 
conceivable  that,  below  this  spot,  an  area  in  the  spinal  cord  might  exist 
injury  of  which  would  not  aifect  the  bladder  function  because  the 
bladder  nerves  would  already  have  left  the  spinal  cord.  Clinical  expe- 
rience, however,  points  to  the  improbability  of  such  a  supposition,  and 
the  diagram  (Fig.  365,  p.  925),  representing  a  deep  exit  of  the  motor 
nerves  of  the  bladder,  should,  therefore,  be  considered  as  accurate. 
The  statements  of  physiologists  in  regard  to  position  of  the  "  bladder 
center"  are  so  contradictory,  and  the  physiologic  methods  of  examining 
this  question  are  so  ambiguous,  that  we  must  provisionally  depend  upon 
clincal  experience.  The  latter  suggests  that  the  human  bladder  inner- 
vation can  be  injured  by  a  lesion  even  at  the  end  of  the  spinal  cord. 

The  Bladder  Functions  in  Peripheral  Affections  of  the  Bladder 
Nerves. — The  function  of  the  bladder  is  rarely  disturbed  in  these 
affections.  In  any  given  case  the  type  of  disturbance  can  be  easily 
explained  by  consulting  the  diagrams. 

Another  Representation  of  the  Bladder  Functions. — The  preceding  diagram 
should  be  regarded  as  wliolly  theoretic.  It  depends  upon  the  unproved 
assumption  of  a  circumscribed  bladder  function  in  the  spinal  cord.  (See  p.  928 
et  seq.  for  arguments  against  such  an  assumption.)  This  assumption  is  based 
upon  the  fact  that  complete  paralysis  of  the  bladder  (p.  942,  No.  1)  has  been 
proved,  both  experimentally  and  clinically,  to  occur  with  disturbances  in  the 
territory  of  the  lowest  part  of  the  spinal  cord.  This  fact  may,  however,  be  per- 
fectly explained  in  another  way  by  assuming  that  the  importance  of  the  lumbar 
sacral  cord  for  the  bladder  functions  depends  upon  the  compact  arrangement  of 
the  sensory  and  motor  fibers  of  the  bladder  at  their  exit  there  from  the  spinal  cord; 
whereas,  higher  up,  they  perhaps  spread  out  diffusely  through  a  large  portion 
of  the  longitudinal  and  cross-sections  of  the  cord.  Although,  without  doubt, 
the  shortest  reflex  arc — i.  e.,  the  shortest  connection  between  the  sensory  and 
motor  bladder  nerves — is  localized  in  the  lowest  portion  of  the  spinal  cord,  this 
does  not  necessarily  exclude  the  circuit  of  the  reflex  arc  from  reaching  high  up 
into  the  spinal  cord  (perhaps  even  to  the  brain).'  The  pathologic  afi'ections  of 
the  bladder  functions  can  be  explained  as  well,  and  perhaps  more  readily,  by 
Fig.  374  than  by  Fig.  373,  provided  that  we  make  such  an  assumption  and  con- 
sider the  mechanism  of  the  bladder  functions  analogous  to  the  mechanism  of  the 
cutaneous  reflexes  (see  p.  779  and  Fig.  368,  p.  928).  In  Fig.  337  we  need  to 
assume  only  that  the  reflex  arcs  for  the  detrusor  reach  high  up  in  the  spinal  cord, 
or  even  as  high  as  the  brain;  whereas,  the  sphincter  reflex  takes  place  princi- 
pally by  shorter  tracts  (in  the  lumbar  enlargement).  This  conception  readily 
explains  the  occurrence  of  retention  of  urine  (paradoxic  incontinence)  in  all 
complete  cross-lesions  situated  above  the  lumbar  enlargement,  for  the  detrusor 
reflex  would  then  be  injured  more  than  the  sphincter  reflex.  This  conception  does 
not  need  to  assume  a  definite  center  to  explain  the  fact  that  severer  bladder 
disturbances  result  from  lesions  of  the  lumbar  enlargement ;  for,  according  to 
this  assumption,  a  lesion  here  affects  the  entire  compact  centripetal  and  centrif- 
ugal bladder  innervation.  Again,  it  explains  most  readily  the  variations  of  the 
less  typical  bladder  affections  in  which  the  bladder  fibers  for  the  different  func- 
tions must  be  assumed  to  be  variously  affected;  for,  when  we  represent  the  reflex 

^  The  theory  that  the  reflex  tracts  of  the  bladder  reach  up  into  the  brain  agrees 
with  the  fact  that  the  bladder  functions  are  not  necessarily  destroyed  by  focal  lesions  of 
the  brain,  as  the  tracts  in  question  must  be  situated  bilaterally  in  the  brain,  while  most 
cerebral  lesions  only  aflect  one  side.  Moreover,  the  exceptional  cases  where  cerebral 
lesions  do  affect  the  bladder  functions  are  most  easily  explained  by  this  assumption. 


944 


EXAMINATION  OF  THE  NERVOUS  SYSTE3L 


<3 


t^^ 


r^ 


^ 


>^ 


apparatus  of  the  bladder  (as  in  Fig.  374)  distributed  through  the  entire  spinal 
cord  and  even  to  a  part  of  the  brain,  it  becomes  perfectly  natural  to  conceive  that 
the  bladder  mechanism  can  be  injured  in  manifold  ways — as  is  especially  the 
case  in  system  diseases  like  tabes. 

So  far  as  the  voluntary  control  of  the  bladder  is  concerned,  Fig.  374  should 
be  regarded  in  the  same  way  as  Fig.  373,  and  should  be  completed  by  adding  the 
voluntary  tracts  for  the  closure  and  relaxation  of  the  sphincter,  as  well  as  those 
innervating  the  abdominal  pressure. 

We  might  add  that  the  principle  of  the  bladder  innervation  is  not  influ- 
enced by  assuming  in  both  Figs.  373  and  374  that 
parts  of  the  reflex  arc  run  in  sympathetic  tracts. 

Mechanism  of  Emptying  the  Rectum  under  Physi- 
ologic and  Pathologic  Conditions. — The  emptying  of  the 
rectum  is  accomplished  in  the  same  way  as  the  empty- 
ing of  the  bladder.  With  the  proper  changes,  what 
has  been  said  about  the  latter  applies  to  the  rectum. 
The  old  conception  of  a  rectal  center  localized  in  the 
liimbar  enlargement  of  the  spinal  cord  (see  Fig.  373) 
becomes  less  probable  when  we  assume  that  the  reflex 
arcs  of  the  rectum  (like  those  of  the  bladder  in  Fig. 
374)  run  far  up  into  the  spinal  cord,  and  perhajDS  even 
into  the  brain.  Either  theory  will  explain  (as  with  the 
bladder)  the  fact  that  lesions  of  the  lumbosacral  cord 
produce  an  actual  paralysis  of  the  rectum;  whereas 
lesions  higher  up  cause  for  the  most  part  a  decided 
retention  of  feces.  Clinically,  however,  the  picture 
of  fecal  accumulation  caused  by  paralysis  of  the  de- 
trusor reflex  or  by  increase  of  the  sphincter  tonus  can 
be  altered  if  the  peristalsis  of  the  upper  part  of  the 
gut,  which  is  not  under  the  direct  control  of  the  spinal 
cord,  is  sufiicient  to  expel  the  fecal  masses  from  the 
rectum  in  spite  of  the  retention.  On  the  other  hand, 
the  picture  of  sphincter  paralysis  in  the  rectum  may 
be  modified  and  much  less  noticeable  if  the  fecal  mas- 
ses are  hard  enough  to  remain  in  the  rectum,  despite 
a  weak  or  absent  closure  of  the  sphincter. 

II.  The  New  Theory  of  Sympathetic  Vesical, 
Rectal,  and  Ejaculatory  Centers  {Goltz,  Freusberg, 
Ewald,  L.  R.  Mi( Her). —The  theory  of  the  spinal  local- 
ization of  the  vesical  and  rectal  centers  has  long  since 
been  shaken  by  the  experiments  of  Goltz,  Freusberg, 
and  Ewald.^  These  authors  demonstrated  that  in 
dogs,  after  the  removal  of  the  lowermost  portion  of 
the  spinal  cord,  which  presumably  contained  the 
vesical  and  rectal  centers,  the  primarily  disturbed 
vesical  and  rectal  functions  became  normal  after  a  time.  The  theory  of  the 
spinal  localization  of  the  centers  for  the  vesical,  rectal,  and  ejaculatory  functions 
had  become  so  deeply  rooted  during  the  preceding  fifty  years,  however,  that  it 
continued  to  dominate  physiologic,  as  well  as  clinical,  teaching.  Since  L.  R. 
Miiller's  recent  important  experiments, •!  have  completely  confirmed  those  of 
Goltz' s  school  and  shown  that  the  centers  for  the  vesical  and  rectal  functions  and 
for  the  male  sexual  act  are  situated  outside  of  the  spinal  cord  in  the  sympathetic 
system,  we  must  determine  to  what  extent  our  clinical  ideas  should  be  revised. 

The  experimental  results  attained  by  Miiller  are  essentially  as  follows  :  If 
the  spinal  cord  of  the  dog  be  divided  above  the  sacral  segments,  or  if  the  sacral 
segments  be  extirpated,  the  result  is  practically  the  same.     At  first  there  is  reten- 

'  Pjluger's  Archiv.,  vol.  viii.,  ix.,  and  Ixiii. 

^  Zeits.f.  NervenheilL,  vol.,  xxi.,  parts  1  and  2. 


Mucous 
(Shhincler 


Fig.  374.— Scheme  of  blad 
der  functions  with  superim 
posed  reflex  arcs. 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  945 

tion  of  the  urine  and  of  the  feces.  The  bladder  may  be  mechanically  evacuated 
by  pressure,  and  if  this  is  not  done  regularly  the  bladder  overflows  (paradoxic 
incontinence).  After  a  time,  however,  this  urinary  and  fecal  retention  disappears 
and  is  replaced  by  periodic  evacuations  differing  from  the  normal  only  in  that 
they  are  involuntary.  Since  this  re-establishment  of  periodic  evacuations  occurs 
even  after  complete  extirpation  of  the  lumbar  and  sacral  cord,  the  central 
mechanism  for  these  functions  evidently  must  be  situated  outside  of  the  spinal 
cord  in  the  sympathetic  system.  Experiments  in  reference  to  the  localization  of 
the  sexual  functions  in  male  dogs  led  to  similar  results.  After  the  extirpation 
of  the  sacral,  and  of  a  great  portion  of  the  lumbar  cord,  the  dogs  are  capable 
not  only  of  erection,  but  also  of  ejaculation.  The  center  for  this  function  must, 
consequently,  also  lie  outside  of  the  spinal  cord.  In  these  experiments,  how- 
ever, the  lesion  of  the  spinal  cord  necessarily  produces  certain  changes  of  the 
functions.  Extirpation  of  the  lowermost  portion  of  the  spinal  cord,  or  simply 
transverse  section,  is  followed  by  a  complete  loss  of  the  influence  of  the  will  upon 
the  evacuation  of  the  bladder  and  rectum,  and  such  evacuation  becomes  purely 
automatic,  as  may  easily  be  recognized  from  the  condition  of  the  animal.  The 
animals  are,  of  course,  anesthetic  for  the  process  of  evacuation.  Immediately 
after  extirpation  of  the  sacral  cord  the  anus  gapes  from  paralysis  of  the  striated 
sphincter,  but  it  gradually  becomes  closed,  evidently  as  a  result  of  the  vicarious 
action  of  the  involuntary  musculature  of  the  internal  sphincter.  The  striated 
sphincter,  however,  remains  paralyzed,  and  the  anal  reflex  (p.  778)  is  perma- 
nently destroyed.  If  the  spinal  cord  is  simply  divided  above  the  sacral  segment 
the  tonus  of  the  sjihincter  and  the  anal  reflex  are  maintained  ;  in  fact,  both  may 
even  be  accentuated.  The  voluntary  perineal  muscles  which  assist  in  the  volun- 
tary closure  of  the  bladder  are  possibly  affected  in  the  same  manner  as  the 
external  sphincter  of  the  anus,  although  Miiller  makes  no  definite  statements  in 
this  connection.  They  are  paralyzed  by  destruction  of  the  sacral  cord,  but  the 
closure  of  the  bladder  is  effected  vicariously  by  the  involuntary  sphincter.  The 
experimental  results  seem  to  indicate  that  reflex  erection  is  associated  with  the 
maintenance  of  the  lowermost  portion  of  the  sacral  cord,  but  that  psychic  erection 
is  dependent  upon  the  maintenance  of  the  lower  dorsal  cord.  The  lower  sacral 
cord  consequently  seems  to  receive  the  sensory  fibers  from  the  penis,  and  to  give 
rise  to  the  genital  reflex,  while  the  centrifugal  fibers  from  the  brain  to  the  sexual 
centers  evidently  leave  the  spinal  cord  in  the  lowermost  dorsal  segment.  Semen 
may  be  discharged  even  after  the  destruction  of  the  lowermost  portion  of  the 
spinal  cord,  but  a  vigorous  reflex  ejaculation  is  dependent  upon  its  integrity — 
i.  e.,  upon  the  innervation  of  the  voluntary  muscles  (bulbocavernosus,  etc.). 

From  these  experimental  data  it  is  easy  to  assume  :  (1)  That  the  actual 
centers  for  the  evacuation  of  the  bladder  and  rectum,  as  well  as  those  for  erection 
and  ejaculation,  are  situated  outside  of  the  spinal  cord  in  the  sympathetic  system; 

(2)  that  motor  fibers  reach  this  sympathetic  apparatus  through  the  spinal  cord 
by  means  of  the  rami  communicantes,  from  the  lumbar  and  sacral  segments;  and 

(3)  that  the  motor  fibers  for  the  striated  muscles  of  the  pelvic  floor,  which  effect 
the  voluntary  closure  of  the  bladder  and  rectum,  arise  directly  from  the  spinal 
cord,  and  have  nothing  to  do  with  the  sympathetic.  The  sensory  impulses  to  the 
brain  are  necessarily  conducted  by  the  spinal  cord.  According  to  this  conception 
the  only  part  played  by  the  spinal  cord  in  the  vesical  and  rectal  fiinctions  is  the 
conduction  of  sensory  impulses  to  the  brain  and  of  voluntary  cerebral  impulses 
for  the  innervation  and  relaxation  of  the  striated  vesicaf  and  rectal  sphincters 
and  for  the  innervation  of  the  abdominal  tension. 

.  Supported  by  his  own  investigations,  as  well  as  by  those  of  Ilehfisch,i  Miiller 
completely  repudiates  the  old  theory  of  the  spinal  centers  for  the  bladder,  rectum, 
and  ejaculation,  and  constructs  the  following  diagram  (Fig.  375)  for  the  explana- 
tion of  the  clinical  symptoms  in  patients  with  affections  of  the  spinal  cord,  in 
which  only  the  sympathetic  plexus  is  to  be  regarded  as  a  central  mechanism. 
According  to  this  new  theory  the  clinical  symptoms  in  the  human  subject  are 

*  Virchow's  Archiv,  vol.  clxi. 
60 


946 


EXAMINATION  OF  THE  NERVOUS  SYSTEM. 


easily  explained  if  we  assume,  with  Miiller,  that  in  all  destructive  lesions  of  the 
spinal  cord,  whether  they  involve  the  sacral,  the  lumbar,  or  higher  regions,  the 
primary  disturbance  is  always  urinary  and  fecal  retention,  followed  by  paradoxic 
incontinence,  that  typical  periodic  evacuations  are  always  established  later,  and 
that  permanent  disturbances  in  affections  of  the  spinal  cord,  like  the  initial  reten- 
tion and  paradoxic  incontinence,  are  due  simply  to  the  absence  of  sensation  as 
well  as  of  the  voluntary  components  of  evacuation.  Further  investigations  are 
necessary,  however,  to  determine  whether  these  suppositions  are  really  in  accord 
with  clinical  observations.  The  peculiar  vesical  disturbances  in  tabes  dorsalis  are 
certainly  easy  of  explanation  by  Miiller' s  theory,  even  without  assuming,  as  does 
Miiller,  that  in  these  cases  the  tabes  is  localized  in  the  sympathetic.  Also 
according  to  Miiller' s  theory  the  sensory  disturbances  in  tabes  are  sufficient  to 
explain  both  the  retention  and  the  slight  phenomena  of  incontinence  in  these 


Iliohypogastric  nerve. 
Sympatlietic  trunk. 


Eami  communieantes. 


Hypogastric  nerve. 
Hypogastric  plexus. 

Nervi  erigentes. 

Pudic  nerve. 

Seminal  vesicle. 

Int.  sphincter  of  bladder. 

Prostate. 

Dorsal  nerve  of  penis. 


M.'"perinEei  profund. 
(compressor  urethrse). 


First  lumbar  vertebra. 
Conus  terminalis. 


Inferior  mesentric  gan- 
glion. 
Hypogastric  ganglion. 

Hemorrhoidal  plexus. 


Hemorrhoidal  nerve. 
Perineal  nerve. 


M.  sphincter  ani  ext. 
M.  sphincter  ani  int. 


Fig.  375. — Diagram  of  the  rectal  and  vesical  innervation  (according  to  Miiller). 

patients,  since  the  regulating  influence  of  the  spinal  cord  and  brain  is  more  or 
less  impaired  as  a  result  of  the  disturbed  vesical  sensibility.  The  sexual  disturb- 
ances in  patients  with  aifections  of  the  spinal  cord  may  also  be  easily  explained 
by  Miiller' s  diagram  if  we  remember  that  the  lesion  hinders  the  transmission  of 
the  psychic  excitations  from  the  lower  dorsal  cord  to  the  sympathetic  sexual 
center,  and  that  variations  of  the  reflex  irritability  of  the  lowermost  portions  of 
the  cord  by  spinal  lesions  may  increase  or  diminish  the  reflex  components  of 
erection  or  ejaculation  (see  above).  The  fact  that  patients  with  destruction  of 
the  sacral  cord  and  complete  motor  and  sensory  paralysis  of  the  lower  half  of  the 
body  are  still  capable  of  procreation  (examples  of  which  are  given  by  Miiller)  is 
best  explained  by  the  new  theory. 

It  must  be  said  that  Miiller's  theory  contains  much  that  is  plausible  in  refer- 
ence to  the  non-striated  musculature  of  the  bladder  and  rectum,  the  spinal  inner- 
vation of  which,  according  to  the  old  theory,  always  seemed  rather  dubious.  His 
experiments  also  seem  to  be  quite  convincing,  but  the  writer,  nevertheless,  believes 
that  they  are  not  entirely  free  from  objection.  For  instance,  these  experiments, 
as  well  as  those  of  Goltz  and  Ewald,  have  not  certainly  demonstrated  that  the 


EXAMINATION  OF  THE  NERVOUS  SYSTEM.  947 

Tesical  and  rectal  functions  are  carried  on  with  the  same  vigor  and  precision  after 
the  destruction  of  the  sjjinal  cord  as  they  were  before,  that  the  strength  of  the 
involuntary  sphincters  and  detrusors  does  not  also  suffer,  and  that  the  degree  of 
distention  of  the  bladder  and  rectum  prior  to  evacuation  is  the  same  without  the 
influence  of  the  spinal  cord  as  it  is  with  it.  If  we  assume,  according  to  the  old 
theory  (p.  943  et  seq.),  that  the  reflex  mechanism  of  the  bladder  and  of  the  rectum 
consists  of  a  number  of  superimposed  reflex  arcs,  it  becomes  quite  plausible  to 
conclude  that  the  lowermost  of  these  arcs  is  situated  in  the  sympathetic,  and  that 
it  is  associated  with  spinal,  and  even  cerebral,  reflex  arcs  in  such  a  manner  that 
in  case  of  necessity  the  sympathetic  arc  may  carry  on  these  functions,  but  that 
the  finer  and  more  vigorous  functions  are  possible  only  with  the  co-operation  of 
the  spinal  cord  and  brain.  It  is  possibly  a  verbal  quibble  whether  we  regard  the 
functions  of  the  sympathetic,  of  the  cord,  and  of  the  brain  as  occurring  in  reflex 
arcs,  or  whether  we  assume  that  the  reflex  function  belongs  only  to  the  sym- 
pathetic, and  that  the  higher  functions  of  the  cord  and  brain  are  excluded  from 
this  reflex.  Since  every  nervous  function  proceeds  upon  the  principle  of  a  reflex, 
however,  the  former  supposition  seems  to  be  fully  justified.  If  we  were  called 
upon  at  present  to  decide  between  the  old  theory  of  spinal  centers  for  the  bladder, 
rectum,  and  erection,  and  Miiller's  theory  of  the  localization  of  these  functions  in 
the  sympathetic,  we  should  be  forced  to  give  the  new  theory  the  preference,  since 
it  is  founded  upon  the  results  of  experiment.  It  would  then  be  necessary  to 
give  a  different  explanation  of  clinical  phenomena  from  that  which  has  been 
offered  in  the  past.  By  the  conception  of  superimposed  reflex  arcs,  however,  it 
seems  to  the  writer  that  the  two  theories  may  be  made  to  harmonize.  The  re- 
corded experiments  are  not  sufficient  to  decide  this  question.  The  vesical  and 
rectal  functions  remaining  after  destruction  of  the  spinal  cord  must  be  more 
accurately  tested,  qualitatively  and  quantitatively,  and  this  test  should  be  clinical 
as  well  as  experimental. 

Examining  the  Vesical  and  Rectal  Functions. 

In  •  examining  the  affected  bladder  and  rectal  functions  the  following  points 
should  be  noted : 

1.  Fulness  of  the  bladder  and  of  the  rectum — to  be  determined  by  palpation 
and  percussion  in  the  case  of  the  bladder,  and  by  digital  examination  in  the  case 
of  the  rectum. 

2.  Condition  of  the  sphincter  tonus — to  be  determined  for  the  bladder  by 
attempting  to  expel  its  contents  mechanically  or  with  the  help  of  the  catheter  ; 
for  the  rectum,  by  digital  examination. 

3.  Sensibility  of  the  bladder  and  rectal  mucous  membranes.  The  occurrence 
or  lack  of  a  desire  for  stool  or  urination  will  decide  this  point.  The  sensibility  of 
the  bladder  can  also  be  determined  by  a  catheter  ;  the  rectum  by  a  digital  exami- 
nation.    Pain  or  pressure  (tenesmus)  accompanying  evacuation  should  be  heeded. 

4.  •  Characteristics  of  the  evacuation  :  Absolute  or  partial  retention  of  the  urine 
and  feces  ;  overflow  of  the  filled  bladder  and  the  rectum  with  pronounced  reten- 
tion and  accentuated  sphincter  tonus  (the  real  paradoxic  incontinence)  ;  overflow 
of  the  filled  bladder  and  of  the  filled  rectum  with  moderate  retention  and  absence 
of  sphincter  tonus  (the  real  Madder  and  rectal  paralysis)  ;  involuntary  evacuation 
by  means  of  the  normal  reflexes  {enuresis) ;  possibility  or  impossibilty  of  favoring 
the  reflex  involuntary  evacuation  (incontinence)  or  of  inhibiting  it.  Iviperative 
incontinence  is  the  name  applied  to  a  special  form  of  incontinence  in  which  the 
only  way  to  avoid  an  involuntary  escape  of  urine  or  feces  is  immediately  to  accede 
to  the  very  first  demand  for  evacuation.  The  fact  that  constipation  often  occurs 
without  any  spinal  cord  affection  makes  it  difficult  to  determine  practically  how 
much  clinical  value  is  to  be  assigned  to  the  condition  of  the  rectal  evacuation. 
Therefore,  before  deciding  that  a  constipation  depends  upon  the  spinal  cord,  it  is 
especially  important  to  examine  points  1,  2,  and  3.  In  any  analysis  of  the 
character  of  evacuation  we  must  also  determine  whether  or  not  the  patient  still 
preserves  the  sensation  of  defecation,  being  careful  to  avoid  confusing  this  sensa- 
tion with  that  of  being  wet  or  soiled. 


948  APPENDIX. 


APPENDIX. 

The  Utility  of  Routine  Plans  and  Stamped  or  Printed  Figures  for  Collecting  and 
Tabulating  the  Results  of  Examination. 

ROUTINE  PLANS. 

In  tabulating  the  condition  of  a  patient  for  certain  special  purposes  it  has  been 
found  very  advantageous  at  the  author's  clinic  to  make  use  of  definite  routine 
plans.  In  this  way  nothing  important  in  the  examination  can  be  forgotten,  and 
the  results  will  be  entered  in  a  carefal  and  summarized  fashion.  These  outlines 
have  proved  of  so  much  value,  and  saved  so  much  time,  that  it  seems  worth 
while  to  give  examples  of  them. 

They  are  of  special  value  in  examining  the  nervous  system,  both  because  the 
points  upon  which  the  complete  examination  depends  are  almost  too  numerous  to 
keep  constantly  in  mind,  and  because  it  is  especially  advantageous  in  this  class  of 
diseases  to  group  the  results  of  examination  in  an  intelligent  way  (see  p.  738). 
Of  course  they  are  also  valuable  in  examining  other  affections.  A  few  examples 
will  illustrate  this,  although  it  scarcely  need  be  mentioned  that  the  outlines  may 
be  modified  or  enlarged  at  pleasure,  according  to  the  special  purpose  of  the 
examiner.  The  following  examples  should  in  no  way  be  considered  as  absolute 
standards,  but  merely  as  illustrations  of  what  the  author  has  found  usefiil. 
Enough  space  upon  the  right  side  of  the  text  should  be  reserved  to  enter  the 
necessary  notes.  For  the  nervous  system  it  is  advisable  to  leave  suflicient  space 
for  the  data  upon  both  sides,  to  correspond  to  the  right  and  left  sides  of  the  body. 
Everything  found  to  be  ' '  normal ' '  should  be  marked  so,  and  everji;hing  which 
has  not  been  examined  should  be  marked  "not  examined."  Naturally,  the 
entire  status  cannot  be  settled  in  every  instance  by  filling  out  the  outlines,  because 
some  conditions  often  require  a  more  detailed  description  ;  but  the  outlines  -will 
serve  to  a  certain  extent  as  a  nucleus  for  the  entire  clinical  picture,  about  which 
everything  else  crj^stallizes.  To  prevent  misunderstanding,  the  author  wishes  to 
call  attention  to  the  fact  that  such  outlines  do  not  in  any  way  take  the  place  of 
the  ordinary  extended  descriptions  of  the  symptoms  of  disease.  Experience 
shows  it  to  be  entirely  impractical  to  use  them,  except  for  certain  special  exami- 
nation. 

I.  OUTLINE  FOR  THE  EXAMINATION  OF  THE  DIGESTION. 

Name. 

Date. 

Appetite.  Stool.  Vomiting  (time,  character). 

Retention  in  the  morning.  Pains         (time,  character). 

Chakacteeistics  of  the  Gastric  Contents  :  ^ 

The  Vomitus :  Mucus,  blood,  leukocytes,  meat  fibers,  starch,  sarcinse,  bacteria. 

The  Expressed  Contents  of  the  Empty  Stomach:  Mucus,  blood,  leukocytes,  meat 
fibers,  starch,  residue  of  other  food,  sarcinte,  bacteria. 

The  expressed  contents  of  the  empty  stomach  after  the  tvithdraival  of  the  gastric  con- 
tents on  the  preceding  evening. 

Butyrometric  Gastric  Examination  : 

Amount  of  test-meal   prepared  .    .  c.c,    containing  .    .  gm.   flour   and  .    .  gm. 

butter. 
Amount  of  test-meal  ingested  .    .c.c. 

^  What  is  not  found  should  be  crossed  out. 


APPENDIX.  949 

Expression  after  .    .minutes.     Amount  expressed :    .    .  c.c. 

N 
Acidity  of  the  expressed  meal:  a  .    .  c.c.  —  NaOH  to  10  c.c.  contents  =  g  HCl. 

(   —  -\-    .    .0  HCl  (acid  excess). 
FreeHCU 

(=—..§  HCI  (acid  deficit). 
Lactic  acid  :    [Shaking  with  ether] . 
Eesidue  estimation  :  300  c.c.  water  added. 

N 
Acidity  of  the  expressed  dilution  :  b  =  .    .c.c.  —  NaOH  =    .    .  §  HCl. 

^    .,  300  .   6  3 

Eesidue  x  ^ —  =    .    .    cc* 

a   —    0 

Total  gastric  contents  (including  residue  estimation)  at  the  time  of  the  expression: 

To  =  .    .  c.c. 
Fat  percentage  of  the  ingested  flour  soup  (estimated  butyrometically):  F  =^  .  .  §. 
Fat  percentage  of  the  expressed  flour  soup  (estimated  butyrometically) :  /  =  .  .  %. 

f  I  fSu        f . 

Eesidual  amount  of  meal  :  Su=  -p- To  =  .    .   c.c.    b    ause  ^  =  ^). 

Amount  of  gastric  juice  :  Ma  =^  To  —  Su  =   .    .c.c. 

a  To  „.,  a  Ma 

Acidity  of  the  pure  secretion :  A  =  -—  =    .    .   §  (because  J~  =  ^  )• 

^         .  .  Ma 

Secretion  quotient:   -^  = 

the  soup  which  passes  through  the  intestine 

Motility  quotient : : Tl  '  — 

"'  ^  soup  ingested 

To 
Summary  of  results :    „    yj,    -A-  = 

Examination  of  the  Filtrate  (of  the  test-breakfast, i-  of  the  vomitus). 

Eeaction  to  free  HCl :    .    .    .  Phloroglucinvanillin  .    .    .  Methylviolet  .    .    . 
Eennin  ferment  .    .    .  Tropaolin. 

Starch  digestion  :  Coloration  of  5  c.c.  of  the  gastric  juice  filtrate  after  addi- 
tion of  .    .c.c.  of  normal  iodid  solution. 
This  color  is  blue,^  violet/  red.^ 
Mett'  s  test  of  digestion :  Diameter  of  the  capillary  tubes  .    . 

N 

1.  1  part  juice  +  15  parts  —  HCl  :  2  X    •    •  mm.  (length  of  digested  albumin). 

2.  1    "  +  31      "       "       "    :  2  X    •    •  mm.  (     "  "  " 

Iodoform  Gltjtoid  Test. 

Control  number  of  the  capsules  .    . 

Appearance  of  the  first  iodid  reaction  in  the  saliva  after  .    .  hours. 

Duration  of  the  reaction. 

Eesults  on  a  healthy  individual. 

2.   OUTLINE  FOR  THE   EXAMINATION   OF  CASES  OF  DIPHTHERIA 
AND  OTHER  ANGINAS. 
Name. 
Age. 
Date. 

day  of  illness. 
Hoarseness. 
Stenotic  phenomena. 

Membrane.  No  visible  membrane.  nasal  cavity.  buccal  cavity, 

tonsils.  pillars   of  palate        soft  palate        posterior  pharyngeal  wall. 

^  What  is  not  found  should  be  crossed  out. 


950 

Other  Locations 

Kind  of  membrane  (  Punctiform. 
in  the  throat   ox<  Patchy, 
vicinity  (.Continuous. 


APPENDIX. 


Tenacious. 
Soft. 


Thick. 

Thin. 

Flimsy. 


Firmly  adherent. 
Easily  wiped  oif. 


Grayish. 
Yellowish, 


Parts  surrounding  the  membranes :  Very  red  swollen  not  much 

changed. 
Lymph  glands  :  not         little         much  swollen. 
Angina    lacunaris  (punctiform  membrane   projecting    from   the   depths   of  the 

crypts)         catarrhalis. 


Fig.  376.— Diagram  to  represent  the  localization  of  the  membrane. 

Results  of  lung  examination. 
Albuminuria. 
Bacteriologic  findings. 

Dry  preparation  (from  where?). 

Culture  (from  where  ?).         Upon  what  medium  ? 
Further  notes. 

3.  OUTLINE  FOR  THE  EXAMINATION  OF  THE  BLOOD. 

Name. 

Date. 

Hemoglobin. 

Number  of  erythrocytes. 

Quotient  (hemoglobin  value  of  the  individual  erythrocyte). 

Number  of  leukocytes. 

Morphologic  Investigation. 

(a)  Fresh  Specimen. 

Formation  of  rouleaux. 
Fibrin. 

Blood-platelets. 
Poikilocytosis. 
(h)  Stained  and  Fixed  Specimen. 
Staining  method. 
Erythrocytes. 
Shape. 
Size. 
Tinctorial   peculiarities  (diminished  hemoglogin,  polychromasia,    basophilic 

granulation). 
Nucleated  reds.  Normoblasts.  Megaloblasts. 

Differentiation  of  the  leukocytes.     (How  many  counted  ?         ). 

Per  cent,  of  the  total  number.  Absolute  number  per  c.mm. 

Neutrophilic  (polymorphonuclear) . 

Eosinophilic. 

Large  mononuclear  without  granulations. 

(Transition  forms). 

Lymphocytes. 

Mast  cells. 

Unusual  forms. 

Malarial  parasites,  bacteria. 

Other  observations. 

(If  there  was  an  autopsy)  condition  of  bone-marrow. 


APPENDIX.  951 

4.  OUTLINE  FOR  THE  EXAMINATION  OF  THE  NERVOUS  SYSTEM. 

(a)  General  Outline 
Date. 
Name. 
Sensorium. 
Intelligence. 
Disposition. 
Memory. 

Speech  (for  details,  see  special  scheme). 
Breathing. 
Pulse. 

Cranial  nerves  (for  details,  see  special  scheme). 
Attitude. 

Gait  (with  eyes  open  and  shut). 
Standing  position  (with  eyes  open  and  shut). 

Voluntary  Motility. 

Neck  : 

Sternocleidomastoid. 

Trapezius. 

Other  muscles  of  the  neck. 
Upper  Extremity  (for  details,  see  special  scheme). i 

Power. 

Coordination. 
Trunk  : 

Intercostal  muscles. 

Diaphragm. 

Abdominal  muscles. 

Muscles  of  the  back. 
Irritative  motor  phenomena  (clonic,   tonic  spasms,  fibrillary  twitchings,  tremors^ 

contractures,  chorea,  athetosis,  etc.). 
Muscular  Atrophies : 

Electric  reaction  of  the  muscles  (for  details,  see  special  scheme). 

Sensibility. 

(To  be  represented   upon   a  chart  of  the  body.^     It  should   be   mentioned 
here  how  the  sensations  of  touch,   pain,   heat,   cold,  and  pressure  were  exam- 
ined). 
Mead  and  Neck : 

Sensation  of  touch. 
■    Sensation  of  pain. 

Sensation  of  heat. 

Sensation  of  cold. 

Localization  of  pain  and  touch. 
Upper  Extremity  : 

Sensation  of  touch. 

Sensation  of  pain. 

Sensation  of  heat. 

Sensatioxi  of  cold. 

Sensation  of  pressure. 

Localization  of  pain  and  touch. 

Innervation  sense,  "power  sense"  (how  examined?). 

Appreciation  and  judgment  of  the  active  movements  (how  examined?). 

Appreciation  of  posture^  (how  examined?). 

Appreciation  of  an  object  by  feeling  it  (how  examined?). 

1  See  (c)  p.  954.  "^  See  p.  955.  '  See  p.  767  et  seq. 


952  APPENDIX. 

Trunk  ■' 

Sensation  of  touch. 

Sensation  of  pain. 

Sensation  of  heat. 

Sensation  of  cold. 

Sensation  of  pressure. 

Localization  of  pain  and  touch. 
Lower  Extremity : 

Sensation  of  touch. 

Sensation  of  pain. 

Sensation  of  heat. 

Sensation  of  cold. 

Sensation  of  pressure. 

Localization  of  pain  and  touch. 

Innervation  sense,  "power  sense"  (how  examined?). 

Appreciation  and  Judgment  of  the  active  movements  (how  examined?). 

Appreciation  of  posture^  (how  examined?). 

Appreciation  of  an  object  by  feeling  it  (how  examined?). 
Spontaneous  pains  {neuralgias,  parenchymatous  pains) . 
Hyperalgesia  of  the  sJcin. 
Sensibility  of  the  nerves  and  muscles  to  pressure. 

Eeflexes. 

Cutaneous  Reflexes  (strength?  alteration?).^ 
Plantar  reflex  (to  pricking). 
Plantar  reflex  (to  tickling). 
Abdominal  reflex  (upper,  lower,  middle). 
C remaster  reflex  (groin  reflex). 
Anal  reflex. 
Other  reflexes. 

Tendon  Reflexes. 
Patellar  reflex. 
Achilles  reflex  (foot  clonus). 
Upper  extremity. 
Periosteal  reflexes. 

Bladder  Functions. 

Fulness  of  the  bladder. 

Condition  of  the  sphincter  tonus  (expression  of  the  bladder,  finally  examining 
with  a  catheter). 

Sensibility  of  the  bladder  mucous  membrane.  Desire  for  evacuation,  urgency, 
tenesmus,  pains. 

Character  of  the  evacuation  :  Absolute  or  partial  retention  ;  overflow  of  a  filled 
bladder  associated  with  a  marked  retention  and  an  increased  sphincter  tonus 
[paradoxic  incontinence)  ;  overflow  of  the  bladder  with  a  moderate  filling 
and  deficient  sphincter  tonus  [actual  paralysis  of  the  bladder);  the  position 
of  the  fundus  (palpation);  evacuation  through  the  normal  reflex,  but  invol- 
untarily [enuresis)  ;  possibility  or  impossibility  of  influencing  the  reflex 
evacuation,  either  favoring  (incontinence,  imperative  incontinence,  p.  947) 
Or  inhibiting  it.  Sensation  produced  by  the  evacuation  to  be  distinguished 
from  the  sensation  of  the  wetting. 

Functions  of  the  rectum  :  Character  of  the  stool  evacuation.  For  the  rest  we 
employ  practically  the  same  scheme  as  for  the  bladder  functions. 

Behavior  of  the  nervous  sexual  apparatus.      (Potency,  etc.) 

Trophic  disturbances  of  the  skin,  hair,  nails,  decubitus,  etc. 

Vasomotor  conditions. 

Additional  notes. 

^  See  p.  767  et  seq.  *  See  p.  786,  Pathologic  K^exes. 


APPENDIX.  953 

(6)  Outline  for  the  Examination  of  the  Cranial  Nerve. 
Date. 
Name. 

I.    Olfactory. 

Smell  (how  tested?  cologne  water,  asafetida,  ol.  anisi). 
Result  of  rhinoscopic  examination. 

II,   Oldie. 

Central  visual  acuity  (with  corrected  refraction). 

Visual  field  (hemiopia,  limitations,  fatigue). 

Result  of  ophthalmoscopic  examination. 

Color  blindness  (how  examined?    Holmgren,  Pfliiger's  flower  contrast). 

III.,  IV.,  VI.   Nerves  of  the  Eye  Muscles.  I 

Direction  of  vision  (conjugate  deviation). 
Conjugate  movements. 

Unilateral  testing  of  the  movements  of  the  eyes. 
Double  vision. 
Convergence  (how  tested?). 
Nystagmus  : 

Horizontal. 

Vertical. 

Rotatory. 
Pupils  : 

Size  under  moderate  illumination. 

Reaction  to  light  (how  tested?). 

Direct. 

Crossed. 

Hemiopic  rigidity  to  light  (to  be  tested  in  hemiopia  and  double  blind- 
ness, how  tested?). 

Narrowing  in  accommodation. 
Accommodation  (how  tested?). 

V.    Trigeminus. 

Sensory  division. 

Face. 

Forehead. 

Conjunctiva  and  cornea  (corneal  reflex). 

Tongue. 

Taste  (how  tested?  salt,  acetic  acid). 

Smell  (how  tested?  acetic  acid,  ammonia). 
Motor  division  (palate  muscles). 
■    Raising  the  jaw. 

Lateral  movement  of  the  jaw. 

Atrophy  of  the  chewing  muscles. 

Electrical  examination  (see  special  scheme). 

VII.  Facial. 

Upper  branch. 

Lower  branch. 

Palate  (position,  voluntary  movement,  speech,  swallowing,  reflex). 

Electrical  examination  (for  details,  see  special  scheme). 

Behavior  of  the  facial  associated  movements. 

Behavior  of  the  facial  affected  movements.  . 

Corneal  reflex,  optical  facial  reflex. 

Mechanical  irritability  (how  tested?). 

Atrophy  of  the  facial  muscles. 


954  APPENDIX. 

VIII.  Acomfic. 

Hearing  in  general. 

Test  of  ttie  air  conduction. 

Test  of  the  bone  conduction  (v.  Bezold's  modification  of  Einne's  test). 

Weber's  test. 

Schwabach's  test. 
Subjective  noises,  dizziness. 
Results  of  otoscopic  examination. 

IX.,   X.,  XI.  Glossopharyngeal    Vagris,  Accessory. 
Taste  (how  tested?  bitter,  sweet?). 
Act  of  swallowing. 
Voice. 

Breathing  and  pulse. 
Remits  of  laryngoscopic  examination. 
Trapezius,   sternocleidomastoideus. 
Atrophies. 
Electrical  examination  (for  details,  see  special  scheme). 

XII.  Hypoglossal. 

Extended  movements. 

Position  of  the  tongue  when  protruded. 

Atrophy  of  the  tongue. 

Fibrillary  movements. 

Electrical  examination  (for  details,  see  special  scheme). 

Speech  (see  special  scheme). 
Other  Remarks. 

(c)  Outlines    for  the  ExaminatioQ  of  Muscular  Atrophies  and  Peripheral 
Motor  Paralyses. 

For  the  exact  examination  of  the  motility  of  the  individual  muscles  and  the 
peripheral  motor  nerves,  the  Bern  Clinic  uses  the  outline  found  upon  pp.  910- 
914.  Ample  room  should  be  left  for  the  entries,  and  the  outlines  for  the  upper 
and  the  lower  extremity  should  be  printed  upon  separate  sheets. 

{d)  Outlines  for  Electrical  Examination. 

Corresponding  results  of  examining  a 
healthy  individual  of  equal  stature 
and  constitution,  for  comparison. 

Date. 

Name. 

Name  of  the  muscle  examined. 

Size  in  sq.  c.  of  the  stimulation  electrode  employed. 

Examination  of  the  Muscle. 

Faradic  Current. 

Eapid  interruption.         Contraction  measured  upon  the  sliding  apparatus. 

Type  of  contraction.         Single  shocks. 
Minimum   contraction  measured  upon  the  sliding  apparatus.         Type  of 

contraction.         Signs  of  fatigue. 

Galvanic  Current. 

Minimal  CaCC  in  milliamperes.         Volt. 

Type  of  contraction. 
Minimal  AnCC  in  milliamperes.         Volt. 

Type  of  contraction. 
Relation  of  CaCC  to  AnCC  in  milliamperes.         Volt. 
Signs  of  fatigue. 


SUPPLEMENT.  955 

Examination  of  the  Nerve. 
Faradic  Current. 

Rapid  interruption.        Contraction  measured  upon  the  sliding  apparatus. 

Type  of  contraction.  Single  shocks. 

Minimum  contraction  measured  upon  the  sliding   apparatus.         Type  of 
contraction.         Signs  of  fatigue. 
Galvanic  Current. 

Minimal  CaCC  in  milliamperes.         Volt. 

Type  of  contraction. 
Minimal  AnCC  in  milliamperes.         Volt. 

Type  of  contraction. 
Relation  of  CaCC  to  AnCC  in  milliamperes.         Volt. 
Signs  of  fatigue. 

(e)  Outline  for  the  Examination  of  the  Speech. 
The  summary  upon  p.  900  may  be  utilized  as  an  outline. 

ILLUSTRATIONS. 

Charts  are  especially  useful  for  recording  the  results  of  physical  diagnosis. 
The  fundamental  rules  recommended  for  their  use  are  mentioned  upon  pp.  159 
etseq.,  164  et  seq.,  249,  260,  268-274,  279,  and  condensed  upon  pp.  321  and  348  et 
seq.  They  are  employed  in  all  the  histories  in  Bern.  Upon  pp.  168-211  and 
821-353  a  large  number  of  pathologic  signs  are  to  be  found.  The  charts  on 
pp.  159-161 — better  double  the  size — are  good  models.  Exact  representations 
are  difficult  to  make  upon  the  ordinary  small  chart.  For  routine  office  practice, 
however,  rubber  stamps  are  very  serviceable. 

Charts  are  quite  as  essential  for  representing  disturbances  of  sensibility.  The 
linear  reproductions  on  pp.  915-920,  Figs.  353-358,  may  be  used  as  charts  repre- 
senting circumscribed  disturbances  of  sensibility.  Those  upon  pp.  772  and  773 
are  better  for  rej^resenting  disturbances  which  affect  a  large  part  of  the  entire 
body  (hemiplegias,  paraplegias,  hysteric  disturbances  of  sensibility).  The  varia- 
tions of  sensibility  can  be  best  expressed  upon  these  charts  by  different  colors 
or  shading. 

Charts  are  also  useful  for  representing  larvngoscopic,  rhinoscopic,  and  otoscopic 
lesions  (Fig.  252,  p.  695,  and  Fig.  267,  p.  702). 

The  results  of  ophthalmoscopic  examination  may  be  very  conveniently  repre- 
sented graphically  in  the  sketch-book  prepared  by  Prof.  Haab  (sold  by  Hofer 
Burger,  in  Zurich).  Both  plates  in  this  book  have  been  made  by  means  of  this 
sketch-book.  The  leaves  are  thickly  colored  to  represent  the  red  ground-tone  of 
the  opthalmoscopic  picture.  White  or  yellow  shades  can  be  produced  by  rubbing 
this  ground-color  more  or  less  vigorously  with  an  eraser  or  a  knife,  and  the  dark- 
red  and  black  tones  can  be  added  with  colored  pencils  or  water-colors.  The 
technic  is  explicitly  described  in  the  sketch-book,  and  any  one  can  easily  acquire 
facility  enough  to  make  very  useful  pictures. 


SUPPLEMENT. 

J.  ANALYSIS  OF  THE  IRREGULAR  PULSE. 

K.  F.  Wenkebach's  1  interesting  research  attempts  to  utilize  Engelmann's^ 
recent  observations  upon  the  properties  of  the  heart  muscle  for  the  clinical  anal- 
ysis of  the  different  kinds  of  irregular  pulse.     To  understand  what  follows,  we 

1  Zeitschr.f.  hlin.  Med.,  1899,  vol.  xxxvi.,  1899,  vol.  xxxvii.,  and  1900,  vol.  xxxix. 
Also,  AVenkebach,  Die  Arrhymthmie  als  Ausdruck  bestimmter  Functionsstdnngen  des  Her- 
zens,  Leipzig,  1903.  *  Pfliiger^s  Archiv,  vol.  Ixii.  and  Ixv. 


956  SUPPLEMENT. 

must  take  for  granted  Engelmann' s  supposition  that  the  physiologic  rhythmic 
stimulation  for  cardiac  activity  proceeds  from  the  opening  of  the  great  veins  into 
the  heart,  the  auricle  and  the  ventricle.  The  normal  heart  action  is  the  physio- 
logic response  of  the  heart  muscle  to  these  physiologic  rhythmic  stimulations.  In 
addition  we  must  accept  as  proved  that  (again  according  to  the  experiments  of 
Engelmann)  there  must  be  differentiated  as  special  properties  of  the  heart- 
muscle  fibers  a  power  to  produce  stimulation,  an  irritability  or  stimulability,  a 
power  of  conducting  stimulation,  and  a  capacity  of  contraction.  These  pecu- 
liarities, Engelmann  maintains,  are  inherent  in  the  muscle  fibers  themselves,  but 
may  be  altered  positively  or  negatively  by  many  influences,  which  proceed  partly 
from  the  nervous  system.  Engelmann  differentiates  positive  or  negative  chrono- 
trophic  influences,  by  which  the  number  of  the  physiologic  automatic  stimulations 
is  increased  or  diminished  in  the  unit  of  time;  positive  or  negative  bathmotrophic 
influences,  which  increase  or  diminish  the  irritability;  positive  or  negative  dromo- 
trophic  influences,  which  increase  or  diminish  the  conduction  power  of  the  heart- 
muscle  fibers;  and,  finally,  positive  and  negative  iiiotrophic  influences,  which  affect 
the  contracting  power  of  the  heart-muscle  fibers. 

"  PARARHYTHMIC  "  PULSE  FROM  EXTRASYSTOLE. 

(The  Ordinary  Intermittent  Pulse  Caused  by  Extr asystole.) 
Wenkebach,  in  the  work  alluded  to  above,  analyzes  first  what  we  ordinarily 
designate  clinically  as  simple  isolated  pulse  intermission.  According  to  ausculta- 
tion and  to  sphygmographic  tracings,  this  very  frequent  anomaly  of  the  pulse  is 
almost  always  to  be  attributed  to  the  appearance  of  extrasystoles.  These  systoles 
are  always  excited  by  unphysiologic  (according  to  Hering '  myogenous)  irritation, 
and  mostly  from  the  ventricular  musculature.  In  the  intermittent  pulse  they  are 
not  potent  enough  to  produce  a  plainly  palpable  pulse  in  the  radial,  but  can  be 
discovered  by  auscultating  the  heart.  Although  sometimes  indefinite,  they  are 
for  the  most  part  exhibited  in  some  fashion  or  other  in  the  _  sphygmographic 
tracings.  Such  extrasystoles  are  observed  experimentally  in  digitalis  poisoning 
and  also  in  increased  resistance  to  the  cardiac  contractions. 

The  peculiarities  of  the  arhythmias  dependent  upon  an  extrasystole  are  to  be 
explained  from  our  physiologic  knowledge  as  follows  :  As  Bowditch  and  Marey 
have  already  shown,  there  occurs  in  the  course  of  the  cardiac  cycle  a  so-called 
refractory  phase  (the  shaded  part  in  Fig.  377,  /)  in  which  the  ventricle  is  non- 
irritable  to  the  invading  stimulus.  This  phase  begins  shortly  before  and  persists 
for  a  short  time  after  systole.  The  further  diastole  advances  the  more  irritable 
the  heart  muscle  becomes,  and  the  slighter  the  stimulation  needed  to  produce  a 
so-called  extrasystole — i.  e.,  an  especial  contraction  independent  of  the  physio- 
logic rhythmic  irritation.  As  a  result  of  the  course  of  the  refractory  phases  the 
extrasystole  is  smaller  the  sooner  it  follows  the  normal  heart  contraction,  or 
the  refractory  phase.  On  the  other  hand,  however,  an  extrasystole  produces  a 
refractory  condition  of  the  ventricle,  which  usually  persists  until  after  the  next 
physiologic  stimulation  has  reached  the  ventricle.  This  next  physiologic  stimu- 
lation has  therefore  ordinarily  no  effect,  but  the  following  one  fiinctionates  prop- 
erly.    Therefore  a  pulse  generally  fails  after  an  extrasystole. 

However,  since  the  rhythm  of  the  physiologic  stimulation  proceeding  from  the 
openings  of  the  veins  is  unaffected  by  these  conditions,  the  ventricle  again  con- 
tracts itself  after  the  expiration  of  the  extrasystole,  exactly  at  the  same  instant 
at  which  it  would  have  contracted  if  the  pause  in  the  following  cardiac  revolution 
had  not  occurred.  Therefore,  after  an  extrasystole  (until  the  following  normal 
systole),  a  pause  ensues  which  exceeds  in  length  the  normal  interval  between  the 
two  pulses.  It  is  called  a  compensatory  resting  pause,  because,  as  a_  result  of 
this  longer  interval,  despite  the  extrasystole,  the  pulse-count  in  the  unit  of  time 
remains  constant.     Engelmann  called  this  phenomenon  the  law  of  the  preserva- 

'  Pjluger's  Archiv,  vol.  Ixxxii.,  and  Prager  med.  Wochenschr.,  vol.  xxvi.,  parts  1  and 
2,  1901. 


SUPPLEMENT.  957 

tion  of  the  physiologic  stimulation  period.  Intermissions  which  depend  upon 
such  extrasystoles  present  the  following  peculiarities:  Let  curve  /(Fig.  377) 
represent  the  radial  pulse  curve  corresponding  to  a  normal  contraction  of  the 
heart.  Then  Curves  //-  V  represent  radial  curves  affected  by  the  introduction 
of  an  extrasystole,  and  the  compensatory  failure  of  the  following  normal  sys- 
tole. As  a  result  of  the  law  mentioned  above  (the  retention  of  the  physiologic 
stimulation  period)  the  normal  systole  which  follows  the  extrasystole  occurs  at 
exactly  the  same  time  as  it  would  have  otherwise,  as  can  be  seen  in  the  figure  by 
comparing  the  apices.  Another  result  of  this  law  is  that  the  pause  between  the 
beginning  of  the  systole  which  precedes  the  extrasystole  and  the  beginning  of  the 
one  which  follows  the  extrasystole  (included  in  the  figure  by  a  bracket)  is  exactly 
twice  as  long  as  the  normal  interval.  Pulse  intermissions  caused  by  extrasys- 
toles can  be  recognized  by  this  peculiarity  in  the  sphygmogram  even  if  the  extra- 


Bfi^WiP^B 

^^ffil 

ImBM 

^^H 

Ell^^^KflH^^^Ei^^^HI^^IQSl^l^l^i 

^^H 

i^^BB 

Fig.  377.— Diagram  of  extrasystoles  and  compensatory  pauses  bv  stimulation  of  the  ventricle  at 

different  times  during  diastole  (after  Engelmann). 


systole  itself  is  hidden  beneath  the  secondary  apex  of  the  pulse  curve.  To  sum- 
marize, we  may  say  that  the  ordinary  intermittent  pulse  is  characterized  by  the 
occurrence  of  an  extrasystole  which  cannot  be  palpated  in  the  radial,  and  that 
the  intermission  measures  exactly  twice  as  much  as  the  preceding  normal  cardiac 
revolution. 

The  sphygmogram  may  present  entirely  different  characters,  depending  upon 
the  pomt  of  time  at  which  the  extrasystole  appears  ;  the  later  in  the  diastole  it 
appears,  the  plainer  the  extrasystole  becomes,  both  in  the  pulse  curve  and  in  aus- 
cultation. It  may  then  present  the  appearance  of  a  normal  but  slightly  antici- 
pated pulse  (Fig.  377,  F).  Quite  vigorous  extrasystoles  produce  two  tones 
audible  over  the  heart;  weaker  ones,  merely  one  first  tone.  Figure  378  repre- 
sents all  transitions  between  an  apjiarently  pure  intermission  with  an  extrasys- 
tole, which  cannot  be  plainly  recognized  by  the  sphygmogram,  through  the 
doubled  apex  curves,  which  are  sometimes  called  a  pulsus  bigeminus,   up  to  a 


958 


SUPPLEMENT. 


pulse-beat  which  apparently  merely  occurs  a  little  too  early.  Wenkebach  assumes 
that  the  so-called  ' '  futile ' '  heart  contractions — i.  e. ,  those  not  palpable  at  the 
radial — must  necessarily  be  extrasystoles.  The  "futility"  of  an  extrasystole 
depends  essentially  upon  the  phase  at  which  it  appears,  and  many  of  the  palpa- 
ble and  auscultatory  peculiarities  which  Quincke  and  Hochhaus  have  assumed  in 
defining  "futile"  contractions  (p.  297  ef  seq.)  must  depend  principally  upon  the 
occurrence  of  the  extrasystole  at  a  definite  phase  of  the  cardiac  cycle.  These 
points  are  not,  therefore,  sufficient  to  differentiate  the  ' '  futile  ' '  contractions  as  a 
certain  specific  sort  of  contraction  from  other  rudimentary  systoles — i.  e.,  extra- 
systoles. 

The  first  systole  after  the  compensatory  pause  (post-compensatory  systole)  is 
ordinarily  more  vigorous  and  produces  more  effect  upon  the  pulse  curve  than  a 


H    1  H  I       9¥ 


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Fig.  378. — Sphygmograph  with  extrasystoles :  In  the  curves  I-V,  which  are  all  taken  from  the 
same  patient,  the  extrasystole  occurs  later  and  later.  In  I  it  does  not  appear,  but  is  recogniza- 
ble only  by  auscultation  and  by  the  occurrence  of  a  pause  twice  as  long  as  normal.  In  V  the 
extrasystoles  in  size  and  time  of  occurrence  might  be  confused  with  the  normal  systoles,  es- 
pecially as  they  alternate  regularly  with  the  latter.  In  V  j  represents  the  normal  systole ;  I ,  the 
extrasystole  (after  Wenkebach). 

systole  which  follows  after  the  normal  interval.  This  is  not  represented  in  Fig. 
877,  but  it  can  be  detected  in  Fig.  378,  /to  V.  It  depends  upon  the  longer  rest 
the  musculature  obtains  and  upon  the  more  complete  diastolic  filling  of  the 
ventricle. 

Extrasystoles  do  not,  however,  always  lead  to  an  intermission  of  the  pulse. 
The  intermission,  and  with  it  the  compensatory  pause  (Fig.  379),  maybe  lacking. 
This  may  be  the  case  when  the  pulse-frequency  is  diminished,  and  as  a  result  the 
"  refractory  "  phase  is  short  in  proportion  to  the  length  of  the  pulse.  The  pulse 
following  extrasystole  then  occurs  at  the  normal  moment  of  time,  so  that  the 
extrasystole  seems  to  be  simply  inserted,  and  the  law  of  the  retention  of  the 
physiologic  stimulation  is  preserved. 

Characteristic  jjulse  curves  will  occur  if  the  normal  cardiac  action  is  altered 


SUPPLEMENT.  959 

by  several  extrasystoles  following  one  after  the  other.  Several  pulses  appearing  at 
abnormal  intervals  then  seem  to  be  inserted  into  a  normal  pulse  curve.  That  even 
this  irregularity  depends  upon  extrasystoles  may  be  seen  from  the  fact  that,  on 
account  of  the  law  of  the  retention  of  the  physiologic  stimulation  period,  the  part 
of  the  pulse  curve  which  contains  the  irregular  pulse — i.  e. ,  the  extrasystoles — can 
be  divided  up  into  an  integral  number  of  normal  pulse  periods.  (See  the  diagram. 
Fig.  377,   VI.) 

When  the  intermissions  in  a  pulse  curve  occur  in  different  kinds  of  groups, 
and  thereby  the  extrasystoles  produce  sometimes  more,  and  sometimes  less,  dis- 
tinct pulses,  and  when  the  post-compensatory  pulse  is  abnormally  long,  and  the 
pulse  following  this  abnormally  small,  then  we  may  lose  entirely  the  regularity 
of  the  rhythm  in  the  ventricle  and  in  the  arterial  pulse  on  account  of  the  extra- 
systole,  even  despite  the  regular  physiologic  stimulation  interval  at  the  venous 
orifices.  Such  an  irregular,  unequal,  and  intermittent  pulse  (which  depends  upon 
extrasystoles)  is,  nevertheless,  quite  different  from  the  so-called  true  irregular 
pulses  which  depend  upon  a  disturbance  of  the  rhythm  originating  in  the  stimu- 
lation in  the  venous  orifices.  Wenkebach  emjihasizes  this  by  saying  that  it  makes 
a  great  difference  whether  a  person  makes  false  steps  here  and  there  and  limjjs 
because  he  has  a  lame  leg  or  because  he  is  walking  upon  a  path  with  holes  or  stones. 
In  difiicult  cases  only  an  exact  measure  of  time  (which  the  Jacquet  sphygmo- 
chronograph  (p.  101)  can  furnish)  will  enable  us  to  decide  whether  the  arhythmia 
depends  upon  extrasystoles  or  upon  an  irregularity  of  the  physiologic  stimulation 
periods  themselves.   Wenkebach  insists  that  the  latter  should  be  called  true  arhyth- 


'    ^     „,  Periode  8-5- 


Fig.  379.— Extrasystole  without  compensatory  pause  (after  Wenkebach). 

mias;  the  former,  pararhythmias.  According  to  this  we  should  speak  of  arhyth- 
mias  from  extrasystoles  as  presenting  a  pararhythmic,  irregular,  unequal,  and 
intermittent  pulse. 

Wenkebach  sometimes  observed  a  characteristic  deviation  from  the  ordinary 
time  relations  in  the  pararhythmic  intermittent  pulse,  in  that  the  compensatory 
rest  was  too  short—i.  e.,  the  intermission  was  shorter  than  double  the  normal 
period.  This  type  is  observed  in  valvular  lesions,  and  shows  that  such  extra  sys- 
toles do  not  proceed  fi-om  the  ventricles,  but  either  from  the  venous  orifices  or 
from  the  auricles.  In  explanation  Wenkebach  reminds  us  of  the  following  experi- 
mentally confirmed  facts.  In  an  extrasystole  arising  from  stimulation  of  the 
venous  openings  the  compensatory  slowing  of  the  pause  after  the  extrasystole 
entirely  fails,  because  when  the  extrasystole  is  produced,  the  stimulability  is 
exhausted  so  that  the  normal  amount  of  time  is  needed  before  another  stimula- 
tion can  be  produced.  In  this  case,  if  the  extrasystole  causes  an  intermission  of 
the  peripheral  pulse,  the  length  of  such  an  intermission  is  less  than  twice  the  nor- 
mal period. 

In  the  extrasystole  proceeding  from  the  auricle  the  pulse  following  the  extra- 
systole may  resemble  that  of  a  ventricular  extrasystole — i.  e. ,  conforming  to  the 
law  of  maintenance  of  the  physiologic  period  of  irritation,  it  may  occur  exactly 
at  the  time  at  which  the  second  normal  systole  would  have  commenced  had  the 
extrasystole  been  absent.  In  case  the  extrasystole  leads  to  an  intermission  of 
the  pulse,  this  intermission  is  also  twice  as  long  as  the  normal  period  of  rest. 
In  other  cases,  however,  -even  when  the  extrasystole  proceeds  from  the  auricle, 


960  ^  SUPPLEMENT. 

the  time  between  two  successive  normal  systoles  or  the  duration  of  the  inter- 
mission may  be  shorter  than  twice  the  normal  period.  According  to  Wenke- 
bach,  this  is  the  case  when  the  extra-irritation  originating  in  the  auricle  also 
produces  a  recurrent  contraction  extending  to  the  site  of  the  origin  of  the  physio- 
logic irritation  at  the  venous  orifices.  In  this  case  the  intermission  is  shortened, 
because,  at  the  moment  when  this  recurrent  contraction  reaches  the  venous 
orifices,  all  of  the  irritation  here  present  is  nullified,  so  that  the  return  of  the 
physiologic  series  of  irritation  is  hastened.  Hering,^  who  has  studied  this  ques- 
tion especially  by  the  help  of  animal  experiments,  reaches  the  diagnostic  result 
that  in  case  the  extrasystole  is  associated  with  normal  compensatory  pauses,  the 
starting-point  of  the  stimulation  causing  the  extrasystoles  is  either  the  ventricle 
or  the  auricle,  but  never  one  of  the  venous  openings  into  the  auricle  ;  and  that 
the  shortening  of  the  compensatory  pause  proves  that  the  stimulation  does  not 
precede  from  the  ventricle,  but  either  from  the  auricle  or  from  the  great  veins. 
According  to  Hering,  the  extrasystoles,  as  has  been  already  mentioned,  are 
always  to  be  attributed  to  the  direct  stimulation  of  the  cardiac  musculature,  and 
the  resulting  irregularity  is  to  be  designated  as  myerethic  irregularity. 

ALLORHYTHMIAS. 

The  regularly  intermitting  pulse  is  so  called  by  Wenkebach.  A  regularly 
intermittent  pulse — i.  e. ,  one  occurring  after  a  certain  number  of  cardiac  beats — 
may  in  exceptional  cases  depend  upon  the  fact  that  the  extrasystoles  leading  to 
the  intermission  occur  at  regular  intervals.  Such  a  regularity,  naturally, 
generally  persists  but  a  short  time.  As  contrasted  with  this,  Muskens  had 
already  noted  that  the  most  probable  explanation  for  the  occurrence  of  regu- 
larly repeated  intermissions  is  ftirnished  by  assuming  a  definite  amount  of 
diminution  of  the  conduction  power  of  the  heart  muscle.  Wenkebach  has  now 
demonstrated,  by  a  careful  analysis  of  pulse  curves,  that  this  is  the  ordinary 
etiology  of  the  regularly  intermitting  pulses.  To  understand  what  follows, 
a  few  words  are  necessary.  Engelmann  represented  the  amount  of  the  con- 
duction power  within  a  certain  section  of  the  heart  as  A-  The  conduction 
power  in  the  venous  sinus  is  represented  as  A  ^,  that  in  the  auricle  as  A  o,, 
and  that  in  the  ventricle  as  A  ^'-  A  «/^  would  then  represent  the  power 
of  conduction  between  the  auricle  and  ventricle,  etc.  The  time  in  which 
the  contraction  stimulation  travels  from  one  place  to  another  depends  upon  the 
conduction  power.  The  interval  As-Vs  (between  the  systole  of  the  auricle  and 
that  of  the  ventricle)  is  of  especial  interest.  During  systole,  not  only  the  stimu- 
lability,  but  also  the  power  of  conduction  A,  is  gradually  recuperated.  With 
this  explanation  it  is  comprehensible  that  if  the  power  of  conduction — e.  g. ,  at 
the  boundary  between  the  auricle  and  ventricle — is  injured  it  may,  after  several 
heart-beats,  become  so  much  depressed  that  finally  the  stimulation  no  longer 
reaches  the  ventricular  musculature  in  sufiicient  force  to  produce  a  contraction ; 
but  that  after  such  a  rest,  in  a  certain  way  forced  upon  the  ventricle,  new  beats 
will  reappear.  Given  a  certain  degree  of  conduction  weakness,  this  process  may 
be  repeated  in  such  a  way  that  one  ventricular  contraction  will  regularly  be  lost 
after  a  certain  number  of  heart-beats,  and  so  groups  of  regular  pulses  will  be 
interrupted  by  an  intermission.  Such  groups  have  for  a  long  time  been  recog- 
nized in  physiologic  experiments,  and  called  Lucian's  periods.  If  we  examined 
the  sphygmogram  in  patients  with  such  a  regularly  intermitting  pulse  more  exactly, 
we  should  find  that  the  intervals  between  the  pulse  beats  within  a  group  vary 
quite  decidedly  from  each  other;  and  that  in  each  group  this  variation  is  repeated 
in  a  perfectly  typical  fashion.  From  a  more  accurate  analysis  of  these  variations 
in  the  inter\^als  of  the  pulse  within  a  group,  Wenkebach  now  shows  that  the 
regular  loss  of  the  pulse  (which  we  are  discussing)  depends  upon  a  negative 
dromotropic  influence  (see  p.  956) — i.  e.,  upon  a  disturbance  of  the  conduction 
power.     After  the  establishment  of  the  pulse  the  first  interval  within  a  group 

^  Pfluger's  Archiv,  vol.  Ixxxii.,  and  Prager  med.  Wochenschr.,  1901,  vol.  xxvi.,  parts 
1  and  2,  1901. 


SUPPLEMENT. 


961 


is  the  largest,  and  the  following  intervals  are  decidedly  smaller ;  but  for  the  most 
part  they  again  increase  somewhat  in  size,  up  to  a  new  intermission.  This  is 
explained  by  assuming  from  what  follows  (and,  moreover,  it  has  been  experi- 
mentally proved  by  Engelmann)  that  the  conduction  power  A  is  injured  most  by 
the  first  contraction  after  pause  and  is  less  markedly  aftected  by  the  following 
contractions.  The  annexed  diagram  (Fig.  380),  taken  from  Wenkebach,  illus- 
trates the  relations  very  clearly. 

The  diagram  is  based  upon  the  above  assumption:  that  A  is  diminished  by 
cardiac  activity  itself  (by  fatigue).  The  horizontal  lines  in  the  figure  are  to  be 
considered  as  time  abscissae.  The  rhythmic  physiologic  stimulations  which  arise 
at  the  venous  orifice  are  marked  at  regular  intervals  upon  the  time  abscissa  p,  20 
units  apart.  The  straight  lines  drawn  obliquely  downward  to  the  right  are  the 
graphic  representations  of  the  course  of  the  stimulation  from  the  venous  orifices 
to  the  auricle  and  ventricle.  The  part  of  the  figure  included  in  the  brace  A 
represents  the  area  of  the  auricle,  that  included  within  the  brace  V  the  area  of  the 
ventricle.  The  points  of  intersection  of  the  oblique  and  horizontal  lines  repre- 
sent the  moments  of  time  at  which  the  physiologic  stimulation,  passing  from  the 
root  of  the  heart  to  its  apex,  first,  crosses  the  auricular  border ;  second,  stimulates 
the  ventricular  contraction.  "Wenkebach' s  own  words  furnish  the  best  explana- 
tion of  the  rest  of  the  diagram :    ' '  The  rate  of  the  stimulation  contraction  at  the 


Fig.  380.— Diagram  to  represent  a  regnlarlv  intermittent  ptilse,  caused  by  disturbance  of  the  con- 
ductivity of  the  heart  muscle  :"One  pulse  is  lost  after  every  four  (after  Weukebach). 

heart  root  Tp  =  20  ;  and  the  interval  p  to  Vs,  that  is  the  time  between  the  stim- 
ulation p  and  the  ventricular  systole  T"*-,  in  a  favorable  case  rafter  a  pause  =  5)  ; 
but  at  the  extreme  case,  where  the  stimulation  is  still  transmitted  just  vigorously 
enough  to  produce  a  ventricular  contraction  =  10.  During  the  contractions  the 
interval  p  to  Vs  is  prolonged  from  5  to  10.  Following  the  experiment,  we  may 
assume  that  after  the  first  systole  of  the  group,  p  to  Vs  is  increased  3  ;  after  the 
following  systoles,  p  to  Vs  is  increased  1  each  time. 

"Should  A  in  each  contraction  remain  equal,  as  is  normally  the  case,  the 
tempo  of  the  ventricular  systole  TVs  would  always  equal  p,  even  if  A  is  ^'^ry 
slight.  A  diminution  of  A  would  occasion  the  jjroportionate  increase  of  TVs.  But 
since  each  systole  has  another  influence  upon  A,  the  case  will  be  quite  dift'erent ; 
and  in  the  instance  given  here,  the  first  interval  (represented  in  the  figure)  of 
ventricular  systole,  T^  Vs  =  23,  being  increased  by  3,  on  account  of  the  increase  of 
the  interval  p  to  Vs  from  5  to  8.  The  following  intervals  of  the  ventricular  sys- 
tole, T^Vs  and  TVs  =  21,  on  account  of  a  further  increase  by  1.  Then,  however, 
the  limit  is  reached,  and  the  fifth  stimulation  is  either  not  transmitted  at  all  or  is 
no  longer  sufficiently  transmitted.  The  ventricular  contraction  tails,  and  an  inter- 
mission results.  The  interval  p  to  Vs  in  this  i)ause  returns  to  5,  and  the  duration 
of  the  intermission  (Tint.)  amounts  to  5  less  than  the  double  of  7/)  ;  that  is  T 
int.  =  2Tp  —  5  =  35.  The  same  process  is  repeated  after  the  intermission.  The 
tempo  of  the  chamber  contraction  then  depends  entirely  upon  the  rapidity  of  dim- 

61 


962 


SUPPLEMENT. 


inution  of  A  in  regular  rhythm  of  the  contraction  stimulation,  and  with  it  the 
increase  of  p  to  Vs.'^'^ 

Wenkebach  found  that  the  time  relations  in  the  accompanying  sphygmogram 
(Fig.  381)  were  in  complete  conformity  with  this  diagram  (Fig.  380),  and  with 
the  explanation  given  for  the  intermission.  We  observe  in  Fig.  381  that  the 
numbers  representing  the  intervals  confirm  the  view  that  the  periods  after  the 
intervals  are  the  longest,  the  following  much  shorter,  and  those  still  later  some- 
what longer  again.  Although  it  cannot  be  recognized  in  the  figure,  a  gradual 
diminution  in  the  power  of  conduction  occurs  toward  the  end  of  a  group  in  the 
pulse  curve,  observed  as  a  diminished  celerity  in  the  ascending  of  the  pulse  wave. 


Fig.  381.— Regularly  intermittent  pulse  with  groups  of  four  pulses  (after  Wenkebach). 

Wenkebach  considers  that  the  exact  measuring  of  the  pulse  curve  shows  the 
size  of  the  interval  of  the  automatic  stimulation  at  the  venous  orifices  Tp,  as  well 
as  the  amount  of  the  diminution  of  conduction  power  in  the  course  of  a  group. 
The  original  article  should  be  consulted  in  this  connection. 

Gaskel  and  Engelmann  have  called  attention  to  the  practical  point  that 
vagus  irritation  diminishes  the  size  of  A-  In  this  way  they  explain  the  allo- 
rhythmia  frequently  occurring  after  vagus  stimulation,  as  well  as  the  appearance 
of  regular  intermissions  (especially  the  bigeminal  and  trigeminal  pulse)  after 
employing  digitalis,  as  this  drug  stimulates  the  vagus.  At  the  same  time  if  there 
is  a  regularly  intermittent  pulse,  digitalis  increases  the  disturbance  of  rhythm, 
because  it  diminishes  A  by  vagus  stimulation.  This  also  explains  how  atropin. 
improves  certain  regular  intermissions,  as  this  poison  depresses  the  vagus  tonus, 
and  thereby  improves  the  conduction  power  of  the  heart  muscle. 

Still  other  kinds  of  allorhythmias  may  arise  from  more  pronounced  diminu- 
tion of  A-  Corresponding  to  the  conception  of  allorhythmia,  these  are  all  char- 
acterized by  a  certain  amount  of  regularity,  or  even  by  perfectly  regular  repetition 
of  the  intermissions — i.  e.,  some  grouping  of  the  pulses.  However,  if  a  longer 
pulse  curve  is  taken,  the  regularity  of  the  grouping  need  not  be  absolutely  even, 
because,  during  the  observation,  varied  influences  may  affect  the  power  of  con- 
duction.    Any  degree  of   gradation    may  occur  between  the  ordinary   regular 


Fig.  382.— So-called  "  regularly  double  intermitting  pulse  "  (pulse-groups  separated  by  two  longer 
cardiac  revolutions)  (after  Wenkebach). 

pulse-rhythm  and  the  regular  pulse  with  half-frequency  (bradycardia)  depending 
upon  the  amount  of  injury  to  the  conduction  power — i.  e.,  the  negative  dromo- 
tropic  influence. 

Such  transitional  forms  are  composed  of  groups  of  6  to  2  pulse  strokes.  The 
regular  intermitting  pulse  in  groups  of  2  strokes  is  nothing  but  a  transformed 
pulsus  bigeminus  alternans.  The  real  pulsus  alternans  (p.  963)  does  not  belong 
here  ;  but,  according  to  Wenkebach,  to  a  disturbance,  not  of  the  rhythm,  but  of 
contractility,  In  another  group  of  cases  the  diminished  power  of  conduction  is 
expressed  by  the  appearance,   after  the  intermission,   of  a  single  systole,  then 

1  Zeiis.f.  klin.  Med.,  vol.  xxxvii.,  p.  482. 


SUPPLEMENT.  963 

another  intermission,  and  then  a  group  of  several  pulse  beats.  This  Wenke- 
bachi  has  called  the  "regularly  double  intermitting  pulse,"  a  term,  however, 
which  might  lead  to  misunderstanding.  Figs.  382  and  383  illustrate  and 
explain  th'e  type.  Still  another  serious  disturbance  of  A  will  produce  regular 
group  formations,  in  which  the  groups  are  separated  by  3,  4,  5,  or  n  cardiac  revo- 
lutions prolonged  through  the  loss  of  a  systole.  Finally,  if  n  =  ^-r^  ,  regular  brady- 
cardia with  half-frequency  occurs,  as  then  only  the  second  stimulation  is  perma- 
nently active. 

In  all  the  cases  thus  far  described  the  diminution  in  conduction  power  goes 
only  so  far  as  to  occasion  the  loss  of  a  systole  more  or  less  often,  but  we  may 
conceive  of  a  case  in  which  two  or  even  several  systoles,  one  immediately  alter 
the  other,  are  lost;  then  longer  pauses—/,  e.,  still  more  pronounced  bradycardia— 
would  result.  Such  an  excessive  bradycardia  may  be  responsible  for  the  phenom- 
enon observed  in  Stokes -Adams  disease.  His's  observations  (]j.  297)  upon  the 
heart  blocking  noticed  in  this  disease  argue  that  a  diminished  conduction  stimu- 
lation is  the  salient  feature. 

Any  allorhvthmia  characterized  by  no  particular  regularity  of  the  grouping 
may  be'  attributed  to  a  defect  of  the  conduction  power,  provided  that  auscultation 
confirms   the   lack   of  extrasystoles.     Further   assistance  will   be   furnished  by 


Fig.  383.— Diagram  to  explain  Fig.  382  (after  Wenkebach). 

noting  that  the  intermissions  are  always  shorter  than  twice  the  normal  periods 
of  cardiac  action  (lack  of  compensatory  rest  which  occurs  with  extrasystoles)  and 
that  within  each  group  the  first  revolution  after  the  intermission  is  the  longest, 
the  following  is  smaller,  and  the  still  later  ones  increase  gradually.  This  can 
easily  be  understood  by  comparing  the  scheme,  and  it  is  very  important  for  the 
diagnosis  of  difficult  cases. 

TRUE  PRIMARY  ARHYTHMIAS. 

We  have  thus  far  described  the  disturbances  in  pulse  rh}i;hm  called  par- 
arhythmias  and  allorhythmias,  which  depend,  upon  the  one  hand,  upon  extra 
systoles,  and,  on  the  other  hand,  upon  diminution  in  the  power  of  conduction. 
Now  we  may  turn  to  what  Wenkebach  calls  the  true  arhythmias,  those  disturb- 
ances of  the  pulse  rhythm  which  depend  upon  a  disturbance  of  the  primary 
stimulation  rhythm  or  of  the  primary  stimulation  strength  at  the  venous  orifices. 
They  can  be  diagnosed  only  by  excluding  the  pararhythmias  and  allorhythmias. 

DISTURBANCES    OF   THE    RHYTHM    FROM    DISTURBANCES    OF 
CONTRACTILITY. 

The  Pulsus  Alternans. 

The  ventricular  contraction  may  fail,  if  the  contractility  of  the  heart  muscle 
has  been  affected,  even  though  the  stimulation  rhythm   remains  normal  and  the 

^  Wenkebach  is  justified  in  calling:  attention  to  the  fact  that  the  terms  pulsus 
bigeminus  and  trigeminus  had  better  be  discarded,  since  he  shows  in  his  particularly 
instructive  book  (p.  171)  that  sphygmograms  requirinff  these  desi.tjnations  are  brought 
about  in  a  number  of  diHerent  ways — by  extrasystoles,  by  disturbed  conductive  power, 
and  by  true  arhythmias — and  that,  consequently,  they  should  not  be  classed  under  one 
common  name. 


964  SUPPLEMENT. 

conduction  power  good.  The  resulting  arhyttimia  will  be  appreciable,  both  to 
palpation  of  the  pulse,  and  in  the  sphygmogram.  In  this  case  it  depends  merely 
upon  negative  inotropic  influences.  A  grouping  of  more  or  less  distinct  regularity 
may  occur  from  the  summation  of  fatigue  phenomena.  These  arhythmias,  which 
the  author  would  describe  as  "intropic  arhythmias,"  can  generally  be  diagnosed 
from  the  differences  in  the  size  of  the  pulses,  although  wdthout  any  marked 
crowding  of  the  periods.  The  pulses  which  fail,  and  to  which,  as  in  para- 
rhythmia,  no  extrasystoles  correspond,  are,  of  course,  excepted. 

The  pulsus  alternans  must  be  discussed  here  among  the  intropic  arhythmias, 
because  it  arises  from  a  disturbance  of  contractility.  A  more  careful  examination 
and  measurement  of  its  pulse  curve  shows  that  it  presents  a  very  characteristic 
deviation  of  rhythm  from  the  normal.  Pulsus  alternans  is  a  pulse  series  with 
large  and  small  pulse  waves  regularly  alternating  with  each  other  at  almost 
equal  intervals  (see  Fig.  43,  p.  125).  Wenkebach  '  has  quite  recently  analyzed 
this  pulse  most  accurately,  and  decided  that  it  depends  upon  a  disturbance  of  the 
contractility  for  the  following  reasons  :  It  certainly  cannot  depend  upon  a  varia- 
tion in  the  intensity  of  the  contraction  stimulation,  because,  as  is  well  known, 
the  heart  always  reacts  maximally,  even  to  a  diminished  stimulation,  provided 
that  the  latter  is  sufficient  to  cause  any  contraction  at  all.  For  the  same  reason 
it  cannot  be  due  to  a  diminished  power  to  conduct  stimulation.  It  is  incor- 
rect to  suppose  that  it  could  depend  upon  a  bigeminal  pulse  with  an  extra- 
systole  occurring  practically  halfway  between  two  normal  systoles ;  because, 
in  the  first  place,  it  is  quite  exceptional  for  extrasystoles  to  persist  so  long 
a  time,  and  because,  besides,  extrasystoles  interposed  almost  in  the  place  of 
the  normal  systoles  would  produce  practically  a  normal  pulse.  AVenkebach's 
explanation  is  better.  He  considers  that  it  depends  upon  a  disturbance  in 
the  contractile  power.  After  a  vigorous  contraction  the  contractile  power  is 
not  sufficiently  recuperated  to  respond  with  an  equally  vigorous  systole  to 
the  next  stimulation.  Wenkebach  appreciates  a  difficulty  in  this  explana- 
tion, for  every  contraction  is  in  one  sense  maximal,  and  whatever  contractile 
power  is  at  its  command  is  utilized,  and  therefore  the  heart  must  be  quite  as 
fatigued  after  a  weaker  contraction  as  after  a  stronger  one.  At  the  same  time 
we  have  no  right  to  assume,  without  anything  further,  that  the  heart  is  recu- 
perated more  quickly  after  a  weak  contraction  than  after  a  strong  one.  Wenke- 
bach believes  that  this  difficulty  can  be  accounted  for  by  assuming  that  the 
stronger  and  weaker  contractions  affect  the  conti'actility  differently  by  not  follow- 
ing equally  rapidly.  B.  F.  Hoffmann,^  in  fact,  did  demonstrate  that  the  con- 
tractions of  the  heart  muscles  occur  more  rapidly  in  a  hypodynamic  condition — 
i.  e.,  with  less  contractile  power — than  with  normal  contractility.  Now,  assum- 
ing that  the  smaller  beats  of  the  pulsus  alternans  occur  more  rapidly  than  the 
larger,  the  pause  from  the  end  of  the  smaller  to  the  beginning  of  the  greater 
pulse  will  be  slightly  lengthened ;  Avhereas,  the  pause  from  the  end  of  the  greater 
to  the  beginning  of  the  smaller  will  be  shortened.  This  can  be  easily  demon- 
strated in  curves  of  the  pulsus  alternans.  As  a  result  the  contractile  power 
recovers  better  after  the  smaller  than  after  the  greater,  and  by  such  an  action 
the  regular  variation  between  the  greater  and  smaller  pulses  will  be  retained. 
Even  the  beginning  of  the  small  pulse  appears  anticipated  in  the  radial  curve, 
as  contrasted  with  the  beginning  of  the  great  pulse,  and  Wenkebach  explains  this 
peculiarity  by  assuming  that  the  small  pulse  waves  are  more  rapidly  transmitted 
to  the  periphery  than  the  large  ones. 

The  alternans  is  then  a  result  of  diminished  contractile  power  of  the  heart 
muscles,  and  is  again  and  again  automatically  reproduced.  Wenkebach  explains 
the  primary  cause  of  the  entire  phenomenon  as  follows  :  With  a  hypodynamic 
condition  of  the  heart — i.  e.,  diminished  contractile  power — if  a  single  physiologic 
irritation  happens  to  occur  somewhat  too  early  it  finds  the  heart  muscle  in  a 
more  hypodynamic  condition  than  the  previous  stimulation  did.     The  resulting 

^  Zeils.f.  klin.  Med.,  1902,  vol.  xliv.,  parts  3,  4,  p.  218. 
*  Pflucjer's  Archiv,  1901,  vol.  Ixxxiv 


SUPPLEMENT.  965 

contraction  will,  therefore,  not  only  be  smaller,  but  also,  according  to  Hoffmann, 
will  be  performed  more  rapidly.  Therefore,  if  the  irritation  of  the  next  stimulus 
does  not  occur  too  late,  the  longer  pause  will  permit  the  contractile  power  to 
recover  perfectly,  and  so  the  following  contraction  will  be  more  vigorous.  This, 
in  turn,  lasting  longer, the  succeeding  pause  will,  as  a  result,  be  shortened,  and, 
consequently,  the  succeeding  contraction  smaller.  This  play  can  be  repeated 
indefinitely,  as  long  as  no  new  factors  enter  the  field.  Hence  one  single  irregu- 
larity of  the  rhythm  is  sufficient  to  produce  a  pulsus  alternans;  and,  jsrovided 
that  the  following  stimulations  are  repeated  at  regular  intervals,  it  may  persist 
for  a  long  time,  until  a  medium-sized  contraction  occurs  and  the  pulsus  alternans 
is  equalized. 

2.  ACIDIMETRJC  TITRATION  OF  FLUIDS  WHICH  CONTAIN  ALKA- 
LINE EARTHS  AND  AMMONIA  SALTS  IN  ADDITION  TO  SALTS 
OF  PHOSPHORIC  ACID. 

(Gastric  Juice,  Urine,  pp.  378  and  541.) 
Moritz  ^  has  recently  suggested  a  method  for  the  acidimetric  titration 
of  fluids,  such  as  the  gastric  juice  and  the  urine,  containing  alkaline 
earths  and  animonium  salts  as  well  as  phosphates,  which  is  entirely 
free  from  objection,  and  which  eliminates  those  inaccuracies  of  titration 
the  existence  of  which  was  demonstrated  by  Nageli  in  his  investiga- 
tions upon  the  acidimetric  titration  of  the  urine  (p.  541). 

Moritz  states  that  the  difficulties  associated  with  the  acidimetric 
titration  of  urine  and  gastric  juice  with  phenolphthalein  are  as  follows : 
1.  The  monalkaline  and  dialkaline  phosphates  in  phosphatic  fluids 
react  with  phenolphthalein  as  they  do  with  litmus,  counterbalancing 
each  other  during  a  certain  period  of  the  titration,  and  consequently 
render  the  end  reaction  indefinite.  2.  The  contained  ammonium  salts 
interfere  with  titration  to  a  certain  extent,  since  ammonia  acts  so  feebly 
upon  the  phenolphthalein  that  more  alkali  must  always  be  added  than 
corresponds  to  the  actual  neutralization.  3.  As  a  result  of  the  weak  alka- 
line reaction  of  the  monalkaline  carbonates  (NaHC03  and  KaHC03),  ^^^ 
carbonic  acid  titration  is  not  exact.  4.  In  the  phenolphthalein  titra- 
tion with  alkali,  the  fluid  seems  to  be  too  acid  from  the  precipitation 
of  indefinite  quantities  of  basic  calcium  salts.  Magnesium  salts  do  not 
produce  similar  disturbances. 

Moritz  has  shown  that  the  difficulties  dependent  upon  the  presence 
of  ammonium  salts,  phosphates,  and  carbonates  may  be  completely 
overcome  and  exact  end  reactions  obtained  by  diluting  the  fluid  to  be 
titrated  with  an  equal  volume  of  concentrated  sodium  chlorid  solution 
which  has  been  prepared  with  boiled  water  freed  of  its  carbonic  acid. 
This  effect  is  doubtless  due  to  an  inhibition  of  dissociation.  After  this 
addition,  a  solution  of  an  alkaline  bicarbonate  reacts  neutrally  with 
phenolphthalein.  After  the  addition  of  the  saline  solution,  according  to 
Moritz,  the  carbonic  acid  is  titrated  to  the  limit  between  the  primary 
and  secondary  salts,  and  the  phosphoric  acid  to  the  limit  between  the 
secondary  and  tertiary  salts.  Moritz  also  eliminates  the  difficulty  de- 
pendent upon  the  presence  of  calcium  salts  by  precipitating  them  by 
the  addition  of  sodium  oxalate. 

*  Arch.  f.  /din.  Med.,  vol.  Ixxx.,  pp.  5  and  G. 


966  SUPPLEMENT. 

According  to  Moritz's  directions,  the  entire  procedure  (both  for  the 
gastric  juice  and  for  the  urine)  is  carried  out  as  follows  : 

The  titration  is  best  performed  in  small  Erlenraeyer  flasks  holding 
about  150  c.c.  About  10  c.c.  of  fluid  are  employed,  to  which  are 
added  about  4  c.c.  of  an  approximately  semi-normal  sodium  oxalate 
solution  (neutralized  ^  sodium  oxalate  solution,  see  p.  378)  and  15  c.c, 
of  a  concentrated  sodium  chlorid  solution.  After  the  addition  of  the 
oxalate,  the  experimenter  should  wait  a  short  time  until  the  calcium 
becomes  precipitated.  This  occurs  almost  instantaneously,  and  when  it 
is  completed  the  saline  solution  is  added.  Two  such  mixtures  are  made 
in  two  similar  flasks,  and  one  is  employed  for  color  comparison.  By 
this  method  the  change  of  color  is  apparent  even  with  dark  gastric 
juices  and  urines.  A  special  procedure  is  necessary  for  urines  contain- 
ing a  phosphatic  precipitate.  If  the  urine  contain  no  carbonate,  the 
phosphatic  precipitate  may  be  dissolved  with  |  acid  ;  the  amount  of 
added  acid  must  be  subsequently  deducted  from  the  result  obtained  by 
titration.  Should  carbonates  be  present  this  procedure  cannot  be  fol- 
lowed, since  the  acid  would  liberate  CO^,  and  the  urinary  acidity  would 
consequently  be  decreased.  In  this  case  the  precipitate  from  a  definite 
quantity  of  well-stirred  urine  is  collected  upon  a  filter,  well  washed, 
and  titrated  (with  methyl  orange  as  an  indicator)  in  the  smallest  volume 
of  ^  acid  that  will  hold  it  in  solution  ;  the  sodium  oxalate  and  sodium 
chloride  are  then  added  as  usual,  and  the  solution  is  titrated  back 
with  ^  KOH  and  phenolphthalein.  The  alkali  equivalent  found  in 
the  precipitate  must  then  be  deducted  from  the  acidity  found  in  the  fil- 
tered urine. 


INDEX. 


Abdomen,  auscultation  of,  286 
cysts  of,  inspection  of,  303 
deeply-placed  solid  masses  in,  dipping  for, 

305 
edema  of,  inspection  of,  301 
fluctuation  of,  305 
free  fluid  in,  dipping  for,  305 

fluctuation  wave    in  diagnosing,   302, 

305 
inspection  of,  302 
inspection  of,  301 
obesity  of,  inspection  of,  301 
palpation  of,  304 
errors  in,  307 
interrupted,  305 
jerky,  305 
results,  general,  305 
special,  308 
percussion  of,  comparative,  215 
sensitiveness  to  pressure,  palpation  in  de- 
termining, 306 
splashing  noise  of,  286,  313 
tumors  of,  deep-lying,  dipping  for,  305 
palpation  of,  306 
Abdominal  aneurism,  307 
breathing,  77 

cysts,  exploratory  puncture  of,  722 
reflex,  777 

viscera,  air-containing,  percussion  of,  196 
disease  of,  asymmetry  of  chest  due  to,  33 
wall,  dilated  veins  in,  inspection  of,  302 
Abducens  nerve,  functions  of,  826 
Abscess  of  liver,  dulness  in,  190 
pulmonary,  sputum  in,  607 
retropharyngeal,  687 

subphrenic,  Litten's  sign  in  diflFerentiat- 
ing  empyema  from,  78 
Acatectic  icterus,  44 
Accidental  albuminuria,  459 
heart  murmurs,  260,  274 

valvular  heart  murmurs  and,  differ- 
entiation, 277 
Accommodation  in  nervous  diseases,  848 

paralysis  of,  848 
Acetic  acid  and  potassium  ferrocyanid  test 
for  albuminuria,  463 
in  gastric  juice,  detection  of,  375 
Acetone  in  urine,  detection  of,  493 
Gunning's  iodoform  test  for,  494 
Legal's  test  for,  495 
Lieben's  iodoform  test  for,  495 
quantitative  estimation  of,  540 
Achilles-tendon  reflex,  778 
Acholia,  color  of  feces  in,  424 
Achroodextrin,  371 
Acid,  acetic,  in  gastric  juice,  377 

beta-oxybutyric.  in    urine,  Darmstadter's 
estimation  of,  540 


Acid,  beta-oxybutyric,  in  urine,  detection  of, 
497 
Kiilz's  test  for,  497 
quantitative  estimation  of,  539 
bile,  in  feces,  445 

in  urine,  detection  of,  474 

Pettenkofer's  test  for,  475 
p-oxybutyric,    in    urine,     Darmstadter's 
estimation  of,  540 
detection  of,  497 
Kiilz's  test  for,  497 
quantitative  estimation  of,  539 
butyric,  in  gastric  juice,  detection  of,  377 
carbolic,  coloring  urine,  454 
chrysophanic,  in  urine,  detection  of,  503 
contents  of  gastric  juice,  diagnostic  notes, 

389 
diacetic,  in  urine,  detection  of,  495 

Gerhardt's  test  for,  496 
fatty,  in  feces,  tests  for,  446 

volatile,  detection  of,  in  gastric  juice,  377 
glycuronic,  in  urine,  detection  of,  492 

Tollen's  test  for,  493 
homogentisic,  in  urine,  detection  of,  497 
hydrochloric,  Gunzburg's  test  for,  373 
in  gastric  contents,  diminution  of,  384 
vomitus  of,  360 
juice,  383 

Mintz's  test,  383 
quantitative  estimation  of,  379 
tests  for,  372 

total  un neutralized,  estimation,  379 
Leo's  method,  380 
Liitke-Martius'  method,  380 
Sjoqvist's  method,  379 
methyl-violet  reaction  for,  372 
phloroglucin-vanillin  reaction  for,  373 
tests  for,  372 

tropseolin  00  reaction  for,  373 
value  of,  373 
lactic.  Boas'  method  of  detecting,  376 
in  carcinoma  of  stomach,  376 
in  gastric  contents,  quantitative  estima- 
tion of,  386 
juice,  tests  for,  374 
in  motor  insufficiency  of  stomach,  376 
in  stenosis  of  stomach,  376 
Strauss'  method  of  determining,  375 
Ufielmann's  reagent  for,  374 
lipuric,  in  urine,  562 

of  gastric  juice,  physiologic  relationship 
of,  388 
quantitative  tests  for,  377 
salicylic,  in  urine,  detection  of,  502 
succinic,  in  echinococcus  fluid,  724 

Hoppe-Seyler  test  for,  724 
sulphuric,  in  urine,  quantitative  estima- 
tion of,  537 

967 


968 


INDEX. 


Acid,  total  organic,  of  gastric  coutents,  quan- 
titative determination,  386 
uric,  556 
■  Hopkin's  estimation  of,  531 

Folin  and  Shaffer's  modification,  531 
Hopkin-Worner  method    of  estimating, 

531 
in  blood,  674 

trarrod's  test  for,  675 
Ludvrig-Salkowski"s  method  of  estimat- 
ing, 530 
murexid  test  for,  556 
quantitative  estimation  of,  529 
valerianic,   in  gastric  juice,  detection  of. 
377 
Acidic  points  of  urine,  estimation,  541 
Acidimetric   titration    of  fluids   containing 
alkaline  earths   and   ammonia  salts, 
965 
of  gastric  juice,  965 
of  urine,  965 
Acidity  of  urine,  determination,  .541 

total,  of  gastric  contents,  Topfer's  method 
of  estimating.  384 
juice,  titration  of,  377.  965 
Acid-staining  bacilli   in   sputum,   isolating 

tubercle  bacilli  from,  595 
Acoustic  nerve.  953 

sphere  of  action,  162 
Acromegaly,  795 
Actinomycosis,  603 
Acusticus    nerve,    865.      See    also  Auditory 

nerve. 
Adenoids,  687 
Addison's  disease,  45 

argyria  and,  differentiation.  46 
arsenic  melanosis   and.  differentiation, 

46 
melasicterus  and.  differentiation,  46 
Adiposity.  26 

After-resonance,  metallic,  157 
Agarophobia,  883 
Agony,  leukocytosis  of,  649 
Agraphia,  896 
association,  897 
conduction.  897 
mixed  forms,  897 
subcortical.  897 
transcortical,  897 
Air  hunger,  84 
Albumin  in  sputum.  605 

in  urine.  458.     See  also  Albuminuria. 
serum-,  in  urine,  detection  of,  460 
Albumineuse.  608 
Albuminimeter.  Esbach's,  505 
Albuminuria,  458 
accidental,  459 
acetic  acid  and  potassium  ferrocyanid  test 

for,  463 
casts  in,  570 
cold  tests  for,  462 
cyclic,  459 
false,  459 
febrile,  460 
heat  test  for,  460 
Heller's  test  for,  462 
metaphosphoric  acid  test  for,  463 
nephritic,  460 
nitric  acid  test  for,  462 
picric  acid  test  for,  463 
renal,  459 
test  for  albumosuria,  466 


Albuminuria,  true,  4.59 
Albuminuric  neuroretiuitis,  704 
Albumoses  in  urine,  465.     See  also  Albumo- 
suria. 
Albumosuria,  465 

albumin  test  for,  446 

Beuce-Jones,  466 

Salkowski's  test  for,  466 

Schulte's  test  for,  467 
Alcohol   amblyopia,   discoloration   of   optic 

disk  in,  706 
Alcoholism,  delirium  of,  739 
Aldor's  modification  of  Salkowski's  test,  467 
Alexia,  896 

cortical,  897 

mixed  forms,  897 

subcortical,  896 

transcortical,  897 
Alimentary  glycosuria,  480,  481 
Alizarins,  381 

Alkalinity  of  blood.  Dare's  test,  615 
Salkowski's  test.  615 

of  urine,  determination,  541 
Alkapton  coloring  urine,  454 

in  urine,  detection  of,  497 
Allihn-Soxhlefs    estimation    of    .sugar    in 

urine.  510 
Allorrhythmia.  960 

auriculoventricular,  298 
AUoxuric  bodies  in   urine,    estimation    of, 

532 
Almen-Xvlander's  test  for  sugar  in   urine, 

485 
Almeu-Schonbein's  test  for  blood  in  feces, 
447 

test  for  hemoglobinuria,  471 
Aloes  in  urine,  detection  of,  503 
Alveolar  epithelium  in  sputum,  588 
Amann's  test  for  indican  in  urine,  477 
Amblyopia,  825 

alcohol,  discoloration  of  optic  disk  in,  706 
Amebse  of  dysentery,  430 
Amimia.  901 

Ammonia  in  urine,  quantitative  estimation 
of,  538 
Schlosiug's  test  for  estimating,  539 
Ammoniomagnesium     phosphate  in  urine, 

558 
Ammonium  urate  in  urine,  558 
Amoeba  coli,  431 

intestinalis  vulgaris,  431 
Amphoric  breathing.  229 
Amusia,  901 

Anacrotic  pulse,  114,  117 
Anacrotism,  129 
Anal  reflex.  778 
Anarthria.  888 

from  aphasia,  899 
Anasarca,  48 
Anemia,  611 

blood  in.  659 

cutaneous  hemorrhage  in,  53 

following  acute  loss  of  blood,  663 
chronic  loss  of  blood.  663 

pernicious,  blood  in.  660 

cutaneous  hemorrhage  in,  53 
eyeground  in.  704 

primary,  blood  in.  659,  660 

secondary,  blood  in,  662 
Anemic  degeneration  of  erythrocytes,  637 

dyspnea,  91 

heart  murmurs,  274 


INDEX. 


969 


Anemic  leukocytosis,  649 
Anesthesia,  756 
dolorosa,  771 

hysteric,  bone  sensibility  in,  766 
Aneurism,  abdominal,  307 
of  aorta,  314,  345 

Oliver-Cardarelli  sign  of,  347 
skiagraph  of,  347,  737 
Anginas,  outline  for  examination  of,  949 
Angioneurotic  edema,  52 
Anguillula  intestinalis  in  feces,  435 

stercoralis  in  feces,  435 
Animal  experiments  for  demonstrating  tu- 
bercle bacilli  in  sputum,  596 
parasites  in  feces,  429 
in  sputum,  592 
in  urine,  578 
Ankle-clonus,  778 

Ankylostoma  duodenale  in  feces,  433 
Anthrax  bacillus  in  blood,  652 

in  feces,  443 
Antifebrin  in  urine,  detection  of,  503 
Antipyrin  in  urine,  detection  of,  502 
Aorta,  aneurism  of,  314,  345 

Oliver-Cardarelli  sign  of,  346 
skiagraph  of,  347,  737 
obliteration  of,  at  mouth  of  ductus  Botalli, 

343 
straddling  of,  344 
Aortic  insufficiency,  328 
capillary  pulse  in,  144 
diastolic  murmur  of,  266,  330 
murmur  of,  266,  330 
pulsus  tardus  of,  334 
stenosis,  332 
tones,  248 

valve,  systolic  murmurs  arising  at,  266 
Ape  hand,  747 

Apex  beat,  289.     See  also  Heart  heat. 
Aphasia,  890 

anarthria  from,  899 
associated,  892,  893 

eflfects  on  written  speech,  896 
conduction,  892,  893 

effects  on  written  speech,  896 
cortical  motor,  893 

effects  on  written  speech,  896 
sensory,  892 

effects  on  written  speech,  896 
diffuse,  898 

disturbances  related  to,  901 
functional,  898 
indefinite,  898 
memory,  898 
optic,  898 
subcortical  motor,  893 

effects  on  written  speech,  896 
sensory,  892 

effects  on  written  speech,  896 
transcortical  motor,  893 

effects  on  written  speech,  896 
sensory,  893 

effects  on  written  speech,  896 
Aphonia,  94 

Aphthous  patches  on  tongue,  683 
Apical  percussion,  171,  172 
Appendicitis,  exploratory  puncture  in,  725 
Appendix,  948 
Apraxia,  901 

Arbutin  coloring  urine,  454 
Areometric  method  of  determining  specific 
gravity  of  blood,  612 


Argyll-Eobertson's  phenomenon,  848 
Argyria,  Addison's  disease  and,  differentia- 
tion, 46 
Arhythmia,  104 
Arhythmias,  intropic,  964 
true,  959 

primary,  963 
Aromatic  products  coloring  urine,  454 
Arsenic  melanosis,   Addison's  disease    and, 

differentiation,  46 
Arterial  liver  pulse,  152,  300 

venous  pulse  and,  differentiation,  147 
wall,  character  of,  in  palpation  of  pulse,  99 
Arteries,  auscultation  of,  282 
Arteriosclerosis,  localized,  systolic  murmur 
from,  283 
pulse  in,  99,  128 
Arthritis  deformans,  skiagraph  of,  736 
Arthropathy,  tabetic,  794 
Arthus  and  Huber's  demonstration  of  action 
of  trypsin,  421  . 

Articular  rheumatism,    acute,  leukocytosis 

of,  647 
Ascaris  lumbricoides  in  feces,  432 
Asiatic  cholera,  feces  of,  443 
Aspergillus  in  sputum,  602 
Aspirated  fluid,   bacteriologic  examination 

of,  713 
Associated  aphasia,  892,  893 

effects  on  written  speech,  896 
movements,  750 
Association  agraphia,  897 
Asthma,  bronchial,  Curschmann's  spirals m, 
585' 
dyspnea  in,  90 
eosinophilia  in,  649 
extension  of  lung  borders  in,  175 
cardiac,  86 
Asymbolia,  901    . 

Asymmetry  of  chest  from  disease,  33,  36 
Atactic  gait,  908 
Ataxia,  752 
central,  753 
cerebellar,  752,  755 
cortical,  753 

Friedreich's,  speech  disturbances  in,  899 
hereditary,  muscle  unrest  in,  750 
pseudo-,  754 

sensation  of  innervation  in,  763 
Atelectasis,  compression,  dulness  of,  209 
dulness  of,  198,  209 
lung  dulness  in,  198,  209 
obstructive,  dulness  of,  209 
obturation,  preventing  bronchial  breath- 
iug,  228 
Athetoid  movements,  750 
Athetosis,  750 
Atony,  gastric,  356 

Atrophic  discoloration  of  optic  disk  in  alco- 
hol amblyopia,  706 
paralysis,  789 

secondary  degenerative  muscular  atro- 
phies after,  790 
Atrophy,  acute  yellow,  of  liver,  cutaneous 
hemorrhage  in,  53 
palpation  in,  310 
muscular,  788.     See  also  Muscular  atrophy. 
neuritic,  of  optic  disk,  705 
of  optic  disk,  705 

nerve  in  glaucoma  simplex,  705 
in  pulsating  exojjhthalmos,  705 
papillitic,  706 


970 


INDEX. 


Atrophy,  papillitic,  after  thrombosis,  706 
retinal,  in  chorioretinitis,  706 
Virchow's,  of  tongue,  683 
Attitude  and  gait,  27 

constrained,  24 
Atypical  fever,  75 

Auditory  nerve,  functions  of,  850,  865 
irritative  phenomena  of,  867 
outline  for  examination  of,  953 
paralysis  of,  865 
Politzer's  test  for,  865 
Einne's  test  for,  865 
Schwabach's  test  for,  866 
Weber's  test  for,  866 
vertigo,  867 
Auriculoventricular  allorrhythmia,  298 
Auscultation,  217 

differentiating  systole  and  diastole  by,  248 

direct,  218 

immediate,  218 

indirect,  218 

instruments  for,  217 

mediate,  218 

of  abdomen,  286 

of  arteries,  282 

of  blood-vessels,  282 

of  brachial  artery,  282 

of  carotid  artery,  282 

of  crural  artery,  282 

of  esophagus,  287,  690 

of  heart,  244 

of  lungs,  242,  243 

of  radial  artery,  282 

of  respiratory  organs,  219 

of  subclavian  artery,  282 

of  veins,  284 

of  vessels,  282 

of  voice  sounds  over  chest,  241 

signs  over  heart,  abnormal,  250 

normal,  244 
technic  of,  219 
Auscultatory  percussion,  158 
Autoscope,  698 

Kirstein's,  699 
Autoscopy  of  larynx,  698 

of  trachea,  698 
Autosuggested  pains,  771 

Baas'  theory  of  vesicular  breathing,  220 

Babinski's  reflex,  787 

Bacillus,  acid-staining,  in  sputum,  isolating 

tubercle  bacilli  from,  595 
anthrax,  in  blood,  653 

in  feces,  443 

in  sputum,  602 
comma,  in  feces,  441 
diphtheria,  examination  for,  684 

Neisser's  stain  for,  686 
influenza,  in  sputum,  598 
mallei  in  blood,  653 

in  sputum,  602 
of  bubonic  plague  in  blood,  653 

in  sputum,  600 
of  cholera  in  feces,  441 
of  dysentery,  Kruse's,  in  feces,  442 
pest,  in  blood,  653 

in  sputum,  600 
pseudodiphtheria,  685 
pyocyaneus  in  sputum,  582 
smegma,  in  sputum,  595 

in  urine,  576 
tubercle,  in  blood,  653 


Bacillus,  tubercle,  in  feces,  440 

in  sputum,  592.  See  also  Tubercle  bacillus 

in  sputum. 
in  urine,  576 
typhoid,  in  blood,  653 
in  feces,  442 
iu  sputum,  602 
Bacteria  in  blood,  652 
staining  of,  652 
in  sputum,  596 

Gram's  stain  for,  596 

Weigert's  modification,  597 
in  urine,  574 
of  feces,  439 

pathogenic,  439 
saprophytic,  in  sputum,  600 
Bacteriologic     examination     of     aspirated 

fluid,  713 
Ballottement,  dipping  in,  305 
Balsam   of  copaiba  in   urine,   detection   of, 

503 
Baresthesiometer,  Eulenburg's,  757 
Barking  cough,  96 

Barnard  and  Hill's  sphygmometer,  140,  141 
Barrel  chest,  30 

Basch's  sphygmomanometer,  134 
Basic  points  of  urine,  estimation,  541 
Basophilic  degeneration,  granular,  of  ery- 
throcytes, 636 
Baunscheidtismus,  45 

Beck-Hirsh  apparatus  for  determining  vis- 
cosity of  blood,  669 
Beckmann's     apparatus     for     determining 

freezing-point  of  urine,  546 
Beckmann-Heidenhain's  crvoscopic  appara- 
tus, 546 
Bed,  posture  in,  23 
Beets,  pigment  of,  in  urine,  455 
Bell's  phenomenon,  863 
Bence-Jones  albumose,  466 
Beta-oxybutyric  acid  in  urine,  Darmstadter's 
estimation  of,  540 
Kiilz's  test  for,  497 
quantitative  estimation  of,  539 
tests  for,  497 
Bial's  test  for  pentoses  iu  urine,  491 
Biermer's  phenomenon,  215 
Bile  acids  in  feces,  445 

in  urine,  detection  of,  474 
Petteukofer's  test  for,  475 
admixture  of,  in  vomitus,  360,  361 
Biliary  pigments  in  urine,  detection  of,  472 
Gmelin's  test  for,  472 

Eosenbach's  modification,  472 
Hammarsten's  test  for,  474 
injaundice,  453 
microscopic  test,  474 
removal  of,  474 
Stockvis'  test  for,  474 
Trousseau's  test  for,  473 
sand,  428 
Bilicyanin,  Stockvis'  test  for,  474 
Bilirubin  icterus,  44 

in  urine,  561 
Biot's  respiration,  81 
Biuret  reaction,  467 
Black  hairy  tongue,  683 
smallpox,  cutaneous  hemorrhage  in,  54 
sputum,  681 
Black-and-blue  spots.  53 
Bladder,  calculus  in,  skiagraph  of,  734 
catarrh  in  gonorrhea,  578 


INDEX. 


971 


Bladder  center,  theory  of,  944 
distended,  palpation  of,  313 
functions,  939 

examination  of,  947 

outline  for,  952 
in  cerebral  affections,  941 
in  diseases  of  spinal  cord,  942 
in    peripheral     affections    of    bladder 

nerves,  943 
physiologic,  mechanism  of,  939 
nerves,   peripheral    affections  of,    vesical 

functions  in,  943 
topographic  percussion  of,  196 
tumors  of,  palpation  of,  310 
Blindness,  706 

after  thrombosis  of  central  retinal  vein, 

706 
note,  901 
psvchic,  901 

simulated  unilateral,  detection  of,  82_p 
Blisters,  pigmentation  of  skin  from,  45 
Bloch's  pneumoscope,  94 
Blocking,  heart,  297 
Blood,  acute  loss  of,  anemias  after,  663 
admixture  of,  in  feces,  426 

in  vomitus,  360 
alkalinity  of.  Dare's  method,  615 

Salkowski's  method,  615 
anemias  after  loss  of,  663 
bacillus  mallei  in,  653 
of  anthrax  in,  652 
of  bubonic  plague  in,  653 
bacteria  in,  652 

staining  of,  652 
casts  in,  651 

chemical  examination  of,  671 
Chenzinsky's  eosin-methylene-blue  stain 

for,  633  " 
chronic  loss  of,  anemias  after,  663 
coagulation  time  of,  615 

Vierordt's  method,  615 
crvoscopy  of,  667 
diiminution  of,  influence  on  pulse  curve, 

120 
diseases,  blood  in,  659 
dried  specimens  of,  631 
Ehrlich's  triple  stain  for,  633 
eosinophilic  cells  in,  642 
examination  of,  609 
chemical,  671 

for  rouleaux  formation,  635 
method  of  obtaining  for,  610 
microscopic,  technic,  631 
outline  for,  950 
fat  in,  652 
fibrin    in,   microscopic  determination  of, 

636 
Francke's  needle  for  obtaining,  610 
freezing-point  of,  667 
fresh,  microscopic  examination  of.  631 
friction  of,  internal,  669 
hemoglobin  in,  616.     See   also  Hemoglobin 

in  blood. 
in  acute  leukemia,  666 
in  anemia,  659 
in  blood  diseases,  659 
in  carbon-dioxid  poisoning,  673 
in  chlorosis,  659 
in  erythemia,  663 
in  feces,  chemical  tests  for,  447 
Schonbein-Almen's  test  for,  447 
spectroscopic  tests  for,  447 


Blood  in  feces,  Teichmann's  hemin  test  for, 
447 
in  hemoglobinuria,  674 
in  hydrogen-sulphid  poisouing,  674 
in  leukanemia,  667 
in  leukemia,  664 
in  lymphatic  leukemia,  665 
in  lymphemia,  665 
in  lymphoid  leukemia,  665 
in  malaria,  653 

staining  of,  655 
in  methemoglobinemia,  674 
in  mixed  leukemia,  666 
in  myelemia,  666 
in  myelogenous  leukemia,  666 
in  myeloid  leukemia,  666 
in  pernicious  anemia,  660 
in  polycythemia,  663 
in  primary  anemia,  659,  660 
in  pseudoleukemia,  661 
in  secondary  anemia,  662 
in  urine,  569 
internal  friction  of,  669 
iodin  reaction  of,  634 

Ehrlich's  stain  for,  634 
iron  tests  for,  with  Jolles'  ferrometer,  671 
Jenner's  test  for,  633 
laked,  titration  of,  614 

Lowy  and  EngeFs  method,  614 
loss  of,  anemias  after,  663 
lymphocytes  in,  640 

inalariar  parasites  in,  653.     See  a.\so  Ma- 
laria, Plasmodia  of. 
mast  cells  in,  642 

microscopic  examination  of,  technic,  631 
molecular  concentration  of,  667 
mononuclear  neutrophilic  cells  in,  642 
morphologic  relations  of,  631,  950 
opaque,  titration  of.  613 

Laudois-von  Jaksch's  method,  613 
osmotic  pressure  of,  667 
parasitic  worms  in,  659 
pest  bacilli  in,  653 
quantity  of,  611 
reaction  of,  613 
specific  gravity  of.  612 

areometric  method,  612 
Hammerschlag's  method.  612 
pycnometric  method,  612 
spirillje  of  recurrent  fever  in,  652 
transitional  cells  in,  641 
tubercle  bacilli  in,  653 
typhoid  bacilli  in.  653 
uric  acid  in,  674 

Garrod's  test  for,  675 
viscosity  of,  669 

Willebrandt's  stain  for  granules  of,  634 
Blood-coloring  matter    in  urine,  469.     See 

also  Hemoglobinuria. 
Blood-corpuscles,  counting  of,  624 
quotient  of,  629 
red.     See  Eri/throcytes. 
volume  of.  in  given  quantity  of  b^ood,  629 
white.     See  Leukocytes. 
Blood-crises,  640 

Blood-granules.  Willebrandt's  stain  for,  634 
Bloodles-sness,  611 
Blood-needles,  610 

Blood-plasms,  specific  gravity  of,  612 
Blood-plates,  650 

counting  of,  651 
Blood-pressure,  106 


972 


INDEX. 


Blood-pressure,  pulse  curve  and,  relations, 

118 
Blood-test,     Heller's,     for     hemoglobinuria, 

470 
Bloody  sweat,  48 
Blue  edema,  797 

sweat,  48 
Boas'  method  of  obtaining  intestinal  juice, 
421 
test  for  lactic  acid,  376 
Boas-E\vald"s  method  of  obtaining  stomach 
contents,  368 
test-breakfast,  368 

examination    of    gastric    functions  by, 
370 
Boat-shaped  chest  of  syringomyelia,  32 
Body  weight,  28 

Bone  fragility  in  nervous  diseases,  793 
marrow,  lymphocytes  iu,  641 
sensibility,  765 
trophic  disturbances  of,  793 
Borborygmi,  286 
Botalli,  duct  of.  potency  of,  344 
Bothriocephalus  latus  iu  feces,  437 
B6ttcher"s  sperm  crystals,  591 
Bottger's  test,  modified,  for  sugar  in  urine, 

485 
Bougies,  esophageal,  688 
Boundaries,  superficial,  160,  161 
Bowles'  phonendoscope.  218 
Box  tone,  209 

|3-oxybutyric  acid   in   urine,  Darmstadter's 
estimation  of,  540 
Kiilz's  test  for,  497 
quantitative  estimation  of,  539 
tests  for,  497 
Brachial  artery,  auscultation  of,  282 
plexus,  localization  of,  932 
motor  roots  of,  934 
Bradycardia,  103 
Brandberg's  estimation  of  proteid  in  urine, 

506 
Breakfast,  test-,  filtrate  of,  examination  of, 
949 
for  stomach  functions,  367 
of  Ewald-Boas,  370 
Breast,  pigeon-,  31,  33 
Breathing.     See  Respiration. 
Breuer's  chamber  for  counting  leukocytes, 

626 
Broca's  area,  888 

Bromin  in  urine,  detection  of,  502 
Bronchi,  examination  of,  direct,  698 
Bronchial  asthma,  Curschmann's  spirals  in, 
585 
dyspnea  in,  90 
eosinophilia  in,  649 
extension  of  lung  borders  in.  175 
breathing,  graphic  expression  for,  348 
obturation  atelectasis  preventing,  228 
pathologic,  226 
physiologic,  222 
casts,  fibrinous,  in  sputum,  586 
whispering,  241 
Bronchiectasis,  sputum  in,  607 
Bronchiolitis  exudativa,  Curschmann's  spir- 
als in,  585 
Bronchitis,  capillarv,  phvsical  examination 
in,  3.53 
croupous,  sputum  iu,  605 
diffuse,  physical  examination  in,  352 
dyspnea  in,  88 


Bronchitis,  fibrinous,  sputum  in,  605 

obstructive  extension  of  lung  borders  in, 

175 
putrid,  sputum  in,  607 
sputum  iu,  605 
Bronchophony,  241 
Bronchopneumonia,  sputum  in,  607 
Bronchopneumonic  infiltrations,  dulness  in, 

208 
Bronchoscopy,  700 
Bronchovesicular  breathing,  231 

inspiration     with     bronchial    expiration, 
graphic  expression  for,  348 
with  prolonged  expiration,  graphic  ex- 
pression for,  348 
Brown-Sequard's  paralysis,  bone  sensibility 

in,  765 
Brucke's  peptone,  Salkowski's  test  for, 466 
Bruit  de  pot  fele,  158 

du  diable,  284 
Bruits  normaux,  244 
Bryson's  sign,  29 
Bubbling  rales,  232 
Bubonic  plague,  bacilli  of,  iu  blood,  653 

in  sputum,  600 
Buccal  mucous  membrane,  examination  of, 

687 
Bulbar  paralysis,  862 

increased  salivary  secretion  in,  864 
reaction  of  degeneration  in,  818 
Butvric  acid  in  gastric  juice,  detection  of, 

377 
Butyrometric    stomach    examination,    948. 
See  also  Stomach,  functions  of. 

Cachetic  leukocytosis,  649 

Cachexias,  severe,  cutaneous  hemorrhage  in, 

53 
Calcareous  concretions  in  sputum,  586 
Calcium  oxalate  in  urine,  556 

sulphate  in  urine,  559 
Calculus  in  ureter,  skiagraph  of,  731 
in  urine,  563 
renal,  skiagraph  of,  732 
vesical,  skiagraph  of,  734 
Capillarv  bronchitis,  phvsical  examination 
in,  353 
pulse,  144 
Capsular  hemianesthesia,  821 
Capsules,  glutoid,  intestiual  digestion  and, 
419 
rubber,  testing  digestion  with,  364 
Caput  medusae,  56,  303 

obstipum  spasticum.  874 
Carbohydrates  in  feces,  446 
Carbonates  iu  urine,  557 
Carbon-dioxid  poisoning,  blood  in,  673 
Carbonization  test  for  sugar  in  urine,  489 
Carcinoma  of  lungs,  dulness  in,  198 
of  rectum,  feces  of,  444 
of  stomach,  diagnosis  by  lavage,  370 
lactic  acid  in,  376 
vomitus  of,  360 
Cardia  bigeminus,  296 
Cardiogram,  298 
Cardiograph,  298 
Cardiohepatic  angle,  187 
Cardiopneumatic  rales,  238 
Cardiosystolic  rales,  238 
Carotid  artery,  auscultation  of,  282 

pulse,  148 
Carphologia,  740 


INDEX. 


973 


Cascara  coloring  urine,  455 

sagrada  in  urine,  detection  of,  503 
Casein  in  feces,  427,  439 
Casts,  fibrinous  broncliial,  in  sputum,  586 

in  albuminuria,  570 

in  blood,  651 

in  urine,  570 

mucous,  in  urine,  572 

testicle,  in  urine,  573 
Catacrotic  pulse,  114 
Catalepsy,  739,  751 
Cataleptic  rigidity,  739,  751 
Catarrh  of  bladder  in  gonorrhea,  578 

mucous,  of  stomach,  vomitus  of,  360 

sputum  in,  605 
Catarrhal  pneumonia,  physical  signs  in,  352 
Catheterization,  fever  after,  69 
Cauda  equina,  topography  of,  937 
Cavernous  breathing,  229 
Cells,  eosinophilic,  in  blood,  642 

epithelial,  in  sputum,  587 

heart,  in  sputum,  588 

mast,  in  blood,  642 
granules  of,  632 

mononuclear  eosinopliilic,  in  blood,  642 
neutrophilic,  in  blood,  642 

of  heart  disease,  589 

pus,  in  urine,  566 

transitional,  in  blood,  641 
Centrifugal  venous  pulse,  positive,  150 

negative,  147 
Centrifugation  of  urine,  553 
Centrifuge,  electrical,  554 
Centripetal  venous  pulse,  positive,  152 
Cercomouas  hominis,  430 
Cerebellar  ataxia,  752,  755 
Cerebral  affections,  functions  of  bladder  in, 
941 

disturbances  of  sensation,  878 

hemianesthesia,  bone  sensibility  in,  765 
from  anatomic  lesions,  879 

hemiplegias,  electric  reaction  in,  876 
reflexes  in,  781,  785 
vasomotor  disturbances  in,  795 

localization,  884 

meningitis,  vomitus  of,  361 

paralyses  of  chewing  muscles,  849 

reflexes,  780 
Cerebrospinal  fever,  herpes  febrilis  in,  62 

posture  in  bed  in,  25 
Cestodes  in  feces,  435 
Charcot's  crystals  in  feces,  432 
Charts  for  physical  diagnosis,  955 
Chemical  examination  of  blood,  671 
of  feces,  444 

of  gall-stones,  method,  429 
of  sputum,  605 
of  urine,  qualitative,  458 

test  for  blood  in  feces,  447 
for  hemoglobinuria,  470 
Chemistry  of  intestines,  418 
Chenzinsky's  eosin-methylene-blue  stain  for 

blood,  633 
Chest,  asymmetry  of,  33,  36 

auscultation  of  voice  sounds  over,  241 

barrel,  30 

boat-shaped,  of  syringomyelia,  32 

circumference  of,  29 

cobbler's,  32 

comparative  percussion  of,  197 

configuration  of,  30 

cracked -pot  resonance  over,  213 


Chest,  deformities  of,  heart  beat  in,  292 

emphysematous,  30 

expansion,  29 

fluctuation  in,  287 

funnel-shaped,  32,  35 

kyphotic,  31 

measurement,  29 

metallic  resonance  over,  212 

noise  of  chink  of  coins  over,  213 

noise  of  spinning-top  over,  213 

paralytic,  30 

pathologic  inspiratory  retraction  of,  79 

percussion  over,  197,  212,  213 

peripneumonic  retraction  of,  80 

phthisic,  31 

rachitic,  31 

resistance  of,  287 

scoliokj'photic,  31 

scoliotic,  31 

shape  of,  30 

localized  prominence  of,  in  coughing,  98 
Chewing  muscles,  cerebral  paralysis  of,  849 
Cheyne-Stokes  respiration,  81 
Chink  of  coins,  noise  of,  158 

over  thorax,  213 
Chloasma  gravidarum,  45 

uterinum,  45 
Chlorids    in    gastric    contents,    determina- 
tion of,  386 
juice,  quantitative    estimation  of,  379, 
381 

in  urine,  quantitative  estimation  of,  534 
Volhard's  estimation,  535 
Chlorin  in  gastric  juice,  quantitative  esti- 
mation of,  381 
Chlorosis,  blood  in,  659 
Choked  disk,  703 

Cholecyanin,  Stockvis'  test  for,  474 
Cholelithiasis,    Eiedel's  projection  of  liver 

in,  311 
Cholera  Asiatica,  vomitus  of,  361 

bacillus  of,  in  feces,  441 

nostras,  feces  of,  443 
vomitus  of,  361 

voice  in,  95 
Cholesterin  in  urine,  561 
Cholesterinuria,  561 

Chorda  tympani,   injury  of,  in  facial  paral- 
ysis, 858 
Chorea,  750 

neurosis,  750 
Choreic  gait,  909 

movements,  750 
Chorioretinitis,  retinal  atrophy  in,  706 
Choroidal  tubercle  in  acute  miliary  tuber- 
culosis, 704 
Chromidrosis,  48 
Chrysarobin  coloring  urine,  455 
Chrysophauic  acid  in  urine,  detection  of,  503 
Chyluria,  561 

Cipolliua's  test  for  sugar  in  urine,  487 
Circulation,  collateral,  in  skin,  55 
effect  of  valvular  lesions  on,  314 
portal,  obstruction  of,  303 
Circulatory  disturbances,  cyanosis  from,  41 

dyspnea  from,  85 
Cirrhosis  of  liver,  303 

palpation  of  liver  in,  310 
pigmentation  of  skin  in,  46 
Claw-hand,  741 

in  ulnar  paralysis,  747 
Cliquetis  metallique,  254 


974 


INDEX. 


Clonic  convulsions,  744 

Closure  rime  of  systole,  115 

Clubbed  fingers,  59 

Coagulable  proteids  of  urine,   detection  of, 

460 
Coagulation  time  of  blood,  615 

Vierordt's  method    of    determining, 
615 
Coal-tar    products,    urinary    pigmentation 

from,  454 
Cobbler's  chest,  32 
Cofl[in-lids,  558 

Cog-wheel    inspiration    with  bronchial    ex- 
piration, graphic  expression  for,  348 

respiration,  226 

vesicular  breathing,    graphic  expression 
for,  348 
Cohu's  stain  for  urinary  sediment,  564 
Coins,  chink  of,  noise  of,  158 

over  thorax,  213 
Cold  tests  for  albuminuria,  462 
Collapse,  venous  systolic,  147 

diastolic,  152 
Collr^teral  circulation  in  skin,  55 
Color  of  feces,  424,  445 

of  flesh,  qualitative  changes  of,  38 

of  skin,  38 

of  sputum,  579,  581 

of  urine,  453 
Colorimetric      estimation    of    dextrose    in 

urine,  512 
Coma,  738 

diabetic,  exaggerated  respiration  in,  91 
Combined  venous  pulse,  152 
Comma  bacillus  in  feces,  441 
Compensation,  valvular,  314 
Compensatory  dilatation  of  heart  chambers, 
316 

disturbances  of  heart,  319 
Complex  reflexes,  781 
Compression  atelectasis,  dulness  of,  209 
Conduction  agraphia,  897 

effects  on  written  speech,  896 
Configuration  of  thorax,  30 
Congestion,  edema  from,  50 

passive,  amount  of  proteid  in,  460 
of  spleen,  palpation  in,  311 
Conjugate  deviations  of  eye,  834 

paralyses  of  eyes,  834 
Consciousness,  disturbances  of,  738 
Consonating  phenomena,  242 

rales,  235 
Constipation,  422 
Constrained  attitudes,  24 
Continued  fevers,   daily  variations  in  tem- 
perature, 68 
Contractions,  clonic,  744 

law  of,  with  galvanic  current,  811 

of  ocular  muscles  in  hysteria,  838 

pupillary,  in  nervous  diseases,  840 
Contractures,  active,  745,  746 

passive,  745,  746 
Conus  terminals,  topography  of,  937 
Converging  movements  of  eyes,  paralysis  of, 

836 
Convulsions,  clonic,  744 

tonic,  744 
Cook's  modification  of  Riva-Eocci's  sphyg- 
momanometer, 141,  142 
Co-ordination  center,  Kronecker's,  722 

disturbances  of,  752 
Copaiba,  balsam  of,  in  urine,  tests  for,  503 


Copper  test  for  sugar  in  urine,  482 
Corneal  sensibility  in  nervous  diseases,  850 

reflex,  850 
Corpuscles,  blood-,  counting  of,  624 
quotient  of,  629 

volume  of,  in  given  quantity  of  blood, 
629 
pus,  in  sputum,  587 
red.     See  Erythrocytes. 
white.     See  Leukocytes. 
Corset  liver,  311 
Cortical  alexia,  897 
ataxia,  753 

lesions,  sensory  disturbances  with,  880 
motor  aphasia,  893 

effects  on  written  speech,  896 
pupillary  reflex  of  Haab,  847 
sensory  aphasia,  892 

effects  on  written  speech,  896 
Costal  breathing,  77 
limitation  of,  78 
Cough, 95 
barking,  96 
dry,  96 
hacking,  97 
in  pertussis,  97 

localized  prominence  of  chest  during,  98 
loose,  96 
moist,  96 
nervous,  96 
Coughing  paroxysms,  97 
Cracked-pot  resonance,  158 

over  thorax,  213 
Crackling  rales,  233,  234,  236 
Cramps,  tonic,  744 

Cranberry  test  for  fasting  stomach,  368 
Cranial  nerve,  eighth,  outline  for  examina- 
tion of,  953 
eleventh,  functions  of,  869 

examination  of,  821,  953,  954 
fifth,  functions  of,  849 

outline  for  examination  of,  953 
first,  examination  of,  821 

outline  for  examination  of,  953 
fourth,  functions  of,  826 

outline  for  examination  of,  953 
ninth,  functions  of,  869 

outline  for  examination  of,  954 
second,  functions  of,  822 

outline  for  examination  of,  953 
seventh,  865.     See  also  Auditory  nerve. 
sixth,  functions  of,  826 

outline  for  examination  of,  953 
tenth,  functions  of,  869 

outline  for  examination  of,  954 
third,  functions  of,  826 

outline  for  examination  of,  953 
twelfth,  functions  of,  875 

outline  for  examination  of,  954 
Cremaster  reflex,  777 
Crepitant  rales,  233,  237 
Crepitatio  indux,  237 

redux, 237 

Crepitation,  237 

cardiac,  238 

hair,  in  auscultation  of  lungs,  243 
Cretinism,  740 
Crises,  blood-,  640 
Crisis,  70 

interrupted,  71 
protracted,  71 
Crossed  double  pictures,  828 


INDEX. 


975 


Crossed  pupillary  reaction,  840 
Croupous  bronchitis,  sputum  iu,  605 
pneumonia,  dulness  in,  208 
fever  curve  of,  69 
left,  physical  examination  in,  351 
sputum  in,  606 
Crural  artery,  auscultation  of,  282 
Cryoscopy  of  blood,  667 
of  urine,  545 

Beckmann's  apparatus,  546 
renal  functions  and,  549 
technic,  546 
Crystalline     trimagnesium      phosphate     in 

urine,  559 
Currant  test  for  fasting  stomach,  368 
Current  murmurs,  origin  of,  262 
Curschmann's  spirals,  585,  591 
Cyanosis,  40 
admixture,  343 
causes,  41 
general,  40 

objective  dyspnea  and,  93 
of  congenital  heart  disease,  41 
Cyclic  albuminuria,  459 
Cylindric  epithelium  in  sputum,  587 
Cylindroids  in  urine,  572 
Cyon's  depressor,  870 
Cyrtometer,  Woillez's,  35 
Cystin  in  urine,  560 
Cystinuria,  560 

Cysts,  abdominal,  exploratory   puncture  of, 
722 
inspection  of,  303 
echinococcus,   fragments  of,  in  urine,  578 

of  liver,  dulness  in,  190 
intrathoracic,    exploratory    puncture   of, 

722 
of  urinary  system,   urea  in,  Salkowski's 

test  for,  724 
ovarian,  paralbumin  in,  724 

Salkowski's  test  for,  724 
pancreatic,  ferments  in,  725 
Cytodiagnosis,  714 

technic  of,  719 
Czaplewsky's  stain   for   tubercle  bacilli  in 
sputum,  594,  593 

Dare's    determination     of    alkalinity    of 

blood,  615 
Darmstadter's  estimation  of  beta-oxybutyric 

acid  in  urine,  540 
Deafness,  psychic,  901 
simulated,  demonstration  of,  867 
tone.  901 
word-,  892 
Decubitus,  791 

acute  unilateral,  792 
Deformities  of  thorax,  displaced  heart-beat 

in, 292 
Degeneration,  erythrocytic,  anemic,  637 
granular  basophilic,  636 
polychromatophilic,  637 
reaction  of,  790,  812 
complete,  813 
in  bulbar  paralysis,  818 
in  infantile  spinal  paralysis,  820 
in  lead  palsy,  820 
in  lead-poisoning,  816 
in  muscular  atrophy,  817,  818 
in  peripheral  paralysis,  816,  817 
in  poliomyelitis,  820 
in  polj'ucuritis,  816 


Degeneration,  reaction  of,  in  rheumatic  fa- 
cial paralysis,  819 
incomplete,  814 
mixed, 814 
Degenerative  muscular  atrophy,  789 

secondary,  790 
Delirium,  739 
maniacal,  739 
muttering,  739 
noisy,  739 
quiet,  739 
tremens,  739 
Deniges'  estimation  of  purin  bodies  in  urine, 

533 
Dermatitis  medicamentosa,  62 
Dermographism,  796 
Desquamation,  63 
Deutero-albumoses    in    urine,   Salkowski's 

test  for,  466 
Dextrocardia,    dislocation   of  heart  dulness 

and,  differentiation,  189 
Dextrose  in  urine,  qualitative  tests  for,  480. 

See  also  Sugar  in  urine. 
Diabete  bronzee,  46 
Diabetes  insipidus  in  nervous  diseases,  797 

mellitus  in  nervous  diseases,  797 
Diabetic  coma,  exaggerated  respiration  in, 
91 
ferric  chlorid  reaction,  Gerhardt's,  for  dia- 
cetic  acid  in  urine,  496 
Diacetic  acid  in  urine,  detection  of,  495 

Gerhardt's  test  for,  496 
Diameter  of  pupils  in  nervous  diseases,  838 
Diaphragm,  hernia  of,  in  lung  region,  211 
skiagraph  of,  735 
phenomenon  and  allied  appearances,  78 
Diaphragmatic  breathing,  77 
Diarrhea,  422,  423 

color  of  feces  iu,  425 
Diastole  and  systole,  auscultation  in  differ- 
entiating, 248 
increased,    dilatation   of    heart  chamber 
from,  316 
Diastolic  murmurs  accentuated  at  beginning 
and  end,  269 
modified,  268 

of  aortic  insufficiency,  266 
of  pulmonary  insufficiency,  268,  338 
of  tricuspid  stenosis,  267 
over  arteries,  282 
over  exophthalmic  goiter.  283 
presystolic  accentuation  of,  269 
pure,  270 
real,  268 
tone,  245 

venous  collapse,  152 
Diazo-reaction  of  Ehrlich,  499 
Dicalcium  phosphate  in  urine,  559 
Dicrotic  pulse,  Landois'  theory  of  origin  of, 

116 
Dicrotism,  129 
Diffuse  bronchitis,  physical  examination  in, 

352 
DiflFusion  icterus,  44 

Digestion,  examination  of  outline  for.  948 
intestinal,  examination  of,  by  glutoid  cap- 
sules, 419 
leukocytosis  of.  646 

proteid,  products  of,  examination  of  gas- 
tric contents  for,  .395 
.'^tarch,  examination  of,  371 
testing  with  potassic  iodid  fibrin,  364 


976 


INDEX. 


Digestive  enzymes  in  feces,  445 

power  of  gastric  juice,  testing,  391 
Digital  examination  of  rectum,  415 
Dilatation  of  heart  chambers,  316 
of  lungs  in  cardiac  affections,  175 
of  stomach,  356 

vomitus  of,  353 
pupillary,  in  nervous  diseases,  839 
Dimethvlamidoazobenzol,  384 
Diphtheria  bacilli,  examination  for,  684 
Neisser's  stain  for.  686 
examination  of,  outline  for,  949 
Dipping,  305 

for  deeply-placed  solid  masses  in  abdomen, 

305 
for  free  fluid  in  abdomen,  305 
in  ballottement,  305 
in  deep-lying  abdominal  tumors,  305 
in  distended  gall-bladder,  305 
in  enlargement  of  gall-bladder,  310 
of  liver,  305 
of  spleen,  305 
Discoloration,  atrophic,  of  optic  disk,  706 
Dislocation  of  heart,  displacements  of  heart- 
beat from,  292 
dulness,  188 
dextrocardia  and,  differentiation,  189 
heart-beat,  pathologic,  191,  192 
of  liver  dulness,  19 
of  splenic  dulness,  194 
Displacements  of  heart-beat,  291,  292 
Distention  of  rectu'm,  416 
Distomum  hepaticum  in  feces,  435 
lanceolatum  in  feces,  435 
pulmonale  in  sputum,  592 
Dittrich's  plugs.  534 

Diverticulum  of  esophagus,   dulness   from, 
209 
from  pressure,  689 
from  stenosis,  vomitus  of,  361 
from  traction,  690 
Doremus  ureometer,  524 

Hind's  modification  of,  524 
Double  heart-beat,  296 
vision,  crossed,  828 
monocular,  830 
non-crossed,  829 
Drechsel-Klimmer's  estimation  of  sugar  in 

urine,  508 
Dropsy,  general.  48 
Drug  eruption,  62 

Drugs,  examination  of  urine  for,  501 
Drunkard's  paralysis,  819 
Dry  cough,  96 

rales,  234 
Ductus  Botalli,  potency  of,  344 
Dulness,  155 
absolute,  156,  163 
deep,  162 
of  heart,  176 

diminution  of,  180 
enlargement  of,  181 
mobility  of,  179 
pathologic  changes  in,  180 
Weil's  explanation  of,  163 
flat,  156 

from  diverticulum  of  esophagus,  209 
from  infarction  of  lung.  208 
from  infiltration  of  lung,  203 
from  inflammation  of  lung,  208 
from  pulmonary  edema,  209 
tuberculosis,  208 


Dulness  from  tumors  of  lungs.  208 
of  mediastinum,  203 
of  pleura,  208 
in  bronchopneumonic  infiltrations,  208 
in  croupous  pneumonia,  208 
in  lung  boundaries,  198 
of  compression  atelectasis,  209 
of  heart,  deep,  176 

diminution  of  180 
enlargement  of,  181 
mobility,  179 

pathologic  changes  in,  180 
dislocation  of,  183 

dextrocardia  and,  diiFerentiation,  189 
position  of  apex  beat  and,  295 
superficial,  170,  176 
diminution  of  180 
enlargement  of,  181 
mobility  of,  179 
pathologic  changes  in,  180 
of  hemothorax.  208 
of  hydrothorax,  202,  205 
of  liver,  190 

dislocations  of,  191 
gross  changes  in,  191 

mobility  of,  191 
relative,  190 
of  lung,  198 

of  obstructive  atelectasis,  209 
of  pleural  exudate,  202 

combined  with  pneumothorax,  206 
of  pulmonary  cavities,  208 
infarctions,  208 
retraction,  209 
pleuritic.  200 
line  of  201 
relative.  156,  163 
splenic,  193 

dislocations  of,  194 
gross  changes  in,  194 
superficial,  160.  163 
of  heart,  170,  176 
diminution  of,  180 
enlargement  of,  181 
mobility  of.  179 
pathologic  changes  in,  180 
of  liver,   changes   in   lower  border  of, 
191.  192 
Dumbness,  congenital,  899 
Duodenum,  stenosis  of,  vomitus  of,  361 
Dupre's  apparatus  for  estimation  of  urea, 

523 
Duroziez's  double  murmur.  282 
Dynamometer,  Oliver's,  141 
Dysentery,  amebae  of,  430 
bacillus  of,  Kruse's,  in  feces,  442 
feces  of,  444 
Dyspnea,  83 
anemic,  91 
expiratory,  90,  92 
febrile,  91 

forced  attitudes  in,  92 
from  circulatory  disturbances,  85 
from  diminution  in  breathing  surface  of 

lung,  85 
from  limitation  of  respiratory  excursions 

of  lung.  85 
from  obstruction  of  upper  air-passages,  86 
from  painful  breathing,  85 
habituation  to,  93 
in  bronchial  asthma,  90 
in  bronchitis,  88 


INDEX. 


977 


Dyspnea  in  emphysema,  90 

in  mitral  insufficiency,  322 

inspiratory,  92 

mixed,  92 

objective,  84 
cyanosis  and,  relations,  93 
subjective  dyspnea  and,  relations,  93 

stridor  of,  88 

subjective,  84 

objective  dj'spnea  and,  93 

uremic,  of  nephritis,  91 

various  types,  85 

whistling  of,  88 

with  tendency  to  slowed  breathing,  87 
Dystrophic  muscular  atrophy,  789 

Eccentric  hypertrophy  of  heart  chamber, 

315 
Ecchymoses,  53 

Echinococcus  cysts,  fragments  of,  in  urine, 
578 
of  liver,  dulness  in,  190 
elements  in  sputum,  586 
fluid,  scolices  in,  723 
succinic  acid  in,  724 

Hoppe-Seyler  test  for,  724 
scolices  in  fluid,  723 
Edema,  49 
abdominal,  inspection  of,  301 
angioneurotic,  52 
blue,  797 

from  congestion,  50 
hydremic,  50 

plethoric,  51 
in  nervous  diseases,  797 
in  paralysis,  797 
in  polyneuritis,  52,  797 
in  urticaria,  52 

iuflammatory,  51 
nephritic,  51 
obstructive,  50 
of  skin,  48,  49 

pulmonary,  dulness  from,  209 
sputum  in,  608 
Efi"usion,   fluid,  in  pericardium,  percussion 

in,  186 
Egg-yellow  reaction  of  Ehrlich,  500 
Egophony,  242 
Ehrlich' s  diazo-reaction,  499 
egg-yellow  reaction,  500 
marfezellen,  642 

stain  for  iodin  reaction  of  blood,  634 
for  tubercle  bacillus  in  sputum,  594 
triple  stain  for  blood,  633 
Ehrlich  and   Lazarus'  eosinophilic    myelo- 
cytes, 642 
Einhorn's  saccharometer,  515 
Ejaculatory  center,  theory  of,  944 
Elastic  fibers  in  sputum,  588 
Weigert's  stain  for,  589 
in  urine,  573 
Elbow-joint  movements  in  nervous  diseases, 

911 
Electric  centrifuge,  554 
examination  of  muscle,  outline  for,  954 
of  nerve,  outline  for,  955 
outlines  for,  954 
irritability,  798 

in  neural  paralysis,  817 
in  tetany,  817 
qualitative,  testing  of,  811 
quantitative,  testing  of,  808 

62 


Electric  irritability,  quantitative,  testing  of, 
808 
faradic  current,  810 
galvanic  current,  809 
reaction,  diagnostic  significance  of,  816 
of  old  peripheral  palsies,  814 
prognostic  significance  of,  819 
Ellis'  line,  201 
Emaciation,  pronounced,  in  chronic  disease, 

27 
Embryocardia,  259,  260 
Embryos  of  filaria  sanguinis  in  urine,  578 
Emodin  in  urine,  detection  of,  503 
Emphysema,  depression  of  upper  liver  bor- 
der from,  192 
diminution  of  cardiac  dulness  in,  180 
dyspnea  in,  90 
liver  borders  in,  192 
lung  borders  in,  174,  175 
of  lungs,  displaced  heart-beat  in,  292 
hyperresonant  tones  in,  209 
interstitial,  respiratory  murmurs  in,  240 
tympanitic  tones  in,  209 
of  skin,  52 
vicarious,  175 
Emphysematous  chest,  30 
murmur,  precordial,  281 
Empyema  necessitatis,  fluctuation  of,  287 
perforating,  sputum  in,  607 
subphrenic   abscess  and,  Litten's  sign  in 
diflfereutiation,  78 
Endocardial  murmurs,  260 

influence  of  breathing  on,  278 
origin  of,  261 

pericardial  rubs  and,  differentiation,  280 
Endocarditis,  ulcerative,  chills  in,  74 

cutaneous  hemorrhage  in,  53 
Engel  and  Lowy's  test  for  laked  blood,  614 
Enteroptosis,  depression,  lung  borders,  175 
of  upper  liver  border  from,  192 
inspection  of,  303 
palpation  in,  306 
Entozoa  in  feces,  432 
Enuresis,  947 
Enzymes,  digestive,  in  feces,  445 

lipolytic,  in  gastric  juice,  403 
Eosin-methylene-blue  stain  for  blood,  Chen- 

zinsky's,  633 
Eosinophilia  in  bronchial  asthma,  649 
in  helminthiasis,  650 
in  infectious  diseases,  650 
in  pemphigus,  650 
in  scarlet  fever,  650 
in  skin  diseases,  650 
in  trichinosis,  650 
in  uncinaria,  650 
Eosinophilic  cells  in  blood,  642 
mononuclear,  in  blood,  642 
leukocytosis,  649.     See  also  Eosinophilia. 
myelocytes,  Ehrlich  and  Lazarus',  642 
Ephelides,  45 

Ephemeral  varieties  of  fever,  69 
Epigastric  pulsation,  300 
Epithelial  cells  in  sputum,  587 

tubules  in  urine,  571 
Epithelium,  alveolar,  in  sputum,  588 
cylindric,  in  sputum,  587 
in  sputum,  587 
in  urine,  565 

of  urinary  tract  in  urine,  565 
preputial,  in  urine,  566 
pulmonary,  in  sputum,  588 


978 


INDEX. 


Epithelium,  renal,  in  urine,  565 

squamous,  in  sputum,  587 

vaginal,  in  urine,  566 
Equilibrium,  disturbances  of,  ocular,  829 
Equinovarus,  741,  747 
Erb's  juvenile  muscular  atrophy,  789 

myotonic  reaction,  815 

point,  801 
Erlanger's  sphygmomanometer,  142 
Erysipelas,  fever  curve  of,  69 

leukocytosis  of,  648 

leukopenia  of,  648 
Erythema  nodosum,  cutaneous  hemorrhage 

from,  54 
Erythemia,  blood  in,  663 
Erythroblasts,  639 
Erythrocytes,  anemic  degeneration  of,  637 

counting  of,  624 

Thoma-Zeiss  apparatus  for,  624 

granular  basophilic  degeneration  of,  636 

hemoglobin  quotient  of,  629 

in  sputum,  588 

microscopic  appearance  of,  636 

nucleated,  639 

number  of,  627,  628 

polychromatophilic  changes  of,  636 

punctate,  638 

ratio  of  leukocytes  to,  628 

resistance  to  hyposmotic  injury,  630 

size  of,  variatiou  in,  638 

staining  capacity  of,  636 

volume  quotient  of,  639 
Erythrocytic  shadows,  638 
Erj^throdextrin,  371 
Esbach'salbuminimeter,  505 

estimation  of  proteid  in  urine,  505 
Esophageal  sounds,  688 
Esophagoscopy,  691 
Esophagus,  auscultation  of,  287,  690 

diverticulum  of,  dulness  from,  209 
from  stenosis,  vomitus  of,  361 
from  traction,  690 

examinatiou  of,  687 

percussion  of,  691 

pressure  in,  diverticulum  from,  689 
measurement  of,  691 

stenosis  of,  689 

diverticulum  from,  varieties  of,  361 
Eulenburg's  baresthesiometer,  757 
Evaporation  test  for  sugar  in  urine,  489 
Ewald  and  Ruber's  test  of  stomach  motilitv, 
363 

and  Sievers'  test  of  stomach  motility,  362 
Ewald-Boas'  method  of  obtaining  stomach 
contents,  368 

test-breakfast,  368 

examination  of  gastric  functions  by,  370 
Exanthemata,  acute,  59 

cutaneous  hemorrhage  in,  53 
Exophthalmic  goiter,  837 

gallop  rhythm  of  heart  tones  from,  259 
systolic  and  diastolic  murmurs  over,  283 
venous  hum  in,  286 
Exophthalmos,  pulsating,  atrophy  of  optic 

nerve  in,  705 
Exploratory  punctures,  707.     See  also  Punc- 
ture, exploratory. 
Expression.  23 

Expulsion  time  of  systole,  115 
Extrapericardial  friction  rub,  239,  280 
Extrasystole,  intermittent  pulse  from,  956 

pararhythmic  pulse  from,  956 


Extremities,  elevation  of,  influence  on  pulse 
curve,  120 
movements  of,  testing,  766,  767 
position  of.  testing,  767 
venous    flow    from,    influence   on    pulse 
curve,  121 
Eyeball,  muscles  of,  functions  of,  826 

paralysis  of,  827 
Eyegrouud,  changes  in,  703 
Eyes,  conjugate  deviation  of,  834 
paralyses  of,  834 
converging  movements  of,  paralysis  836 
region  of,  motor  innervation  of,  826 

Fabee   and   Penzoldt's    test  of   absorbing 

power  of  gastric  mucous  membrane,  361 
Face,   diminished  sensibility  of,  in  paraly- 
sis, 864 
skin  of,  abnormal  redness  of,  39 
Facial  nerve,  functions  of,  850 

outline  for  examination  of,  953 
paralysis,  851 
central,  853 

diminished  sensibility  of  face  in,  864 
injury  of  chorda  tympani  in,  858 
lagophthalmus  in,  851,  862 
nucleoproteid,  857 
pains  in,  864 
rheumatic,  reaction  of  degeneration  in, 

819 
supranuclear,  853 
symptomatology  of,  851 
spasms,  864 
Facies  Hippocratica,  24,  49 
Falling  drops,  noise  of,  236 

in  pneumothorax,  241 
False  albuminuria,  459 
Faradic  current  in  testing  irritability,  810 

laws  of  contraction  with,  811 
Fascicular  twitching,  748 
Fastigium  of  typhoid  fever,  71 
Fasting  stomach,  contents  of,  368 
cranberry  test  for,  368 
currant  test  for,  368 
Fat  in  blood,  652 
in  feces,  tests  for,  446 
in  urine,  561 
splitting  of,  438 
utilization  of,  438 
Fat-needles  in  feces,  438 
Fat-stools  in  diseases  of  pancreas,  444 
Fatty  acids  in  feces,  tests  for,  446 
volatile,  in  gastric  juice,  377 
Febricula,  69 
Febrile  albuminuria,  460 

dyspnea,  91 
Febris  herpetica,  62 
Fecal  concretions,  429 
tumors,  308 
vomiting,  361 
Feces,  admixture  of  blood  in,  426 
of  mucus  in,  426 
amount  of,  422,  423 
anguillula  intestinalis  in,  435 

stercoralis  in,  435 
animal  parasites  in,  429 
ankylostoma  duodenale  in,  433 
anthrax  bacillus  in,  443 
appearance  of,  424,  445 
ascaris  lumbricoides  -in,  432 
bacillus  of  cholera  in,  441 
of  tuberculosis  in,  440 


INDEX. 


979 


Feces,  bacteria  of,  439 

pathogenic,  440 
bile  acids  in,  445 
blood  in,  chemical  tests  for,  447 

Schonbein-Almen's  test  for,  447 

spectroscopic  tests  for,  447 

Teichmann's  hemin  test  for,  447 
bothriocephalus  latus  in,  437 
carbohydrates  in,  446 
casein  in,  428,  439 
cestodes  in,  435 
Charcot's  crystals  in,  432 
chemical  examination  of,  444 
color  of,  424,  445 
concretions  in,  429 
consistence  of,  423 
digestive  enzymes  in,  445 
distomum  hepaticum  in,  435 

lanceolatum  in,  435 
entozoa  in,  432 
enzymes  in,  445 
examination  of,  422 
fat-needles  in,  438 
fats  in,  splitting  of,  438 

tests  for,  446 

utilization  of,  438 
fatty  acids  in  diseases  of  pancreas,  444 

tests  for,  446 
fermentation  of,  after  evacuation,  439 
flukes  in,  435 
hydrobilirubin  in,  445 
in  Asiatic  cholera,  443 
in  carcinoma  of  rectum,  444 
in  cholera  nostras,  443 
in  diseases  of  pancreas,  444 
in  dysentery,  444 
in  typhoid  fever,  443 
indigestible  food  residue  in,  439 
intestinal  sand  in,  428 
Kruse's  bacillus  of  dysentery  in,  442 
microscopic  examination  of,  438 
mucin  in,  446 

muscle  fibers  in,  utilization  of,  438 
nematodes  ascarides  in,  432 
neoplastic  fragments  in,  427 
odor  of,  425 

oxyuris  vermicularis  in,  432 
peptone  in,  446 
pieces  of  tumors  in,  427 
pigment  of,  445 
proteids  in,  utilization  of,  438 
protein  in,  446 
proteoses  in,  446 
protozoa  in,  429 
pus  ir.,  427 
reaction  of,  444 
round  worms  in,  432 
saginata  in,  437 
shape  of,  423 
soaps  in,  tests  for,  446 
starch  in,  utilization  of,  438 
streptococci  in,  443 
tfenia  in,  436  ' 

mediocanellata  in,  437 
solium  in,  436 
tapeworms  in,  435 
trematodes  in,  435 
trichina  spiralis  in,  435 
tricocephalus  dispar  in,  434 
typhoid  bacilli  in,  442 
urobilin  in,  445 
Fehling's  test  for  sugar  in  urine,  484 


Fehling-Soxhlet's  estimation    of   sugar    in 

urine,  507 
Fermentation,  examination  of  stomach  con- 
tents for,  396 

of  feces  after  evacuatian,  439 

test  for  sugar  in  urine,  488 
gas-volumetric,  514 
quantitative,  for  dextrose  in  urine,  513 
Ferrometer,  JoUes',  671 
Fetal  rhythm  of  heart  tones,  259 
Fever  after  catheterization,  69 

after  operation,  69 

course,  68 

for  longer  periods,  68 

curve,  68 

daily  variations,  68 

ephemeral  varieties,  69 

relapses,  74 

tachycardia  and,  101,  102 

type,  68 
Fibrillary  twitching,  748,  790 
Fibrin  in  blood,  microscopic  determination, 
636 

in  sputum,  585 

in  urine,  detection  of,  465 
Fibrinogen  in  urine,  detection  of,  464 
Fibrinous  bronchial  casts  in  sputum,  586 

bronchitis,  sputum  in,  605 
Filaria  sanguinis,  embiyos  of,  in  urine,  578 
Filehue's  theory  of  C'heyne-Stokes  respira- 
tion, 82 
Filtration  of  urine,  553 
Fingers,  claw-like  position  of,  741 

clubbed,  59 

little,  movements  of,  in  nervous  diseases, 
911,  912 
Fischer-von    Jaksch  test  for  sugar  in  urine, 

487 
Fistula  noise,  pulmonary,  in  pneumothorax, 

241 
Flask,  fractionation,  494 
Flea-bites,  cutaneous  hemorrhage  from,  53 
Fleischl-Miescher  hemometer,  619 
Flesh  color,  qualitative  changes  of,  38 
Flexibilitas  cerea,  751 
Flint's  murmur,  331 
Floating  kidney,  palpation  of,  310 
Floccillation,  740 
Fluctuation,  abdominal,  305 

in  thorax,  determination  of,  287 

of  empyema  necessitatis,  287 

of  purulent  pleurisy,  287 

wave  in  diagnosis  of  free  fluid  in  abdomen, 
302,  305 
Fluid   effusion  in   pericardium,   percussion 

in,  186 
Flukes  in  feces,  435 
Flush,  hectic,  40    - 
Folin  and  Shafier's  modification  of  Hopkin's 

uric-acid  estimation,  531 
Food  particles,  incrustations  of,  with  organic 
salts,  429 

residue,  indigestible,  in  feces,  439 
Foot-clonus,  778 
Foot-joint  movements  in  nervous  diseases, 

913 
Foot-phenomenon,  778 
Foramen  ovale,  patent,  343 
Forced  laughter,  751 

movements,  7ol 
Foreign  bodies  in  sputum,  586 
Fractionation  flask,  494 


980 


INDEX. 


Fragility  of  boues  in  nervous  diseases,  723 
Francke's  needle  for  obtaining  blood,  610 
Frankel's  nasal  speculum,  701 

pueumococci  in  sputum,  598 
Wolf's  stain  for,  598 
Frank's  theory  of  icterus  neonatorum,  43 
Freckles,  45 

Freezing-point.     See  Cryoscopy. 
Fremissement,  heart,  301 
Fremitus,  tactile,  testing  of,  288 

vocal,  testing  of,  288 
Frey's  irritation  hairs,  758 

testing  sense  of  pain  by,  760 

sphygmograph,  109 
Friction,  internal,  of  blood,  669 

rub,  extrapericardial,  239 
pleural,  239 
pleuropericardial,  239 
pseudopericardial,  239 

sounds,  in  pulmonary  auscultation,  243 
Friedreich's  ataxia,  muscle  unrest  in,  750 
speech  disturbances  in,  899 

diastolic  venous  collapse,  152 

phenomenon,  215 
Frohlich's  method  of  measuring  chest,  29 
Fungi,  ray,  in  sputum,  603 
Funnel,  separatory,  375 
Funnel-shaped  chest,  32,  35 
Furunculosis,  63 
Futile  heart  contractions,  297 

Gaiffe's  reducteur  de  potential,  806 
Gait  and  attitude,  27 

atactic,  908 

choreic,  909 

hemiparetic,  908 

hemiplegic,  908 

of  hip-joint  disease,  909 

of  paralysis  agitans,  909 

of  propulsion,  909 

of  retropulsion,  909 

of  sciatica,  909 

paraparetic,  908 

pathologic,  908 

spastic,  908 

staggering,  909 
Gall-bladder,  distended,  dipping  in,  305 

enlargement  of,  310 
Gallop  rhythm  of  heart-tones,  258,  259 

Potain's  systolic,  259 
Gall-stones,  428,  429 

chemical  examination  of,  429 

chills  in,  74 
Galvanic  current  in  testing  electric  irrita- 
bility, 809 
laws  of  contraction  with,  811 

vertigo,  883 
Gamgee-Grutzner's   demonstration  of    lipo- 
lytic activity,  421 
Gangrene,  pulmonary,  sputum  in,  607 
Garland's  line,  201    ' 
Garrod's  thread  test  for  uric  acid  in  blood, 

675 
Gartner's  sphygmomanometer,  139 
Gas  fermentation,  examination  of  stomach 

contents  for,  396 
Gastric  juice,   acetic  acid  in,  detection  of, 
377 
acids  of,  diagnostic  notes  upon,  389 
physiologic  relationship,  388 
qualitative  examination  for,  372 
antiseptic  qualities  of  vomitus  of,  359 


Gastric  juice,  butyric  acid  in,  detection  of, 
377 
chlorids  in,  quantitative  estimation  of, 

379,  381 
chlorin  in,  quantitative  estimation  of, 

381 
digestive  power  of,  391 
hydrochloric  acid  in,  383 
Mintz's  test  for,  383 
quantitative  estimation  of,  379 
tests  for,  372 

unneutralized,  estimation  of,  379 
Leo's  method,  380 
Liitke-Martius'  method,  380 
Sjoqvist's  method,  379 
hyperacidity  of  vomitus  of,  358 
hypersecretion  of  vomitus  of,  358 
lactic  acid  in,  tests  for,  374 
lipolytic  enzyme  in,  403 
pepsin  in,  391.     See  also  Pepsin. 
qualitative  examination  for  acids,  372 
quantitative  tests  for  acids,  377 
rennin  in,  examination  for,  394 

zymogen  in,  examination  for,  394 
specific  gravity  of,  370 
supersecretion  of  vomitus  of,  358,  360  . 
titration  of,  total  acidity  of,  377,  965 
valerianic  acid  in,  detection  of,  377 
volatile  fatty  acids  in,  detection  of,  375 
vertigo,  883 
Gastritis,  phlegmonous,  vomitus  of,  360 

suppurative,  vomitus  of,  .360 
Gastrodiaphany,  367 
Gastrorrhcea  acida,  vomitus  of,  358,  360 
Gas-volumetric  fermentation  test  for  sugar 

in  urine,  514 
Geriiusche,  245 
Gerhardt's  phenomenon,  214 
test  for  diacetic  acid  in  urine,  496 
tone  change,  214 
Gerrard's  apparatus  for  estimation  of  urea, 

522 
Girdle  pain,  770 

Glanders,  pulmonary,  sputum  in,  602 
Glands,  mesenteric,  tumor  of,  palpation  of, 
310 
parotid,  secretory  nerve  of,  functions,  869 
retroperitoneal,  tumor  of,  palpation  of,  310 
thyroid,   enlarged,    systolic  and  diastolic 
murmurs  over,  283 
Glaucoma  simplex,  atrophy  of  optic  nerve 

in,  705 
Globulin  in  urine,  detection  of,  464 
Glossopharyngeal  nerve,  functions  of,  869 
outline  for  examination  of,  954 
sensory  tibers  of,  869 
Glossy  skin,  792 
Glucose  in  urine,  qualitative  tests  for,  480. 

See  also  Sugar  in  urine. 
Gluing  of  respiratory  passages,  582 
Gluteal  reflex,  778 
Glutoid  capsules,  examination  of,  intestinal 

digestion  by,  419 
Glycosuria,  480 

alimentary,  480,  481 
physiologic,  480,  481 
transitory,  in  nervous  diseases,  797 
Glycuronic  acid  in  urine,  detection  of,  492 

Tollen's  test  for,  493 
Gmelin's  test  for  biliary  pigments  in  urine, 

472 
Goiter,  exophthalmic,  837 


INDEX. 


981 


Goiter,    exophthalmic,    gallop    rhythm    of 
heart  tones  from,  259 
systolic  and  diastolic  murmurs  over,  283 
venous  hum  in,  286 

Gonorrhea,  catarrh  of  bladder  in,  578 
pyelitis  in,  578 

Gonorrheal  threads  in  urine,  573 

Gouty  deposit,  skiagraph  of,  729 

Gowers'  hemoglobiuometer,  617 

Grafe's  sign,  838 

Gram's  stain  for  bacteria  in  sputum,  596 
Weigert's  modification,  597 

Granular  basophilic  degeneration  of  erythro- 
cytes, 636 

Granules,  blood-,  Willebrandt's  stain,  634 
mast-cell,  632 
Zollikofer's,  634 

Grape  sugar  in  urine,  480.     See  also  Sugar  in 
urine. 

Graphic  expressions  for  physical   signs   in 
pulmonary  cases,  348 

Gravel,  biliary,  428 

Great-toe  movements   in  nervous  diseases, 
914 

Green  sputum  in  tumors  of  lung,  581 

Grutzner-Gamgee's  demonstration  of  lipo- 
lytic activity,  421 

Gums,  examination  of,  681 
lead  line  ou,  682 

Gunning's  iodoform  test  for  acetone  in  urine, 
494 

Giinther's  stain  for  bacteria  in  blood,  652 

Giinzburg's  reagent,  373 

Gutbrod-Skoda's  theory  of  weakened  apex 
beat  in  aortic  stenosis,  334 

Gutta  cadeiis,  236 

Gypsum  in  urine,  559 

Haab's  reflex,  847 

Habituation  to  respiratory  obstruction  and 

dyspnea,  93 
Hacking  cough,  97 

Hair  crepitation  in  auscultation  of  lungs, 
243 

irritation,  760 
von  Frey's,  758 

testing  sense  of  pain  by,  760 

tension  value  of,  759 
Hairy  tongue,  black,  683 
Half-beat  of  heart,  296 
Half-moon-shaped  space,  193 
Hallucinations,  739 
Hamraarsten's    test   for  biliary   pigments, 

474 
Hammerschlag's  estimation  of  pepsin,  391 

of  specific  gravity  of  blood,  612 
Hand,  ape,  747 

claw-,  in  ulnar  paralysis,  747 

preacher's,  747 
Hand-clonus,  778 
Hard  palate,  examination  of,  687 
Harpooning,  728 
Harrison's  groove,  31 
Head,  shape  of,  36 

size  of,  36 

square-shaped,  37 
Hearing-power,  Pollitzer's  test  for,  86 

Rinne's  test  for,  865 

Schwabach's  test  for,  866 

Weber's  test  for,  866 
Heart  action,  frequency  of,  pulse  curve  and, 
117,  120 


Heart  action,    stimulated,    gallop    rhythm 
from,  259 
apex  beat,  289.     See  also  Heart-heat. 
apex  of,  systolic  retraction  at,  295 
auscultation  of,  244,  250 
-beat,  289 
altered,  296 
cause  of,  essential,  291 
dlfi"usion  of,  292 
disappearance  of,  294 
dislocation  of,  291,  292 
double,  296 
half-,  296 
heaving,  293 
intensification  of,  292 
intensity  of,  290 
Miiller's  heaving,  293 

vibrating,  294 
position  of,  abnormal,  295 
slow  heaving,  293 
twin, 296 

under  normal  conditions,  290 
vibrating,  294 
weakening  of,  294 
blocking,  297 
cells  in  sputum,  588 

chambers,    abnormal    communication   of, 
343 
alterations   of  size  of,  laws  governing, 

314 
dilatation  of,  316 
hypertrophy  of,  315 
changes  in,  heart-beat  in,  291 
compensatory  disturbances  of,  314,  319 
contractions,  futile,  297 

ineffectual,  297 
crepitation,  238 
disease,  cells  of,  588 

congenital  cyanosis  of,  41 
dilatation  of  lungs  in,  175 
dislocation    of,    displacements    of  heart- 
beat from,  292 
dulness,  position  of  apex  beat  in,  295 
deep,  176 

diminution  of.  180 
enlargement  of,  181 
mobility  of,  179 
pathologic  changes  in,  180 
dislocation  of,  188 

dextrocardia  and,  differentiation,  189 
superficial,  170,  176 
diminution  of,  180 
enlargement  of,  181 
mobility  of,  179 
pathologic  changes  in,  180 
enlargement  of,  increase  of  dulness  from, 
181 
percussion  in,  182 
fremissement,  301 

insufficiency  of,  gallop  rhythm  from,  259 
left,  valvular  lesions  of,  321 
murmurs,  260 

accidental,  260,  274 

valvular  murmurs    and,   differentia- 
tion, 277 
anemic.  274 
functional,  274 

in  multijde  valvular  disease,  271 
inorganic,  274 
insufficiency,  264 

localization    of,   in    multiple    valvular 
lesions,  271 


982 


INDEX. 


Heart  murmers,  palpation  of,  301 
relative,  274 

tones  and,  differentiation,  260 
valvular,  260,  263 
accidental  murmurs  and,  differentia- 
tion, 277 
exact  time  relations  to  heart  tones, 

268 
from  insufficiency  of  valves,  263 
from  regurgitation,  263 
from  stenosis  of  valves,  263 
functional,  263 
intensity  of;  264 
localization    of,   in    simple    valvular 

lesions,  266 
loudness  of,  264 
organic,  263 
quality  of,  264 
timbre  of,  264 
muscular  sound  of,  245 
pendulum  rhythm  of,  249 
rales,  238 
region,  inspection  of,  289 

palpation  of  289 
right,  valvular  lesions  of,  334 
thrill,  301 
tones,  244 

division  of,  255 

exact  time  relations  of  valvular  mur- 
murs to,  268 
fetal  rhythm  of,  259 
first,  reduplication  of,  254,  255,  257 

splitting  of,  255,  257 
gallop  rhythm  of,  258.  259 
loudness  of,  alterations  in,  250 
murmurs  and,  differentiation,  260 
pendulum  rhythm  of,  259 
reduplication  of,  254,  255,  257 
second,  reduplication  of,  255,  257 

splitting  of,  255,  257 
splitting  of,  255,  257 
timbre  of,  alterations  in,  254 
triple  rhythm  of,  258 
topographic  percussion  of,  176 
valves,  insutiiciencv  of,  valvular  murmurs 
from,  263 
stenosis  of,  murmur  of,  264 
valvular  murmurs  from,  263 
valvular  lesions  of,  314 

alterations  of  size  of  heart  chambers 

in,  laws  governing,  314 
combinations  of  heart  murmurs  from, 

271 
combined,  341 
congenital,  343 
effect  on  circulation,  314 
individual,  321 
left,  321 

localization  of  murmurs  in,  266 
multiple     localizing      murmurs     in, 

271 
pathologic  phvsiology  of,  foundations 

of,  314 
right,  334 
Heat  test  for  albuminuria,  460 

for  hemoglobinuria,  470 
Heaving  beat  of  heart,  293 
Hebetude,  738 
Hectic  fever,  fever  curve  of,  74 

flush,  40 
Hehner-Maly's  estimation   of  hydrochloric 
acid  in  gastric  juice,  382 


Heidenhain-Beckmann's  cryoscopic  appara- 
tus, 545 
Heller's  test  for  albuminuria,  462 

for  hemoglobinuria,  470 
Heller-Moore's  test  for  dextrose   in   urine, 

481 
Helminthiasis,  eosinophilia  in,  650 
Hematoblasts,  650 
Hematocrit,  629 
Hematogenous  icterus,  44 
Hematoidin  crystals  in  urine,  561 
Hematoporphyrin  in  urine,  453 
Salkovcski's  test  for,  472 
tests  for,  471 
Hematoporphyrinuria,   453 
Salkowski's  test  for,  472 
tests  for,  471 
Hematospectrophotometer,  623 
Hematuria,  453,  469 
Hemianesthesia,  capsular,  821 
cerebral,  bone  anesthesia  in,  765 

from  anatomic  lesions,  879 
hysteric,  879 
spinal,  879 
Hemidrosis,  48 

Hemin    test,  Teichmann's,  for   hemoglobi- 
nuria, 470 
Hemiopia,  homonymous,  825 
Heniiopic  pupillary  reaction,  843 

reaction,  840 
Hemiparetic  gait,  908 
Hemiplegia,  742,  743 

cerebral,  electric  reaction  in,  816 
reflexes  in,  781,  785 
vasomotor  disturbances  in,  795 
gait  of,  908 
motor,  characteristics  of,  876 

pseudobulbar  symptoms  of,  878 
spinal,  903 
Hemiplegic  gait,  908 
Hemisystole,  296 

Hemoglobin  in  blood,  tests  for,  616 
Fleischl's  hemometer  for,  619 
Gowers'  hemoglobinometer  for,  617 
hematospectrophotometric,  623 
Hoppe-Seyler's    colorimetric     double 

pipet  for,  624 
Sahli's  hemometer  for,  620 
under  pathologic  conditions,  628 
in  urine,   453,  469,  561.  See  also  Hemoglo- 
binuria. 
quotient  of  erythrocytes,  629 
Hemoglobinometer,  Gowers',  617 
Hemoglobinuria,  453,  469,  561 
blood  in,  674 

chemical  detection  of,  470 
heat  test  for,  470 
Heller's  blood-test  for,  470 
periodic,  469 

Schonbein-Almen's  test  for,  471 
spectroscopic  test  for,  471 
Teichmann's  hemin  test  for,  470 
Hemometer,  Fleisclil-Miescher,  619 

Sahli's,  620 
Hemoptysis,  sputum  in,  609 
Hemorrhage,  cutaneous,  52-54 

pulmonary,  sputum  in,  608 
Hemorrhagic  infarction  of  lung,  sputum  in, 
608 
purpura,  eyeground  in,  704 
Hemothorax,  dulness  of,  208 
Hereditary  ataxia,  muscle  unrest  in,  750 


INDEX. 


983 


Hernia,  diaphragmatic,   in  region  of  lung, 
tones  in,  211 
skiagraph  of,  735 
Herpes  febrilia,  61 

in  cerebrospinal  fever,  62 
in  malaria,  62 
in  meat-poisoning,  62 
High-pressure  stases,  321 
Hill  and  Barnard's  sphygmometer,  140,  141 
Hinds'  modification  of  Doremus  ureometer, 

524 
Hip-joint  disease,  gait  of,  909 

movements  in  nervous  diseases,  912 
Hirsch-Beck     apparatus     for    viscosity    of 

blood,  669 
History,  17 

taking,  18,  20 
Hoarse  voice,  94 
Homogentisic  acid   in  urine,   detection  of, 

497 
Hook-worm,  new  world,  434 
Hopkin's  estimation  of  uric  acid,  531 

Folin  and  Shaflfer's  modification,  531 
Hopkin-Worner's  estimation  of  uric  acid, 

531 
Hoppe-Seyler  colorimetric  double  pipet,  624 
test  for  succinic  acid  in  echinococcus  fluid, 
724 
Hour-glass  stomach,  367 
Huber's  test  for  motility  of  stomach,  363 
and  Arthur's   demonstration   of    trypsin 

action,  421 
and  Ewald's  test  for  motility  of  stomach, 
363 
Huckleberries,  pigment  of,  in  urine,  455 
Hiifner's  apparatus  for  estimating  urea,  520 
Hiifner-Knop's  method  of  estimating  urea, 

520 
Hum,  venous,  284 

in  exophthalmic  goiter,  286 
Hutchinson's  teeth,  678,  680 
Hydatid  thrill,  306 
Hydremic  edema,  50 
plethora,  611 
plethoric  edema,  51 
Hydrobilirubin  in  feces,  445 
Hydrocephalus,  37 
Hydrochinoii  acetate  in  iirine,  detection  of, 

497 
Hydrochloric-acid  deficit,  384 
vomitus  of,  360 
Giinzburg's  reagent  for,  373 
in  gastric  juice,  383 
Mintz's  test,  383 
quantitative  estimation  of,  379 
tests  for,  372,  383 
methyl-violet  reaction  for,  372 
phloroglucin-vanillin  reaction  for.  373 
tests  for,  372,  383 

total  unneutralized,  estimation,  379 
Leo's  method,  380 
Lvitke-Martius'  method,  380 
Sjoqvist's  method,  379 
tropaeolin  00  reaction  for,  373 
Hydrogen  sulphid  poisoning,  blood  in,  674 
Hydronephrosis,  renal  tumor  from,  310 

urea  content  of,  724 
Hydroquinone  coloring  urine,  454 
Hydrothorax,  dulness  of,  202,  205 
Hyperacidity   of  gastric  juice,  vomitus  of, 

358 
Hyperalgesia,  771 


Hyperalgesic  zones  of  skin,  774 

Hyperdicrotism,  131 

Hyperesthesia,  771 

Hyperpyrexia,  67 

Hypersecretion  of  gastric  juice,  vomitus  of, 

358 
Hypertrophy,  muscular,  788 
of  heart  chambers,  315 
eccentric,  315 
secondary,  316 
simple,  315 
of  tonsils,  687 
Hypesthesia,  756 
Hypnotic  conditions,  739 
Hypodicrotism,  130 
Hypoglossus  nerve,  functions  of,  875 

outline  for  examination  of,  954 
Hyposmotic    injury,  resistance   of  erythro- 
cytes to,  630 
Hysteria,  blue  edema  of,  797 

contractions  of  ocular  muscles  in,  838 
disturbances  of  consciousness  in,  738 

of  speech  in,  899 
major,  739 
Hysteric    anesthesias,  bone  sensibility   in, 
765 
hemianesthesia,  879 
pains,  771 
paralysis,  electric  reaction  in,  816 

Icterus,  42 
acatectic,  44 

bile  pigments  in  urine  in,  453 
bilirubin,  44 
difl'usion,  44 
hematogenous,  44 
in  infectious  diseases,  43 
neonatorum,  43 

Frank's  theory  of,  43 
obstructive,  42 
sputum  in,  581 
sweat  in,  47 
urobilin,  44 
Idiomuscular  mechanical  irritability,  797 
Ileus,  intestinal  tumor  iu,  302 
Illusions,  739 
Imbecility,  740,  741 
Imperative  incontinence,  947 
Inanition,  empty   intestines  in,   inspection 

of,  304 
Incontinence,  imperative,  947 

paradoxic,  942 
Indican  in  urine,  454 
tests  for,  475 
Am  aim's,  477 
Taflfe's,  476 
Obermayer's,  476 
Indigo  in  urine,  454,  561 

detection  of,  475 
Indol,  red,  in  urine,  detection  of,  477 
Infants,  weight  of,  28 
Infarction,  chills  in,  74 
of  lung,  dulness  from,  208 
hemorrhagic,  sputum  in,  608 
Infectious   diseases,   enlargement  of  spleen 
in,  312 
eosinophilia  in,  650 
icterus  in,  43 
leukocytes  in,  646 
inflammations,  leukocytosis  of,  649 
leukocytosis,  646 
leukopenia,  646 


984 


INDEX. 


Infectious  pleurisy,  acute,  717 
Infiltration  of  lung,  duluess  from.  203 
Inflammation,    infectious,    leukocytosis    of, 
649 
of  lung,  duluess  from,  203 
Inflammatory  edema,  51 

liver  pulse.  152 
Influenza  bacillus  iu  sputum,  598 
Inguinal  reflex,  777 
Innervation,  motor,  of  eye  region.  826 
sensation  of.  in  ataxia.  763 
testing.  762 
Inoscopy.  719 

Inspiration,   cog-wheel,    graphic    expression 
for.  343 
mixed,  graphic  expression  for.  348 
vesicular,  graphic  expression  for,  348 
Instabilite  clioreiforme.  750 
Instrumental  percussion,  153 
Instruments  for  auscultation.  217 
for  examiuatiou  of  stomach,  364 
lusuflicieuey,  aortic,  32S 
murmur  of,  330 
mitral.  321 

dyspnea  in,  322 
murmur  of.  323 
pulmonary,  338 

diastolic  murmur  of,  338 
pulsus  celer  of,  339.  S40 
tricuspid.  335 
Insufliation  of  rectum,  417 
Intelligence,  disturbances  of.  740 
Intention  tremor,  743 

in  multiple  sclerosis,  749 
Intermittent  fevers,  daily  variations  in  tem- 
perature. 65 
spleen  of,  palpation  of.  312 
pulse  from  extrasystole,  956 
Interrupted  crisis.  71 

fevers,  daily  variations  in  temperature,  68 
Interscapular  reflex,  775 
Interstitial  pulmonary  emphysema,  respira- 
tory murmurs  in.  240 
Intestinal  concretions.  429 

digestion,  examination  of.  hv  glutoid  cap- 
sules. 419 
juice.  Boas'  method  of  obtaining,  421 
noises,  peristaltic,   palpation  of.  313 
obstruction,  vomitus  of.  361 
sand  in  feces.  423 
tumor  in  ileus.  302 
worms  in  vomitus.  361 
Intestines,  absorption  in.  examination.  413 
chemistry  of.  examination,  413 
concretions  of.  429   . 
digestion   of.  examination  of.  by  glutoid 

capsules.  419 
empty,  in  inanition,  inspection  of,  304 
examination  of.  415 
functions  of.  examination.  418 
motility  of,  examination,  418 
movements  of.  frequency.  422 
liquid,  stratification  of.  423 
tumor  of.  palpation  of,  309 
Intra-abdominal   pressure,    increase  of.   dis- 
placed heart-beat  from.  292 
Intracellular  iodin  reaction  of  blood.  634 
Intrathoracic    cvsts,    exploratorv  puncture 

of  722 
Intropic  arhythmias.  964 
lodid  fibrin,  potassic.  testing  digestion  with, 
364 


lodid.  potassic.   testing  absorbing  power  of 

gastric  mucous  membrane  by,  361 
Iodin  in  urine,  detection  of.  501 

reaction  of  blood.  634 

Ehrlich's  stain  for.  634 
of  leukocytes.  634 
lodipin  in  testing  motility  of  stomach,  363 
Iodoform   test,    Gunning's,    for  acetone  in 
uriue,  494 
Lieben's,  for  acetone  in  urine,  495 
Iron  tests  for  blood  \\ii\x  Jolles'  feiTometer, 

671 
Irradiation  of  pain.  774 
Irritability,  electric.  798 

faradic  current  for.  310 

galvanic  current  for,  309 

idiomuscular.  mechanical,  797 

in  neuralparalysis,  817 

iu  tetany.  317 

mechanical,  testing.  797 

qualitative,  testing  of.  311 

quantitative,  testing  of.  508 
Irritation  phenomena,  speech   disturbances 

from,  900 
Isomaltose  in  urine,  detection  of.  490 
Itching  cutaneous  diseases,  pigmentation,  45 

Jack  tuhes.  364 

Jaff'e's  reaction  for  kreatinin  in  urine.  534 

test  for  indican  in  urine.  476 
Jaksch-Fischer  test  for  sugar  in  urine,  457 
Jaksch-Landois'    titration  of  opaque  blood, 

613 
Janeway's  sphygmomanometer,  143 
Jaquet's  sphygmograph,  111 
Jaundice.  42.     See  also  Icterus. 
Jaw  reflex,  349 
Jendrassik's  theorv  of  genesis   of  reflexes,. 

780 
Jenner's  stain  for  blood,  633 
Joint  reflexes.  778,  730 

trophic  disturbances  of,  793 
Jolles"  ferrometer,  iron  tests  for  blood  with, 

671 

Keenig's  sign.  Plate  12.  opposite  page  746 

Kidney,  calcultis  in,  skiagraph  of,  732 
epithelium  of,  in  urine.  565 
floating,  palpation  of.  310 
functions  of.  crvoscopv  of  urine  for  studv 

of.  549  '  ' 

movable,  palpation  of,  310 
topographic  percussion  of.  195 
tumor  of.  from  hydronephrosis,  310 
palpation  of.  310 
Kirstein's  autoscope.  699 
examination  of  larynx,  698 

of  trachea.  693 
tongue  spatula  for  autoscope,  700 
Kjeldahl's  apparatus.  530 

estimation  of  nitrogen  in  urine,  526 
of  proteid  in  urine,  505 
Klimmer-Drechsel's  estimation  of  sugar  in 

urine.  505 
Knee  phenomenon,  77^ 
Knee-joint  movements  in  nervous  diseases,, 

913 
Knop-Hufner's  estimation  of  urea.  520 
Koch's  stain  for  malarial  plasmodia,  656 
Kreatinin  in  urine,  estimation  of,  534 
Jaffe's  reaction  for.  534 
Weyl's  reaction  for,  534 


INDEX. 


985 


Kronecker's  co-ordination  center,  722 
Kruse's  bacillus  of  dysentery  in  feces,  442 
Kiilz's  test  for  beta-oxybutyric  acid  in  urine, 

497 
Kyphotic  chest,  31 

Lactic  acid.  Boas'  test  for,  376 
in  carcinoma  of  stomach,  376 
in  gastric  juice,  tests  for,  374 
in  motor  insufficiency  of  stomach,  376 
in  stenosis  of  stomach,  376 
of  gastric  contents,  quantitative  estima- 
tion of,  376 
Strauss'  determination  of,  375 
Uffelmann's  reagent  for,  374 
Lactose  in  urine,  490 
Laennec's  souffle  voile,  230 

theory  of  vesicular  breathing,  220 
Lagophthalmus  in  facial  paralysis,  851,  862 
Laked  blood,  titration  of,  614 

Lowy  and  Engel's  method,  614 
Lancinating  pains,  770 
Landois'  theory  of  dicrotic  pulse,  116 
Landois-vonJaksch's    titration     of    opaque 

blood,  613 
Laryngeal  branches  of  vagus,  869 

mirror,  692 
Laryngoscopy.  693 
combined,  701 
direct,  698 
with  mirror,  693 
Larynx,  autoscopy  of,  698 
examination  of,  direct,  698 
orthoscopy  of,  698 
Laughter,  forced,  751 

sardonic,  24 
Lavage,  rectal,  417 

Laws  of  contraction  with  faradic    current, 
811 
with  galvanic  current,  811 
Lazarus  and  Ehrlich's  eosinophilic  myelo- 
cytes, 642 
Lead  in  urine,  detection  of,  501 
line  on  gums,  682 

palsy,  reaction  of  degeneration  in,  820 
Lead-poisoning,  reaction  of  degeneration  in, 

816 
Legal's  test  for  acetone  in  urine,  495 
Lehmann's  estimation  of  dextrose  in  urine, 

509 
Leidenfrost's  phenomenon,  632 
Leo's  estimation  of  total  unneutralized  hy- 
drochloric acid,  330 
Leptothrix  buccalis  in  sputum,  600 
Lethargy,  738 
Letters,  test  for,  900 
Leucin  in  urine,  561 
detection  of,  497 
Sherer's  test  for,  499 
Leukanemia,  blood  in,  667 
Leukemia,  acute,  blood  in,  666 
blood  in,  664 

cutaneous  hemorrhage  in,  53 
lymphatic,  blood  in.  665 
chronic,  blood  in,  665 
lymphoid,  blood  in,  665 
mixed,  blood  in,  666 
myelogenous,  blood  in,  666 
myeloid,  blood  in.  666 
spleen  of,  palpation  of.  312 
Leukocytes,  counting  of,  626 
Breuer's  chamber  for,  626 


Leukocytes,  counting  of,  differential,  643 

diminution  in,  645.     See  also  Leukopenia. 

in  infectious  diseases,  646 

increase  in,  645.     See  also  Leukocytosis. 

iodin  reaction  of,  634 

irritation  forms,  643 

mononuclear,  641 

number  of,  under  phvsiologic  conditions, 
627 

pathologic.  642 

polymorphonuclear  neutrophilic,  641 

polynuclear,  427,  641 

proportions,  643 

ratio  of,  to  erythrocytes,  628 

varieties  of,  640 
Leukocytosis,  645 

after  cold  baths,  646 

anemic,  649 

cachectic,  649 

eosinophilic.  649.     See  also  EosinophUia. 

infectious,  646 

medicinal,  649 

of  acute  articular  rheumatism.  647 

of  agony,  649 

of  digestion,  646 

of  erysipelas,  646 

of  infectious  inflammations,  649 

of  malaria,  648 

of  measles,  643 

of  meningitis.  647 

of  newborn,  646 

of  perityphlitis,  C4!) 

of  pertussis,  648 

of  pneumonia,  646 

of  pregnancy,  646 

of  scarlet  fever,  648 

of  septicemia,  648 

of  suppuration,  649 

of  tetanus,  649 

of  tuberculosis,  649 

of  typhoid  fever,  646 

of  varicella,  648 

physiologic.  645 

polvnuclear  neutrophilic,  649 

toxic.  649 
Leukopenia.  645 

infectious,  646 

of  erysipelas.  648 

of  malaria,  648 

of  measles.  648 

of  pneumonia,  646 

of  scarlet  fever,  648 

of  typhoid  fever,  646 
Leukoplakia,  683 

buccalis,  683 
Levulose  in  urine.  490 
Levden-Moebius' j  uvenile  muscular  atrophy, 

789 
Lieben's  iodoform  test  for  acetone  in  urine, 

495 
Liebig's  estimation  of  urea,  520 
Ligne  du  cordon.  35 
Limbeck's    modification     of    Hamburger's 

test  for  resistance  of  erythrocytes  to  hypo- 
tonic saline  solutions,  630 
Lindt's  method  of  rhinopharyngoscopy,  687 
Lipemia,  652 

Lipolytic  activity,  Grutzner-Gamgee  demon- 
stration  of,  421 

enzyme  in  gastric  juice,  403 
Lips,  examination  of,  678 
Lipuria,  562 


986 


INDEX. 


Lipuric  acid  in  urine,  562 
Litten's  sign,  78 

in  differentiation  of  empyema  from  sub- 
phrenic abscess,  78 
Little-finger  movements  in  nervous  diseases, 

912 
Little-toe  movements  in  nervous   diseases, 

914 
Liver,  abscess  of,  dulness  in,  190 

acute  yellow  atrojihy  of,  cutaneous  hem- 
orrhage in,  53 
palpation  in,  310 
arterial  pulse,  152 
border,  upper,  depression  of,  192 
cirrhosis  of,  303 

palpation  of  liver  in,  310 
pigmentation  of  skin  in,  46 
corset,  311 
dulness,  190 

dislocations  of,  191 
gross  changes  in,  191 
in  abscess  of  liver.  190 
in  echiuococcus  cysts  of  liver,  190 
mobility  of,  191 
relative,  190 

superficial,  changes  in  lower  border  of, 
192 
in  upper  border  of,  191 
enlargement  of,  dipping  in,  305 

palpation  of,  310 
low  position  of,  palpation  of,  310 
palpation  of.  in  cirrhosis,  310 
pulsation  of.  300 
pulse,  arterial,  152,  300 

inflammatory,  152 
topographic  percussion  of.  190 
tumor  of,  palpation  of.  310 
venous  pulse,  151 
Localization,  cerebral,  8S4 

cross-section,  of  spinal  cord,  920 
longitudinal,  of  spinal  cord.  920 
of  brachial  plexus,  932 
of  functions  in  spinal-cord  segments,  930 
of  lumbosacral  plexus,  932 
segmental,  of  cutaneous  sensibilitv,  922 
of  motility.  926 
of  reflexes.  927 
of  spinal  cord,  920 
spinal,  920 
Location,  sense  of,  764 
Lohnstein's    fermentation     saccharometer, 

515 
Loose  congh,  96 

Lower  extremities,  movements  of,   in   ner- 
vous diseases,  912 
Low-pressure  stases.  321 
Lowy  and  Engel's  test  for  laked  blood,  614 
Ludwig  Cyon's  depressor.  870 
Ludwig-Salkowski's  estimation  of  uric  acid, 

530 
Lumbar  puncture.  725 

region,  skiagraph  of,  730 
Lumbosacral  cord,  topography  of,  937 
plexus,  localization  of,  932 
motor  roots  of,  934 
Lungs,    abnormalities    of.   cardiac    dulness 
and, 181 
abscess  of,  sputum  in,  607 
absent  mobility  of,  174 
active  mobility  of,  173 
apices  of,  percussion  of,  171,  172 
auscultation  of,  errors  in,  242 


Lungs,  auscultation  of,  friction  sounds  in,  243 
hair  crepitation  in,  243 
muscle  sounds  in,  243 
borders,  abnormal  position  of,  175 
depression  of,  in  enteroptosis,  175 
dilatation  of,  in  cardiac  affections,  175 
diminished  mobility  of,  174 
dulled  note  within,  198 
expiratorv  position    of,   percussion   of, 

168 
extension  of,  175 
hyperresonant  tones  within,  209 
inspiratory  position    of,  percussion   of, 

168 
mobility  of,  absent,  174 
diminished.  174 
passive.  173 
passive  mobility  of.  173 
retraction  of,  175.  176 
topographic  percussion  of,  168 
tympanitic  tones  in,  209 
carcinoma  of,  dulness  in.  198 
cavities  of.  dulness  of,  20: 

exploratorv   puncture    to    demonstrate, 

721 
hyperresonant  tones  in,  211 
metallic  resonance  in.  212 
tympanitic  tones  in,  211 
dulness,  198 
edema  of,  dulness  from,  209 

sputum  in,  608 
emphvsema  of.    displaced   heart-beat  in, 
292 
hyperresonant  tones  in,  209 
interstitial,  respiratory  murmurs  in,  240 
tympanitic  tones  in,  209 
fistula  noise  in  pneumothorax,  241 
gangrene  of,  sputum  in.  607 
glanders  of,  sputum  in,  602 
hemorrhage  of.  sputum  in.  603 
hemorrhagic  infarction  of,  sputum  in,  608 
infarction  of.  dulness  from,  208 
hemorrhagic,  sputum  in,  608 
infiltration  of,  dulness  from.  208 
inflammation  of.  dulness  from,  208 
neoplasms   of.   fragments   of.    in   sputum, 

591 
palpation  of.  287 
partial  consolidations  of,  mobility  of  lung 

borders  in.  174 
pulsation  in  region  of,  abnormal,  287 
reflex,  162 

retraction  of,  dulness  of.  209 
stones,  586 
tissue  in  sputum.  583 
topographic  percussion  of.  168 
tumors  of,  dulness  from,  208 
green  sputum  in.  581 
vesicular  breathing  in,  225 
unilateral  retraction  of,  displaced   heart- 
beat in.  292 
Liitke-Martius'   estimation   of  total  unneu- 

tralized  hydrochloric  acid.  330 
Lymphatic  leukemia,  blood  in,  665 
Lymphemia,  blood  in.  665 
Lymphocytes  in  blood,  640 
in  bone-marrow,  641 
large,  641 
Lymphocytosis.  650,  717 
Lymphoid  leukemia,  blood  in,  665 
Lymphomatoses,  classification  of,  662 
Lysis,  70 


INDEX. 


987 


Madder,  pigment  of,  in  urine,  455 
Malaria,  blood  in,  653 
staining  of,  655 
fever  curve  of,  73 
herpes  febrilis  in,  62 
leukocytosis  of,  648 
leukopenia  of,  648 
Plasmodia  of,  653 
counting,  656 
crescents  of,  658 
diagnostic  significance  of,  656 
flagellate  forms  of,  658 
Koch's  stain  for,  656 
Maunaberg's  stain  for,  655 
Romonowski's  stain  for,  655 
Euge's  stain  for,  656 
varieties  of,  657 
Maltose,  371 

in  urine,  490 
Malv-Hehner's  estimation  of  hydrochloric 

acid,  382 
Maniacal  delirium,  739 
Maunaberg's  stain  for  malarial  plasmodia, 

655 
Manometer,  Sahli's,  pocket  mercury,  136 
Markzellen,  Ehrlich's,  642 
Marrow,  lymphocytes  in,  641 
Martius'  normal  cardiogram,  298 
Masque  des  femmes  enceintes,  45 
Mast-cell  granules,  632 
Mast-cells  in  blood,  642 
Measles,  cutaneous  hemorrhage  in,  53 
leukocytosis  of,  648 
leukopenia  of,  648 
Measui-ement,  29 

chest,  29 
Meat-iioisoning,  herpes  febrilis  in,  62 
Mechanical  irritability,  idiomuscular,  797 
of  muscles,  797 
of  nerves,  797 
Mediastinum,  tumors  of,  dulnesa  from,  208 
Medicinal  leukocytosis,  649 

pigments  in  urine,  454 
Megaloblasts,  639,  640 
Megastoma  entericum,  430 
Melanemia,  651 
Melanin  in  urine,  561 
detection  of,  477 
Melanogen  in  urine,  detection  of,  477 
Melanosarcoma,  45 
Melanosarcomatosis,  45 
Melanosis,   arsenic,    Addison's   disease  and, 

differentiation,  46 
Melanotic  tumor,  color  of  urine  in,  454 
Melasicterus,  42 

Addison's  disease  and,  differentiation,  46 
Memory  aphasias,  898 
disturbances  of,  741 
Meniere's  disease,  867 
Meningitis,  cerebral,  vomitus  of,  361 
cerebrospinal,   posture  in  bed  in,  25 
leukocytosis  of,  647 
Mensuration,  29, 
Mental  condition,  24 
Mercury  in  urine,  detection  of,  501 
Mering's  exiierinients  on  potassic  iodid,  362 
reflex,  413 

test-breakfast   for    absorptive  power    of 
stomach,  397 
Mesenteric   glands,    tumor  of,  palpation  of, 

310 
Metallic  after-resouauce,  157 


Metallic  breathing,  229 
resonance,  157,  212 

stick-pleximeter  for,  158 
Metamorphosed  breathing  murmur,  230 
Metaphosphoric-acid   test  for  albuminuria, 

463 
Meteorism,  inspection  of,  302 
Methemoglobinemia,  blood  in,  674 
Methyl  violet     reaction     for     hydrochloric 

acid,  372 
Mett's  determination  of  pepsin,  392 
Micrococcus  catai-rhalis  in  sputum,  600 

tetragenus  in  sputum,  600 
Micro-organisms  in  urine,  574 
Microphone,  218 
Midclavicular  line,  167 
Miescher-Fleischl  hemometer,  619 
Mikulicz's  method  of  measuring  intra-eso- 

phageal  pressure,  691 
Miliaria,  62 
alba,  62 
crystallina,  62 
rubra,  62 
Miliary  tuberculosis,  acute,  choroidal  tuber- 
cle in,  705 
sputum  in,  606 
physical  examination  in,  353 
Mintz's  determination  of  free  hydrochloric 

acid,  383 
Mirror  larvngoscopy,  693 

subglottic,  698 
Mitral  defects,  cyanosis  from,  41 
insufiiciency,  321 
dvspnea  in,  322 
m\irmur  of,  323,  266 
systolic  murmur  of,  266 
lesions,  reduplication  of  second  heart-tone 

in,  257 
stenosis,  324 

murmurs  of,  267,  328 
thrill  in,  301 

triple  rhythm  of  heart  tones  in,  258 
tones,  246,  247,  248 
Mixed  breathing,  222,  231 
dyspnea,  92 

inspiration     with    bronchial    expiration, 
graphic  expression  for,  348 
with  prolonged   expiration,  graphic  ex- 
pression for,  348 
leukemia,  blood  in,  666 
Moebius-Leyden's  juvenile   muscular  atro- 
phy, 789 
Mohrenheim's  groove,  282 
Moist  cough,  96 

rales,  232 
Moisture  of  skin,  47 
Molecular  concentration  of  blood,  667 

of  urine,  545 
Monocrotism,  130,  131 

Mononuclear  eosinophilic  cells  in  blood,  642 
leukocytes,  641 

neutrophilic  cells  in  blood,  642 
Moore-Heller's  test  for  dextrose  in  urine, 

481 
Morbus  Addisoni,  45 

argyria  and,  diflerentiation,  46 
arsenic  melanosis  and,    differentiation, 

46 
melasicterus  and.  differcjitiation.  46 
Moritz's  icidinu^tric  titration  of  fluids,  965 
Morning-star  balls,  .5,")9 
Motility,  examination  of,  741 


988 


INDEX. 


Motility,  gastric,  vomitus  of,  358 
of  intestines,  examination,  418 
of  stomach,  examination  without  stomach 
tube,  362 
iodipiii  in  testing,  363 
judgment  of,  370 
salol  in  testing,  362 
raw,  special  examination  of  stomach  for, 

413 
segmental  localization  of,  926 
voluntary,   outline   for    examination  of, 
951 
Motor  aphasia,  cortical,  893 

effects  on  written  speech,  896 
subcortical,  893 

effects  on  written  speech,  896 
transcortical,  893 

effects  on  written  speech,  896 
fibers  of  vagus,  869 
hemiplegia,  characteristics  of,  876 
pseudobulbar  symptoms  of,  878 
innervation  of  eye  region,  826 
irritation,  phenomena  of,  744 
nerves,  laws  of  contraction   for,    with   fa- 
radic  current,  811 
mechanical  irritability  of,  797 
paralysis,  peripheral,  examination  of,  910, 

954 
points,  800 

roots  of  brachial  plexus,  934 
of  lumbosacral  plexus,  934 
trigeminus,  functions  of,  849 
weakness,  741 
Mountain  vertigo,  883 
Mouth,  examination  of,  677 

palpation  of,  677 
Mouvement  de  bascule,  874 
Movable  kidney,  palpation  of,  310 
Movements,    active,    of    extremities,  judg- 
ment of,  766 
associated,  750 
athetoid,  750 
choreic,  750 

conception  of,  judgment  of,  762 
forced,  751 

of  elbow-joint  in  nervous  diseases,  911 
of  finger  in  nervous  diseases,  911 
of  foot-joint  in  nervous  diseases,  913 
of  great-toe  in  nervous  diseases,  914 
of  hip-joint  in  nervous  diseases,  912 
of  knee-joint  in  nervous  diseases,  913 
of  little-finger  in  nervous  diseases,  912 
of  little-toe  in  nervous  diseases,  914 
of  lower  extremity  in  nervous  diseases, 

912 
of    shoulder-blade    in    nervous    diseases, 

910 
of  shoulder-joint  in  nervous  diseases,  910 
of  thumb  in  nervous  diseases,  912 
of  toe  in  nervous  diseases,  914 
of  upper  extremitv  in  nervous  diseases, 

910 
of  wrist-joint  in  nervous  diseases,  911 
passive,  of  extremities,  testing,  767 
Mucin  in  feces,  446 

substances  resembling,  detection  in  urine, 
468 
Mucopurulent  sputum,  580 
Mucor  in  sputum,  602 
Mucous  casts  in  urine,  572 

catarrh  of  stomach,  vomitus  of,  360 
membrane,  buccal,  examination  of,  687 


Mucous  membrane  of  stomach,  potassic  iodid 

for  testing  absorbing  power,  361 
secretion  of  stomach,  examination  of,  395 
sediments  in  urine,  468,  562 
Mucus,  admixture  of,  in  feces,  426 
Muller"s  heaving  heart-beat,  293 

vibrating  apex  beat,  294 
Multiple  myeloma,  emaciation  in,  27 
sclerosis,  disturbances  of  speech  in,  899 

intention  tremor  in,  749 
Mumps,  648 

Murexid  test  for  uric  acid,  556 
Murmur,  breathing,  in    interstitial   pulmo- 
nary emphvsema,  240 

indefinite,  230 

metamorphosed,  230 

mixed,  222,  231 
bronchial,  physiologic,  222 
current,  origin  of,  262 
diastolic,    accentuated   at  beginning  and 
end,  269 

modified,  268 

of  aortic  iusuflBciency,  266 

of  pulmonary  insufficiency,  268,  338 

of  tricuspid  stenosis,  267 

over  arteries,  282 

over  exophthalmic  goiter,  283 

presystolic  accentuation  of,  269 

pure,  270 

real,  268 
Duroziez's  double,  282 
endocardial,  260 

influence  of  breathing  on,  278 

origin  of,  261 

pericardial    rubs    and,    differentiation, 
280 
Flint's,  331 

heart,  260.     See  also  Heart  murmurs. 
nun's,  284 
of  aortic  insufiiciency,  330 

stenosis,  333 
of  mitral  iusuflBciency,  323 

stenosis,  267,  328 
of  pulmonary  stenosis,  340 
of  stenosis  of  heart-valves,  264 
over  veins,  284 
paracardial,  279 

precordial,  emphysematous,  281 
prediastolic,  268,  270 
pressure  over  arteries,  282 
presystolic,  268 

pure,  269 
respiratory,  vesicular,  220 
spinning-top,  158 

over  thorax,  213 
squeezing,  690 
squirting,  690 
swallowing,  690 
systolic,  at  aortic  valve,  266 

of  mitral  insufficiency,  266 

of  pulmonary  stenosis,  267 

of  tricuspid  insufiiciency,  267 

over   arterial    and    auriculoventricular 
orifices,  differentiation,  268 

over  arteries,  282 

over  exophthalmic  goiter,  283 

over  subclavian  artery,  283 
Muscle  sense,  764 

sounds  in  auscultation  of  lungs,  243 
Muscles,  chewing,  cerebral  paralyses  of,  849 
electric  irritability  of,  798 

qualitative,  testing  of,  811 


INDEX. 


989 


Muscles,   electric   irritability  of,    quantita- 
tive, testing  of.  808 
faradic  current,  810 
galvanic  current,  809 
examination  of,  electric,  954 
eyeball,  functions  of,  826 

paralysis  of,  827 
fibers  of,  in  feces,  utilization  of,  438 
laws  of  contraction  for,  with  faradic  cur- 
rent, 811 
with  galvanic  current,  811 
mechanical  irritability  of,  797 
ocular,  contractions  of,  in  hysteria,  838 

external,  functions  of,  826 
trophic  disturbances  of,  788 
volume  of,  788 
Muscular  atrophy,  788 
degenerative,  789 
dystrophic,  789 
Erb's  juvenile,  789 
examination  of,  910,  954 
inactivity,  788 

Leyden-Moebius'  juvenile,  789 
myopathic,  789 
neuritic,  789 
nuclear,  789 
progressive,  789 

reaction  of  degeneration  in,  817,  818 
secondary  degenerative,  790 
simple  non-degenerative,  788 
spinal,  789 
hypertrophy,  788 
pseudohypertrophy,  788 
sensibility,  764 
sound  of  heart,  245 
Musical  rales,  234 
Mustard  plasters,  pigmentation  of  skin  from, 

45 
Muttering  delirium,  739 
Myasthenic  reaction,  816 
Mydriasis,  alternating,  839 

in  nervous  diseases,  839 
Myelemia,  blood  in,  666 
Myelin  in  sputum,  588 

kernels,  723 
Myeloblast,  643 
Myelocytes,  642 

eosinophilic,  Ehrlich  and  Lazarus',  642 
Myelogenous  leukemia,  blood  in.  666 
Myeloid  leukemia,  blood  in,  666 
Myeloma,  multiple,  emaciation  in,  27 
Myerethic  irregularity  of  pulse,  960 
Myopathic  nuisciilar  atrophy,  789 
Myosis  in  nervous  diseases,  839 
in  progressive  paralysis,  839 
in  tabes  dorsalis,  839 
Myotonia,  752 
Myotonic  reaction,  815 
Myxedema,  741,  795 

Naphthalene  coloring  urine,  4.54 
Narrowing,  pupil larv,  in  nervous  diseases, 
839 
to    convergence     and     accommodation, 
847 
Nasal  speculum,  Frankel's,  701 
Needle,  blood-,  610 

Francke's,  610 
Neelsen-Ziehl  stain  for  tubercle  bacilli  in 

sputum,  .594 
Neisser's  stain  for  diphtheria  bacilli,  686 
Nematodes  ascarides  in  feces,  432 


Neoplasms  of  lung,  fragments  of,  in  sputum, 

591 
Neoplastic  fragments  in  feces,  427 
Nephritic  albuminuria,  460 
Nephritis,  casts  in  urine  in,  570 
chronic,  pulse  in,  128 
edema  of,  51 
gallop  rhythm  from,  259 
uremic  dyspnea  of,  91 
Nerve,  abducens,  functions  of,  826 

acoustic,  outline  for  examination  of,  953 
acusticus,  865.  ^qh  &\so  Auditory  Nerve. 
auditory,  865.  See  also  Auditory  Nerve. 
bladder,   peripheral  aflections  of,  vesical 

functions  in,  943 
cranial,  examination  of,  829,  953 
electric  irritability  of,  798 

qualitative,  testing  of,  811 
quantitative,  testing  of,  808 
faradic  current,  810 
galvanic  current,  809 
examination  of,  electric,  outline  for,  955 
facial,  functions  of,  850 

outline  for  examination  of,  953 
paralysis  of,  851.    See  also  Facial  Paraly- 
sis. 
spasm  of,  864 
glossopharyngeal,  functions  of,  869 
outline  for  examination  of,  954 
sensory  fibers  of,  869 
hypoglossal,  outline   for  examination  of, 
954 
functions  of,  875 
mechanical  irritability  of,  testing,  797 
motor,  laws  of  contraction  for,  with  fa- 
radic current,  811 
mechanical  irritability  of,  797 
oculomotor,  function  of,  826 
of  skin,  sensory,  peripheral  distribution 

of,  915 
olfactory,  examination  of,  821,  953 
optic,  atrophy  of,  705 

examination  of,  822,  953 
secretory,  of  parotid  gland,  functions  of, 

869 
spinal  accessory,  functions  of,  870 
trigeminal,  functions  of,  849 

outline  for  examination  of,  953 
trochlear,  function  of,  826 
vagus,  869.     See  also  Vagus. 
Nervous  cough,  96 

Nervous  system,  examination  of,  738,  951 
psychical  examination  of,  738 
spinal,  examination  of,  910 
Neural  paralysis,  electric  irritability  in,  817 

progressive  muscular  atrophy,  789 
Neuralgic  pains,  770 
Neuritic  atrophy  of  optic  disk,  705 

muscular  atrophy,  789 
Neuroretinitis,  albuminuric,  704 
Neurosis  chorea.  7.50 
traumatic,  reaction  in,  816 
tremor  of,  749 
Neurotonic  reaction.  815 
Neutrophilic      leukocvtosis,      polynuclear, 
649 
pseudolymphocytes.  642 
New  growths,  fragments  of,  in  urine,  573 
Newborn,  leukocytosis  of,  646 
Newton's  rings,  624 
New-world  hook-worm,  434 
Nitric-acid  test  for  albuminuria,  462 


990 


INDEX. 


Nitrogen  in  urine,  Kjeldahl's  estimation  of, 

526 
Noise,  audible,  in  pneumothorax,  240 

of  chinli  of  coins,  158 
over  tliorax,  213 

of  falling  drops,  236 

in  pneumothorax,  241 

of  spinning-top,  158 
over  thorax,  213 

peristaltic,  intestinal,  palpation  of,  313 

pleural  splashing,  in  pneumothorax,  240 

pulmonary  fistula,  in  pneumothorax,  241 

splashing,  of  abdomen,  palpation  of,  286, 
313 
of  stomach,  356 

water-whistle,  iu  pneumothorax,  241 
Non-cousonating  r&les,  235 
Non-resonant  rales,  235 
Normoblasts,  639,  640 
Note-blindness,  901 
Nubecula  of  urine,  452,  468 
Nuclear  muscular  atrophy,  789 

reflexes,  784 
Nucleated  red  cells,  639 
Nucleo-albumiu  in  urine,  468 
Nucleoproteid  facial  paralysis,  857 
Nucleus,  oculomotor,  components  of,  833 
Nun's  murmur,  284 
Nutrition,  27 
Nylander-Almen's  test  for  sugar  in  urine, 

485 
Nystagmus,  838 

Obeemayee's  test  for  indicau  in  urine,  476 
Obesity,  abdominal,  inspection  of,  301 
Objective  examination,  17 
Oblique  reflex,  777 

Obstructive  atelectasis,  dulness  of,  209 
preventing  bronchial  breathing,  228 

bronchitis,  extension  of  lung  borders  in, 
175 

edema,  50 

icterus,  42 
Ocular  disturbances  of  equilibrium,  829 

muscles,  contractions  of,  in  hysteria,  838 
external,  functions  of,  826 

vertigo,  829 
Oculomotor  nerve,  functions  of,  826 

nucleus,  components  of,  833 
Odor  of  feces,  425 

of  sputum.  583 
Oedeme  bleu  des  hysteriques,  42 
Oidium  albicans  in  sputum,  603 
Oil,  sandalwood,  in  urine,  503 
Olfactory  nerve,  examination  of,  821,  953 
Oligochromemia,  pallor  and,  38 
Oligopnea,  84 
Oliguria,  450 

Oliver's  dynamometer,  141 
Oliver-Cardarelli  sign,  299,  346 
Olives,  689 

Omentum,  tubercular,  palpation  of,  310 
Opaque  blood,  titration  of  613 

Landois-von  Jaksch's  method,  613 
Operation,  fever  after,  69 
Ophthalmoscopy,  703 
Optic  aphasias,  898 

disk,  atrophic  discoloration  of,  706 
atrophy  of,  705 
neuritic  atrophy  of,  705 

fibers,  diagnosis  of  lesions  of,  824 

nerve,  atrophy  of,  705 


Optic  nerve,  examination  of,  822,  953 

neuritis,  703 
Oral  rales,  232 

Orcin  test  for  pentoses  in  urine,  491 
Orientation  lines,  166 
Orthopnea,  24 
Orthoscopy  of  larynx,  698 

of  trachea,  698 
Osmotic  pressure  of  blood,  667 

of  fluids  obtained  by  puncture,  716 
of  urine,  545 
Otoscopic  examinations,  867 
Ovarian  cysts,  paralbumin  in,  724 
Salkowski's  test  for,  724 

tumors,  inspection  of,  303 
Oxaluria,  557 

Oxymethylanthraquinone  reaction,  504 
Oxyuris  vermicularis  in  feces,  432 

Pains,  auto-suggested,  771 
girdle,  770 
hysteric,  771 
in  facial  paralysis,  864 
irradiation  of,  774 
lancinating,  770 
neuralgic,  770 
parenchymatous,  770 
points  of,  760 
reflex  of,  pupillary,  847 
sensibility  of  skin  to,  759 

irritation  hairs  for  testing,  760 
sensitiveness  to,  771 
spontaneous,  770 
suggested,  771 
Palate,  hard,  examination  of,  687 
paralysis  of,  687 
reflex,  absence  of,  687 
soft,  examination  of,  684 
Pallor,  38 

oligochromemia  and,  38 
Palpation,  98 
abdominal  sensitiveness  and,  306 
in  acute  yellow  atrophy  of  liver,  310 
in  enteroptosis,  306 
in  tumors  of  abdomen,  306 
of  abdomen,  304.     See  also  Abdomen,  paU 

pation  of. 
of  acute  splenic  swelling,  311 
of  distended  bladder,  313 
of  enlargement  of  gall-bladder,  310 
of  liver,  310 
of  spleen,  311 

in  infectious  diseases,  312 
in  typhoid  fever,  312 
of  floating  kidney,  310 
of  heart  murmurs,  301 

region,  289 
of  liver  in  cirrhosis,  310 
of  low  position  of  liveP;  310 
of  lungs,  287 
of  mouth,  677 
of  movable  kidney,  310 
of  passive  congestion  of  spleen,  311 
of  peritoneal  friction-rub,  313 
of  pharvnx,  677 
of  pleura,  287 
of  precordia,  289 

of  splashing  noise  of  abdomen,  286,  313 
of  spleen  of  intermittent  fever,  312 
of  leukemia,  312 
of  pseudoleukemia,  312 
of  tubercular  omentum,  310 


INDEX. 


991 


Palpation  of  tumors  of  bladder,  310 
of  intestine,  309 
of  kidney,  310 
of  liver,  310 

of  mesenteric  glands,  310 
of  pelvis,  310 

of  peritoneum,  tubercular,  310 
of  retroperitoneal  glands,  310 
of  spleen,  310 
of  stomach,  309 
percussion,  154 
Pancreas,  diseases  of,  fat-stools  in,  444 

feces  in,  444 
Pancreatic  concretions,  429 
cysts,  pancreatic  ferments  in,  725 
ferments  in  cysts,  725 
Panniculus  adiposus,  27 
Papillitic  atrophy,  706 

after  tlirombosis  of  central  retinal  vein, 
706 
Pappenheim's  stain    for  tubercle  bacilli  in 

sputum,  595 
Paracardial  murmurs,  279 
Paradoxic  incontinence,  942 

pupillary  reaction,  847 
Paraglobulin  in  urine,  detection  of,  464 
Paralbumin  in  ovarian  cysts,  724 

Salkowski's  test  for,  724 
Paralysis,  741 

agitaus,  gait  of,  909 

tremor  in.  749 
atrophic,  789 
secondary  degenerative  muscular  atro- 
phies after,  790 
Bell's,  663 

Brown-Sequard's,  bone  sensibility  in,  765 
bulbar,  862 

increased  salivary  secretion  in,  864 
reaction  of  degeneration  in,  818 
cerebral,  of  chewing  muscles,  849 
conjugate,  of  eyes,  834 
drunkard's,  819 
edema  in,  797 

facial,  851.     See  also  Facial  paralysis. 
hysteric,  electric  reaction  in,  816 
incomplete,  741 

lead,  reaction  of  degeneration  in,  820 
motor  peripheral,  examination,  910,  954 
neural,  electric  irritability  in,  817 
of  accommodation,  848 
of  auditory  nerve,  865 
of  converging  movements  of  eyes,  836 
of  facial  nerve,  851.     See  also  Facial  paral- 
ysis. 
of  muscles  of  eyeball,  827 
of  palate,  687 
peripheral,  electric  reactions  of,  814 

reaction  of  degeneration  in.  816,  817 
posticus,  872 
progressive,  disturbances  of  speech  in,  899 

myosis  in,  839 
psychic,  electric  reaction  in,  816 
rheumatic  facial,  reaction  of  degeneration 

in,  819 
sensory,  testing  of,  756 
skin  changes  in,  792 
sleep,  819 

spastic,  reflexes  in,  786 
spinal,  reaction  of  degeneration  in,  820 
ulnar,  claw-hand  in,  747 
vasomotor,  cyanosis  from,  42 
Paralytic  chest,  30 


Paralytic  dilatation  of  heart  chamber,  316 

phenomena,  disturbances  of  speech  from. 
899 

strabismus,  828 
Paraparetic  gait,  908 
Paraphasia,  892 
Paraplegic  gait,  908 
Pararhythmias,  true,  959 
Pararhythmic  pulse  from  extrasystole,  956 
Parasites,  animal,  in  feces,  429 
in  sputum,  592 
in  urine,  578 

malarial,  653.     See  also  Malaria,   Plasmo- 
dia of. 

vegetable,  in  sputum,  592 
Parasitic  worms  in  blood,  659 
Parenchymatous  pains,  770 
Paresis,  741.     See  also  Paralysis. 
Paresthesia,  769 
Paretic  gait,  spastic,  908 
Parotid  gland,  secretory  nerve  of,  functions 

of,  869 
Paroxysmal  tachycardia,  103 
Paroxysms,  coughing,  97 
Patellar  reflex,  778 

Pavy's  estimation  of  sugar  in  urine,  508 
Pectoriloquy,  242 
Pectus  cariuatum,  31 
Pelvis,  tumors  of,  palpation  of,  310 
Pemphigus,  eosinophilia  in,  649 
Pendulum  rhythm  of  heart,  249,  259 
Penetrating  venous  pulse.  152 
Pentoses  in  urine,  Bial's  test  for,  491 
detection  of,  490 
orcin  test  for,  491 
Salkowski's  test  for,  491 
ToUen's  test  for,  491 
Pentosuria.  490.     See  also  Pentoses  in  urine. 
Penzoldt   and    Faber's   test    for    absorbing 

power  of  gastric  mucous  membrane,  361 
Pepsin,  examination  for,  391 

Hammerschlag's  method,  391 
Mett's  method.  392 
Peptone  in  feces,  446 

in  urine,  465.  See  also  Albumosuria. 
Peptonuria,  465.  See  also  Albumosuria. 
Perception,  postural.  767 

testing  of.  766 

touch,  testing  of,  768 
Percussion,  153 

auscultatory,  158 

charts,  159 

comparative,  197 
of  abdomen,  215 
of  thorax,  197 

deep,  1,55,  162 

dull  tympanitic,  155 

dulness  in,  1.55.     See  also  Dulness. 

immediate,  153 

in  enlargement  of  heart,  192 

in  fluid  ('ff"usion  in  pericardium,  186 

instrumental.  153 

light,  155.  160,  161 

mediate,  1.53 

non-tynipanitic,  155 

of  esophagus,  691 

over  thorax,  212 

change  in  pitch  of,  213 

palpation,  154 

qi^ality  of,  1.55 

resonant,  1.55.     See  also  J?esonance. 

st/ong,  1.5,5,  162 


992 


INDEX. 


Percussion,  superficial,  155,  160 
topographic,  159 

of  air-containing  abdominal  viscera,  196 
of  bladder,  196 
of  heart,  176 
of  kidneys,  195 
of  liver,  190 
of  lungs,  168 
of  spleen,  193 
of  uterus,  196 
Perforating  empyema,  sputum  in,  607 
serous  pleurisy,  sputum  in,  608 
ulcer  in  tabes,  791 
Pericardial  rub,  279 

endocardial    murmur  and,    differentia- 
tion, 280 
graphic  expression  for,  349 
splashing,  281 
Pericarditis,  347 
dry,  347 
exudative,  347 
Pericardium,  exploratory  puncture  of,  722 

fluid  effusion  in,  percussion  in,  186 
Perimeter,  822 

Periodic  hemoglobinuria,  469 
Periosteal  reflexes,  778,  780 
Peripheral  accessory  nerve,  functions  of,  870 
affections  of  bladder  nerves,  vesical  func- 
tions in,  943 
distribution  of  seusorv  cutaneous  nerves, 

915 
motor  paralysis,  examination  in,  910,  954 
paralyses,  electric  reactions  of,  814 

reaction  of  degeneration  in,  816,  817 
vagus,  functions  of,  869 
Peripneumonic  groove,  80 

retraction,  80 
Peristaltic  intestinal  noises,  palpation  of,  313 
Peritoneal  cavity,  accumulation  of  air  in, 
inspection  of,  302 
friction-rub,  palpation  of,  313 
Peritoneum,  tuberculous  tumors  of,  palpa- 
tion of,  310 
Peritonitis,  acute  diffuse,  302 
Perityphlitic  exudations,  308 
Perityphlitis,  leukocytosis  of,  649 
Pernicious  anemia,  blood  in,  660 
cutaneous  hemorhage  iu,  53 
eyeground  in,  704 
Persisting  interval  of  systole,  115 
Perturbatic  critica,  71 
Pertussis,  cough  in,  97 

cutaneous  hemorrhage  in,  54 
leukocytosis  of,  648 
whoop  of,  97 
Pest  bacilli  in  blood,  653 

in  sputum,  600 
Petechise,  53 
Pettenkofer's  test  for  bile   acids  in  urine, 

475 
Pharynx,  examination  of,  677 

palpation  of,  677 
Phenacetin  in  urine,  detection  of,  503 
Phenol  in  urine,  detection  of,  502 
Phenolphthalein,  384 
Phenomen  des  orteils,  787 
Phenylhydrazin  test  for  sugar  in  urine,  487 
Phlegmonous  gastritis,  vomitus  of,  360 
Phloroglucin-vanillin    reaction   for   hydro- 
chloric acid,  373 
Phonendoscope,  218 
Bowles'  method,  218 


Phosphates,    amorphous  earthy,    iu    urine, 
557 
crystalline  trimagnesium,  in  urine,  559 
dicalcium,  in  urine,  559 
earthy,  in  urine,  537 
in  urine,  amorphous  earthy,  557 
crystalline  trimagnesium,  559 
dicalcium,  559 

earthy,  estimation  of,  separate,  537 
quantitative,  536 
total,  537 

uranium  nitrate  for,  537 
total,  estimation  of,  537 
triple,  558 
triple,  iu  urine,  558 
Phosphorus-poisoning,     cutaneous     hemor- 
rhage in,  53 
Phthisic  chest,  31 

Phymatorrhusiu  in  urine,  detection  of,  477 
Physical  signs  in  pulmonary  cases,  graphic 

expressions  for,  348 
Picric-acid  test  for  albuminuria,  463 
Pigeon  breast,  31,  33 
Pigmentation,  abnormal,  of  skin,  45 
of  itching  cutaneous  diseases,  45 
of  skin,  45 
Pigments,   biliary,   in   urine,   detection   of, 
472.     See  also  Biliary  pigments  in  urine, 
medicinal,  urine  and,  454 
of  beets  in  urine,  455 
of  feces,  445 

of  huckleberries  in  urine,  455 
of  madder  in  urine,  455 
skatol  in  urine,  detection  of,  477 
urinary,  normal,  453 
pathologic,  453 
Pinqueculse,  43 
Pipet,  Hoppe-Seyler,  624 
Piria's  test  for  tyrosin  in  urine,  498 
Pityriasis  tabescentium,  63 
Plague,  bubonic,  bacilli  of,  in  blood,  653 

in  sputum,  600 
Plantar  reflex,  777,  787 
Plasma,  blood,  specific  gravity  of,  612 
Plasmodia,  malarial,  653.    See  also  Malaria, 

Plasmodia  of. 
Plasters,    mustard,    pigmentation   of    skin 

from,  45 
Platysma,  sign  of,  743 
Plethora,  hydremic,  611 
Pleura,  palpation  of,  287 
pulsation  in  region  of,  abnormal,  287 
tumors  of,  dulness  from,  208 
Pleural  exploratory  punctures,  721 
exudate,  dulness  of,  202 

when  combined  with  pneumothorax, 
206 
fluids,  diagnostic  value  of,  716 
friction-rub,  239 

splashing  noise  in  pneumothorax,  240 
Pleurisy,  acute  infectious,  717 

diminished  vesicular  breathing  in,  225 
perforating  serous,  sputum  in,  608 
purulent,  fluctuation  of,  287 
retraction  of  lung  borders  in,  176 
right,   with   effusions,  physical  signs  in, 
350 
Pleuritic  adhesions,   mobility  of  lung  bor- 
ders in,  174 
dulness,  200 

exudations,  displaced  heart-beat  in,  292 
rub,  graphic  expression  for.  349 


INDEX. 


993 


Pleuropericardial  rub,  239,  280 
Pleximeter,  154,  155 
Plexor,  ]54 

Plexus,  brachial,  localization  of,  932 
motor  roots  of,  934 
lumbosacral,  localization  of,  932 
motor  roots  of,  934 
Pneumatometry,  93 
Pneumocardia,  cardiac  dulness  in,  180 
Pneumococci,  Frankel's,  in  sputum,  598 

Wolfs  stain  for,  598 
Pneumoconioses,  color  of  sputum  in,  581 
Pneumonia,   catarrhal,    physical    signs    in, 
352 
croupous,  dulness  in,  208 
fever  curve  of,  69 
left,  physical  examination  in,  351 
sputum  in,  606 
Ehrlich's  egg-yellow  reaction  in,  500 
leukocytosis  of,  646 
leukopenia  of,  646 
lung  dulness  in,  198 
Pneumonomycosis  aspergillina,  602,  603 

mucorina,  602,  603 
Pneumopericardium,  metallic  resonance  in, 

212 
Pneumoscope  of  Bloch,  94 
Pneumothorax,  cardiac  dulness  in,  180 
dulness  of  pleural  exudate  in,  206 
falling-drop  noise  in,  241 
heart-beat  in,  292 
hyperresonaiit  tones  in,  211 
metallic  resonance  in,  212 
noises  audible  in,  240 
pleural  splashing  noise  in,  240 
pulmonary  fistula  noise  in,  241 
skiagraph  of,  733 
tympanitic  tones  in,  211 
upper  liver  border  in,  192 
vesicular  breathing  in,  225 
vy^ater-whistle  noise  iu,  241 
Poikilocytes,  636 

endoglobular  changes  in,  637 
Poikilocytosis,  636 

Poisoning,  carbon -dioxid,  blood  in,  673 
hydrogeu-sulphid,  blood  in,  674 
lead-,  reaction  of  degeneration  in,  816 
meat-,  herpes  febrilis  in,  62 
phosphorus-,  cutaneous  hemorrhage  in,  53 
Poisons,  cyanosis  from,  42 

in  urine,  501 
Polarimetric  estimation  of  sugar  in  urine, 

515 
Polaristrobometer,  Wild's,  516,  517 
Poliomyelitis,   reaction  of  degeneration  in, 

820 
Politzer's  sound-meter,  865 
Polychromatophilic  changes  of  erythrocytes, 

636 
Polycrotism,  129 
Polycythemia,  blood  in,  663 
Polymorphonuclear  neutrophilicleukocytes. 

641 
Polyneuritis,  acute,  sweat  in,  797 
edema  in,  52,  797 
reaction  of  degeneration  in,  816 
Polynuclear  leukocytes,  427,  641 
neutrophilic  leukocytosis,  649 
Polypnea,  84 
Polyuria,  450 

Portal  circulation,  obstruction  of,  303 
vein,  thrombosis  of,  303 

63 


Posner's  estimation  of  pus  in  urine,  568 

stain  for  urinary  sediment,  565 
Posoriasis  linguae,  683 
Posticus  paralysis,  872 
Postural  perception,  767 
Posture  in  bed,  23 
active,  24 

iu  cerebrospinal  meningitis,  25 
passive,  24 
pathologic,  908 
Potain's  explanation  of  gallop  rhythm,  259 
stomach  pump,  364 
systolic  gallop  rhythm,  259 
Potassic  iodid  fibrin,  testing  digestion  with, 

364 
Potassium  ferrocyanid   and  acetic  acid  test 
for  albuminuria,  463 
testing  absorbing  power  of  stomach  with, 
361 
Power  sense,  testing,  762 
Preacher's  hand,  747 
Precordia,  inspection  of,  289 
palpation  of,  289 
pulsations  iu,  299 
Precordial  emphysematous  murmur,  281 

terror,  84 
Prediastolic  murmurs,  268,  270 
Pregnancy,  leukocytosis  of,  646 
Preputial  epithelia  in  urine,  566 
Pressure  diverticulum  of  esophagus,  689 

points,  758 
Presystolic  accentuation   of  diastolic  mur- 
mur, 269 
murmurs,  268 
pure,  269 
Prickly  heat,  62 

Progressive  muscular  atrophies,  789 
dystrophy,  789 
paralysis,  disturbances  of  speech  in,  899 
Propeptonuria,  465.     See  also  Albumosuria. 
Propulsion,  gait  of,  909 

Proteids,  amount  of,  in  passive  congestion, 
460 
coagulable,  of  urine,  detection  of,  460 
digestion  of,  products  of,  395 
.  in  feces,  detection  of,  460 
method  of  removing,  463 
quantitative  estimation  of,  505 
Brandberg's  method,  506 
Esbach's  method,  505 
Kjeldahl's  method,  505 
Eoberts-Stolnikow's  method,  506 
utilization  of,  438 
Protein  in  feces,  446 
Proteoses  in  feces,  446 
Protozoa  in  feces,  429 
Protracted  crisis,  71 
Pseudo-atasia,  754 

Pseudobulbar  symptoms  of  motor  hemiple- 
gia, 878 
Pseudocrisis,  71 
Pseudodiphtheria  bacilli,  685 
Pseudogall-stones,  428 
Pseudohemisystole,  297 
Pseudohypertrophy,  muscular,  788 
Pseudoleukemia,  blood  in,  661 

spleen  of,  palpation  of,  312 
Pseudolymphocytes,  neutrophilic,  642 
Pseudomucin  iu  ovarian  cysts,  724 

Salkowski's  test  for,  724 
Pseudopericardial  rub,  239,  280 
Psychic  blindness,  901 


994 


INDEX. 


Psychic  deafness,  901 

paralysis,  electric  reaction  in,  816 
Ptosis,  833 

congenital,  834 
sympathetic,  833 
Puerile  breathing,  223 

Pulmonary   cases,   graphic  expressions  for, 
physical  signs  in,  348 
epithelium  in  sputum,  588 
infarctions,  dulness  of,  208 
insufficiency,  338 

diastolic  murmur  of,  268,  338 
pulsus  celer  of,  339,  340 
stenosis,  340 
murmur  of,  340 
systolic  murmur  of,  267 
tones,  248 

tuberculosis,  cutaneous  hemorrhage  in,  53 
dulness  from,  208 
Ehrlich's  diazo-reaction  in,  500 
physical  signs  in,  351 
pigmentation  of  skin  in,  45 
sputum  in,  606 
Pulsating  exophthalmos,  atrophy  of  optic 

nerve  in,  705 
Pulsation,  abnormal,  in  region  of  lungs,  287 
of  pleura,  287 
epigastric,  300 
in  precordia,  299 
of  liver,  300 
Pulse,  alternate,  125 
anacrotic,  114,  117 
arterial,  of  liver,  152 

venous  pulse  and,  differentiation,  147 
beat,  individual,  characters  of,  104 
bigeminal,  123 
capillary,  144 
carotid,  148 
catacrotic,  114 
celerity  of,  105 

in  sphygmogram,  127 
characters  of,  100 
combined  qualities  of,  108 
curve,  blood-pressure   and,    relations   be- 
tween, 118 
celerity  of,  127 
diagnostic  significance,  121 
explanation  of,  114 
factors  influencing,  114,  120 
frequency  of  pulse  and,  123 
influence  of  breathing  on,  118 
of  cardiac  activity  on,  120 
of  compression  of  vascular  trunks  on, 

121 
of  diminution  of  blood  on,  120 
of  elevation  of  extremity  on,  120 
venous  flow  from  extremity  on,  121 
shape  of,  influence  of  cardiac  action  on, 

117 
specific,  131 

tension  of  pulse  and,  129 
volume  of  pulse  and,  124 
dicrotic,  108 

Landois'  theory  of,  116 
diminution  of,  103 
equality  of,  125 
frequency  of,  100 

in  sphygmogram,  123 
increase  of,  101.     See  also  Tachycardia. 
hard,  108 

high  pressure  in,  130 
hyperdicrotic,  131 


Pulse,  hypodicrotic,  131 
in  arteriosclerosis,  99,  128 
in  chronic  nephritis,  128 
inequality  of,  125 
intermittent,  123 

from  extrasystole,  956 
irregular,  123 

absolutely,  104 

analysis  of,  955 

partially,  104 
liver,  arterial,  152,  300 

inflammatory,  152 
low  pressure  in,  130 
myerethic  irregularity  of,  960 
normal  pressure  in,  129 
palpation  of,  99 

character  of  arterial  wall  in,  99 
paradoxic,  125,  126 
pararhythmic,  from  extrasystole,  956 
regular,  123 
relaxed,  108 
rhythm,  104,  123 

disturbances  of  contractility,  963 

irregularities  of,  104 
size  of,  105 
soft,  108 
splenic,  300 
tardy,  105,  127,  128 

of  aortic  stenosis,  334 
tense,  108 
tension  of,  106 

in  sphygmogram,  129 
trigeminal,  123 

venous,  arterial  pulse  and,  difierentiation, 
147 

combined,  152 

difiiculties  in  distinguishing  kinds,  152 

negative,  147 
centrifugal,  147 
presystolic,  147 

of  liver,  151 

penetrating,  152 

physiologic,  147 

positive  centrifugal,  150 
centripetal,  152 

regurgitating,  150 

varieties  of.  147 

Volhard's    procedure    for    determining 
phases  of,  152 
volume,  105 

in  sphygmogram,  124 
Pulsus  alternans,  125,  963 
bigeminus,  123 

alternans,  125 
celer,  105,  127,  128 

of  pulmonary  insuflSciency,  339,  340 
durus,  108 
eqnalis,  125 
inequalis,  125 

periodicus,  125 
intercidens,  123 
intermittens,  123 
irregularis,  123 
mollis,  108 
paradoxus,  125,  126 
tardus,  105,  127,  128 

of  aortic  stenosis,  334 
trigeminus,  123 
Punctate  erythrocytes,  638 
Punctures,  exploratory,  707 

in  appendicitis,  725 

in  diseased  conditions,  721 


INDEX. 


995 


Punctures,  exploratory,  methods  of,  707 
of  abdominal  cysts,  722 
of  intrathoracic  cysts,  722 
of  pericardium,  722 
of  spleen,  725 
osmotic  pressure  of  fluids  obtained  by, 

716 
pleural,  721 
results  of,  707 
syringes  for,  707 

to  demonstrate  pulmonary  cavities,  721 
lumbar,  725 
Pupillary  contraction  in  nervous  diseases, 
840  ^ 
dilatation  in  nervous  diseases,  839 
immobility,  hemiopic,  843 
light  reaction  in  nervous  diseases,  846 

reflex,  840 
narrowing  in  nervous  diseases,  839 

accommodation,  847 
pain  reflex,  847 
phenomena  in  nervous  diseases,  838 

of  Westphal,  847 
reaction,  crossed,  840 
■  hemiopic,  843 
paradoxic,  847 
reflex  of  Haab,  847 

hemiopic,  843 
rigidity,  reflex,  846 
Pupils,  Argyll-Eobertson's,  846 
diameters  of,  in  nervous  diseases,  838 
inequality  of,  in  nervous  diseases,  839 
irregularity  in  shape  of,  in  nervous  dis- 
eases, 839 
rigidity  of,  in  nervous  diseases,  846 
tester  for,  845 
Westphal' s,  847 
Purin  bodies  in  urine,  Denige's  estimation, 
533 
estimation  of,  532 
Salkowski's  estimation,  532 
Purpura,  cutaneous  hemorrhage  in,  52,  53 
hsemorrhagica,  changes  of  eyegrouud  in, 

704 
pulicosa,  53 

variolosa,  cutaneous  hemorrhage  in,  54 
Purulent  pleurisy,  fluctuation  of,  287 

sputum,  580  ' 

Pus,  74 
cells  in  urine,  566 
corpuscles  in  sputum,  587 
in  feces,  427 
in  urine,  471 

Posuer's  estimation,  568 
in  vomitus,  360 
Putrid  bronchitis,  sputum  in,  607 
Pvciiometric  determination  of  specific  grav- 
ity of  blood,  612 
Pyelitis  in  gonorrhea,  578 
Pyemia,  chills  in,  74 

cutaneous  hemorrhage  in,  53 
Pyloric  stenosis,  302 

examination  of  stomach  for,  414 
Pyopneumothorax,  left,  physical  examina- 
tion in,  350 
Pyramidon  in  urine,  503 
Pyrocatechin  coloring  urine,  454 

Quartan  fever,  73 

Quetelet's  table  of  body  measurements,  29 

of  body  weight,  28 
Quotidian  fever,  73 


Eachitic  chest,  31 

rosary,  31 

teeth^  679 
Eachitis,  37 

Eadial  artery,  auscultation  of,  282 
Eales,  226,  232 

bubbling,  232 
coarse,  232 
fine,  232 
large,  232 
small,  232 

cardiac,  238 

cardiopneumatic,  238 

cardiosystolic,  238 

consonating,  235 

crackling,  233,  234,  236 

crepitant,  233,  237 

dry,  234 

graphic  expressions  for,  349 

moist,  232 

musical,  234 

non-consouating,  235 

non-resonant,  235 

oral,  232 

resonant,  235 

snapping,  234 

subcrepitant,  233 

transmission  of,  232 
Eaw  mobility,  examination  of  stomacli  for, 

413 
Eay  fungi  in  sputum,  603 
Eectal  functions,  939 

examination  of,  947 
Eectum,  carcinoma  of,  feces  in,  444 

center,  theory  of,  944 

digital  examination  of,  415 

distention  of,  416 

emptying,  944 

examination  of,  415 

injections  of  water  into,  417 

insufliation  of,  417 

lavage  of,  417 

sounding  of,  417 
Eecurrent  fever,  curve  in,  74 
spirillse  of,  in  blood,  652 
Eed  corpuscles.     See  Erythrocytes. 

indol  in  urine,  detection  of,  477 
Eeducteur  de  potential,  806 
Eeduction  tests  for  sugar  in  urine,  482 

significance  of,  485 
Eeflex,  abdominal,  777 

Achilles-tendon,  778 

anal,  778 

Babinski's,  787 

center,  783 

cerebral,  780 

complex,  781 

corneal,  850 

cr em  aster,  777 

cutaneous,  777 

outline  for  examination  of,  952 

examination  of,  776,  952 

gluteal,  778 

Haab's,  847 

hemiopic  pupillary,  843 

in  cerebral  hemiplegias.  781,  785 

in  spastic  paralyses,  786 

in  transverse  lesions  of  spinal  cord,  782 

inguinal,  777 

interscapular,  778 

jaw,  849 

Jendrassik's  theory  of,  780 


996 


INDEX. 


Eeflex,  joint,  778,  780 
lung,  162 
Mering's,  413 
nuclear,  784 
oblique,  777 
origin  of,  779 
palate,  absence  of,  687 
patellar,  778 
pathologic,  786 
periosteal,  778,  780 
plantar,  777,  787 
pupillary,  hemiopic,  843 
light,  840 
pain,  847 
rigidity,  846 
quantitative  alterations  of,  786 

significance,  784 
segmental  localization  of,  927 
sensation,  774 
spinal,  constancy  of,  779 

frequency  of,  779 
tendon,  778,  780 
outline  for  examination  of,  952 
Eegurgitating  venous  pulse,  150 
Eelapses  of  fever,  74 

Remittent  fever,  variations  in  fever  of,  68 
Eeual  albuminuria,  459 
Eenuin  in  gastric  juice,  394 

zymogen  in  gastric  juice,  394 
Eesonance,  155 
cracked-pot,  158 

over  thorax,  213 
metallic,  157 

in  pneumopericardium,  212 
in  pneumothorax,  212 
in  pulmonary  cavities,  212 
over  thorax,  212 

stick-pleximeter    method  of   apprecia- 
ting, 158 
non-tympanitic,  156 
tympanitic,  156 
Eesonant  rales,  235 
Eesorein  coloring  urine,  454 
Eespiration,  abdominal,  77 
accessory,  92 
amphoric,  229 
asymmetric,  79 
auxiliary,  92 
Biot's,  8*1 

bronchial,  graphic  expression  for,  348 
pathologic,  226 

different  kinds  of,  229 
obturation      atelectasis      preventing, 
228 
physiologic,  222 
bronchovesicular,  231 
cavernous,  229 
character  of,  77 
Cheyne-Stokes,  81 
cog-wheel,  226 

vesicular,  graphic  expression  for,  348 
costal,  77 

limitation  of,  78 
diaphragmatic.  77 
endocardial  murmurs  and,  278 
exaggerated,  in  diabetic  coma,  91 
frequency  of,  abnormalities  in,  80 
under  physiologic  conditions,  77 
indistinct,  graphic  expression  for,  348 
influence  on  pulse  curve,  118 
metallic,  229 
mixed,  222,  231 


Eespiration  murmur  in  interstitial  pulmo- 
nary emphysema,  240 
indefinite,  230 
metamorphosed,  230 
normal  type,  77 
painful  dyspnea  from,  85 
pathologic  variations  in  type  of,  77 
puerile,  223 

rhythm  of,  abnormalities  in,  80 
vesicular,  220 
absence  of,  224 
alterations  of,  223 
cog-wheel,  226 
diminution  of,  224 
graphic  expressions  for,  348 
impure,  225 
increased,  223 
rough,  225 
sharp,  223 
systolic,  222 
weakened,  224 

with  prolonged  expiration,  225 
Eespiratory  murmur,  vesicular,  220 
obstruction,  habituation  to,  93 
organs,  auscultation  of,  219 
passages,  gluing  of,  582 
phenomena  of  motion  in  veins,  145 
tone  change,  215 
Eetina,  nerve  fibers  of,  705 
Eetinal  atrophy  in  chorioretinitis,  706 
vein,   central,    thrombosis    of,   blindness 
after,  706 
Eetroperitoneal  glands,  tumor  of,  palpation 

of,  310 
Eetropharyngeal  abscess,  687 
Eetropulsion,  gait  of,  909 
Eevilliod's  signs,  855 
Ehamnus  in  urine,  detection  of,  503 
Eheumatic  facial  paralysis,  reaction  of  de- 
generation in,  819 
Eheumatism,  acute   articular,    leukocytosis 

of,  647 
Ehinopharyngoscopy,  direct,  687 

Lindt's  method,  687 
Ehinoscopy,  701 
anterior,  701 
posterior,  701 
Ehonchi,  232.     See  also  Rales. 
Ehubarb  in  urine.  455 

detection  of.  503 
Eiekets,  34 
Eiedel's  projection  of  liver  in  cholelithiasis, 

311 
Eiegel's  test-meal,  368 

diagnostic  importance,  396 
Eienne's  test  for  hearing-power,  865 
Eigidity,  cataleptic,  739,  751 
Eisus  sardonicus,  24 
Eiva-Eocci's  sphygmomanometer,  136 

Cook's  modification,  141,  142 
Eobert's    quantitative   areometric    test    for 

sugar  in  urine,  513 
Eoberts-Stolnikow's  estimation  of  proteid  in 

urine,  506 
Eomberg's  sign.  909 
Eomonowski's  stain  656 
Eontgen-ray  examinations,  729 
in  aortic  aneurism,  347 
ia  examination  of  stomach,  367 
of  aneurism  of  aorta,  737 
of  arthritis  deformans,  736 
of  calculus  in  ureter,  731 


INDEX. 


997 


E6ntgen-ray  of  chronic  tubercalosis,  735 

of  gouty  deposits,  729 

of  hernia  of  diaphragm,  735 

of  lumbar  region,  730 

of  pneumothorax,  732 

of  renal  calculus,  732 

of  vesical  calculus,  734 
Rose  spots,  60 

Eosenbach's  modification   of  Gmelin's  test 
for  biliary  pigments,  472 

reaction,  477 

theory  of  Cheyne-Stokes  respiration,  83 
Eosenstein's  theory  of  weakened  apex  beat 

in  aortic  stenosis,  334 
Eoseola,  60 
Eotary  vertigo,  881 
Eouleaux  formation,  635 
Round  worms  in  feces,  432 
Eubber  capsule,  testing  digestion  with,  364 
Buhner's  test  for  sugar  in  urine,  488 
Euge's  stain  for  malarial  plasmodia,  656 
Eumpel's  diflFerentiation  of  esophageal  dila- 
tations and  diverticula,  692 
Eusty  sputum,  580 

Sabek  shin,  792 
Saccharometer,  Einhorn's,  515 

Lohnstein's,  515 
Saginata  in  feces,  437 
Sahli's  hemometer,  620 

pocket  mercury  manometer,  136 
test  for  motility  of  stomach,  363 
theory  of  systolic  retraction  at  apex,  295 
of  vesicular  breathing,  221 
Sahli-Seiler's  butyrometric  examination    of 
stomach  functions,  397.     See  also  Stom- 
ach, functions  of. 
universal  test  meal,  368,  397 
Salicylic  acid  in  urine,  detection  of,  502 
Saliva,  secretion  of,  687 

increased,  in  bulbar  paralysis,  864 
Salkowski's  determination  of  alkalinity   of 
of  blood,  615 
estimation  of  purin  bodies  in  urine,  532 
test  for  albumoses,  466 
for  biliary  pigments,  473 
forBrucke's  peptone,  466 
for  deutero-albumoses,  466 
for  hematoporpbyrin,  472 
for  paralbumin  in  ovarian  cysts,  724 
for  pentoses,  491 
for  peptone,  Brucke's,  466 
for  urea  in  urinary  cysts,  724 
Salkowski-Ludwig's  estimation  of  uric  acid, 

530 
Salol  coloring  urine,  454 

in  testing  motility  of  stomach,  362 
Salts,  organic,  incrustations  of  food  particles 

with,  429 
Sand,  biliary,  428 

intestinal,  in  feces,  428 
Sandalwood  oil  in  urine,  detection  of,  503 
Santonin  in  urine,  455 

detection  of,  503 
Saprophytic  bacteria  in  sputum,  600 
Sarcinse  in  si)atum,  602 
Sardonic  laugh,  24 
Scaphoid  belly,  304 

Scarlet  fever,  cutaneous  hemorrhage  in,  53 
eosinophilia  of,  650 
leukocytosis  of,  648 
leukopenia  of,  648 


Scars,  63 

Schlosing's  estimation  of  ammonia  in  urine, 

539 
Schonbein-Almen's  test  for  blood  in  feces, 

for  hemoglobinuria,  471 
SchondorflTs  estimation  of  urea.  526 
Schrotter's  fermentation  tube,  489 
Schulte's  test  for  albumosuria,  467 
Schwabach's  test  for  hearing-power,  866 
Sciatica,  gait  of,  909 

Sclerosis,  multiple,    disturbances  of  speech 
in,  899 
intention  tremor  in,  749 
Scoliokyphotic  chest,  31 
Scoliosis,  36 

right,  32 
Scoliotic  chest,  31 
Scotoma,  significance  of,  823 
Scurvy,  cutaneous  hemorrhage  in,  53 
Seasickness,  883 

Secretion,  disturbances  of,  in  nervous  dis- 
eases, 796 
mucous,  of  stomach,  examination  of,  395 
of  saliva,  687 

increased,  in  bulbar  paralysis,  864 
sweat,  abnormalities  of,  in  nervous  dis- 
eases, 796 
Secretory  nerve  of  parotid  gland,  functions 

of,  869 
Sediment  of  urine,  553 
Cohn's  stain  for,  564 
examination,  553 
inorganic,  analytic  scheme  of,  563 
mucous,  562 
non-organic,  555 
organic,  564 
preservation  of,  564 
staining  of,  564 
Posner's  stain  for,  565 
Sedimentation  of  tubercle  bacilli  in  sputum, 
595 
urinary,  553 
Seegen's  modification  of  Trommer's  test  for 

sugar,  484 
Segmental  localization  of  cutaneous  sensi- 
bilitv,  922 
of  motility,  926 
of  reflexes,  927 
of  spinal  cord,  920 
Segments,  spinal-cord,  localization  of  func- 
tions in,  930 
Seiler-Sahli's  butyrometric  examination  of 
stomach  functions,  397.     See  also  Stom- 
ach, functions  of. 
universal  test-meal,  368,  .397 
Senna  in  urine,  455 

detection  of,  503 
Sensations,  ability  to  localize,  764 
cerebral  disturbances  of,  878 
girdle,  770 
of  innervation  in  ataxia,  763 

testing,  762 
of  vibration,  765 
reflex,  774 
sympathetic,  774 
Sense  of  location,  764 
of  strength,  testing,  762 
power,  testing  of,  762 
stereognostic,  768 
Sensibility,  hone,  in  Browu-Sequard's  paral- 
ysis, 765 


998 


INDEX. 


Sensibility,  bone,    in    cerebral    hemi-anes- 
thesia,  765 
in  hysteric  anesthesias,  765 
in  syringomyelia,  765 
in  transverse  lesions  of  spinal  cord,  765 
testing  of,  765 
corneal,  in  nervous  diseases,  850 
cutaneous  segmental  localization  of,  922 
diminished,  in  facial  paralysis,  864 
muscular,  764 

of  abdomen  to  pressure,  palpation  in,  306 
of  skin,  testing,  759 

irritation  hairs  for,  760 
outline  for  examination  of,  951 
pressure,  757,  772 
tactile,  testing,  757 
testing  of,  756 
technic,  769 
thermal,  of  skin,  testing,  761 
to  pain,  771 
Sensory  aphasia,  cortical,  892 

effects  on  written  speech,  896 
subcortical,  892 

effects  on  written  speech,  896 
transcortical,  893 

effects  on  written  speech,  896 
branches  of  vagus,  869 
cutaneous  nerves,  peripheral  distribution 

of,  915 
disturbances  with  cortical  lesions,  880 
fibers  of  glossopharyngeal  nerve,  869 
functions,   complicated,   examination  of, 
766 
simple,  examination  of,  757 
irritation,  phenomena  of,  769 
paralysis,  testing,  756 
trigeminus,  functions  of,  849 
Separatory  funnel,  375 
Septicemia,  leukocytosis  of,  648 
Septum,  ventricular,  343 
Serum  in  urine,  detection  of,  464 

test,  Widal's,  in  typhoid  fever,  675 
Serum-albumin  in  urine,  detection  of,  460 
Serum-globulin  in  urine,  detection  of,  460 
Shadows,  erythrocytic,  638 
Shaffer  and  Folin's  modification  of  Hopkin's 

estimation  of  uric  acid,  531 
Sherer's  test  for  leucin  in  urine,  499 
Shock,  systolic  valve,  300 
Shoulder-blade  movements  in  nervous  dis- 
eases, 910 
Shoulder-joint  movements  in  nervous  dis- 
eases, 909 
Siever    and    Ewald's  test  for  motility  of 

stomach,  362 
Signe  de  I'orbiculaire,  855 
Simulated  deafness,  867 

unilateral  blindness,  825 
Single-day  fevers,  69 
Sinking  of  sputum,  582 
Sjoqvist's  estimation  of  total  unneutralized 

hydrochloric  acid,  379 
Skatol  pigments  in  urine,  detection  of,  477 
Skin,  changes  in,  over  paralyzed  parts,  792 
circulation  in,  collateral,  55 
collateral  circulation  in,  55 
color  of,  38,  45 
desquamation  of,  63 
diseases,  59 

eosinophilia  in,  650 
itching,  pigmentation  of,  45 
edema  of,  48,  49 


Skin,  emphysema  of,  52 
examination  of,  38 
glossy,  792 
hemorrhage  into,  52,     See  also  Hemorrhage, 

cutaneous. 
hyperalgesic  zones  of,  in  diseases  of  deeper 

organs,  774 
icteric  coloration  of,  42.     See  also  Icterus. 
moisture  of,  47 
nerves  of,  sensory,  peripheral  distribution 

of,  915 
of  face,  abnormal  redness  of,  39 
pigmentation  of,  45 
reflexes  of,  777 

outline  for  examination  of,  951 
sensibility   of,  segmental  localization  of, 
922 
to  pain,  testing,  759 

irritation  hairs  for,  760 
swelling  of,  48 

thermal  sensibility  of,  testing,  761 
trophic  affections  of,  59,  791 
turgidity  of,  48 
Sleep  paralysis,  819 
Sleepiness,  738 

Small-pox,  black,  cutaneous  hemorrhage  in, 
54 
cutaneous  hemorrhage  in,  53 
Smearing  of  respiratory  passages,  582 
Smegma  bacilli  in  sputum,  595 

in  urine,  576 
Snapping  rales,  234 
Soaps  in  feces,  tests  for,  446 
Soft  palate,  examination  of,  684 
Somnambulism,  739 
Somnolence,  738 
Souffle  voile  of  Laennec,  230 
Sound  perceptions,  subjective,  from  nervous 

diseases,  867 
Sounding  of  rectum,  417 
Sound-meter  of  Politzer,  865 
Soxhlet-Allihn's  estimation  of  sugar  inurine, 

510 
Soxhlet-Fehling's   estimation    of   sugar   in 

urine,  507 
Spasms,  clonic,  744 
facial,  864 
tonic,  744 
Spastic  gait,  908 
paralyses,  reflexes  in,  786 
paretic  gait,  908 
Specific  gravity  of  blood,  612 
of  gastric  juice,  370 
of  urine,  451 
estimation  of  amount  of  urea  by,  519 
Spectroscope,  direct-vision  hand,  447 
Spectroscopic  detection  of  hemoglobinuria, 
471 
test  for  alkalinity  of  blood.  Dare's,  6i5 
for  blood  in  feces,  447 
Speculum,  examination  of  rectum  with,  416 

Frankel's  nasal,  701 
Speech,  disturbances  of,  from  irritation  phe- 
nomena, 900 
from  lesions  of  conducting  fibers,  888 
from  lesions  of  speech-area,  888 
from  paralytic  phenomena,  899 
in  Friedreich's  ataxia,  899 
in  hysteria,  899 
in  multiple  sclerosis,  899 
in  nervous  diseases,  888 
in  progressive  paralysis,  899 


INDEX. 


999 


Speech,  functions  of,  testing,  900 
letters,  900 
words,  900 
tract,  conception  of,  888 
Speech-area,    lesions     of,     disturbances    of 

speech  from,  888 
Spermatozoa  in  urine,  573 
Sphygmograph,  application  of,  132 
Jaquet's,  111 
of  von  Frey,  109 
Sphygraography,  109 
Sphygmomanometer,  Erianger's,  142 
Gartner's,  139 
Janeway's,  143 
Kiva-Rocci's,  136 

Cook's  modification,  141,  142 
Stanton's,  144 
von  Basch's,  134 
Sphygmomanometry,  134 
Sphygmometer,  Hill  and  Barnard's,  140 

pocket,  141 
Spinal  accessory  nerve,  functions  of,  870 
cord,  diseases  of,  functions  of  bladder  in, 
942 
localization  of,  920 
segments  of,  localization  of  functions  in, 

930 
transverse  lesions  of,  bone  sensibility  in, 
765 
electric  reaction  in,  816 
reflexes  in,  782,  785 
vasomotor  disturbances  in,  796 
hemianesthesia,  879 
hemiplegia,  903 
localizations,  920 
muscular  atrophy,  789 
nervous  system,  examination  of,  910 
paralysis,  infantile,  reaction  of  degenera- 
tion in,  820 
reflexes,  constancy  of,  779 
frequency  of.  779 
Spinning-top,  noise  of,  158 

over  thorax,  213 
Spirillae  of  recurrent  fever  in  blood,  652 
Spirometry,  93 

Splashing  noise  of  abdomen,  palpation  of, 
286,  313 
pleural,  in  pneumothorax,  240 
pericardial,  281 
sounds  of  stomach,  356 
Spleen,  congestion  of,  passive,  palpation  of, 
311 
enlargement  of,  dipping  in,  305 

in    infectious    diseases,    palpation     of, 

312 
in  typhoid  fever,  palpation  of,  312 
palpation  of,  311 
exploratory  puncture  of,  725 
of  intermittent  fever,  palpation  of,  312 
of  leukemia,  palpation  of,  312 
of  pseudoleukemia,  palpation  of,  312 
swelling  of,  acute,  palpation  of,  311 
topographic  pereussion  of,  193 
tumor  of,  palpation  of,  310 
Splenic  dulness,  193 
dislocations  of,  194 
gross  changes  in,  194 
pulse,  300 
Splitting  of  heart  tone,  255,  257 
Spontaneous  pains,  770 
Spritzen,  283 
Sputa  fundum  petentia,  582 


Sputum,   acid-staining  bacilli  in,  isolating 

tubercle  bacilli  from,  595 
air  content  of,  582 
albumin  in,  605 
alveolar  epithelium  in,  588 
amount  of,  579 
animal  parasites  in,  592 
appearances  of,  583 
aspergillus  in,  602 
bacillus  anthracis  in,  602 

mallei  in,  602 

of  bubonic  plague  in,  600 

of  tuberculosis  in,  592.    See  also  Tuber- 
cle bacillus  in  sputum. 

pyocyaneus  in,  582 

typhoid  in,  602 
bacteria  in,  596 

Gram's  stain  for,  596 

Weigert's  modification,  597 
black,  581 

Bottcher's  crystals  in,  591 
calcareous  concretions  in,  586 
characteristics  of,  583,  605 
Charcot's  crystals  in,  591 
chemical  examination  of,  605 
color  of,  579 

in  pneumoconioses,  581 
consistence  of,  579 
crystals  in,  590,  591 
Curschmaun's  spirals  in,  585,  591 
cylindric  epithelium  in,  587 
distomum  pulmonale  in,  592 
Dittrich's  plugs  in,  584 
echinococcus  elements  in,  586 
elastic  fibers  in,  588 

Weigert's  stain  for,  589 
epithelium  in,  587 
erythrocytes  in,  588 
examination  of,  578 

chemical,  605 

microscopic,  586 
fibrin  in,  585 

fibrinous  bronchial  casts  in,  586 
foreign  bodies  in,  586 
fragments  of  neoplasms  of  lung  in,  591 
Frankel's  pneumococci  in,  598 

Wolf's  stain  for,  598 
green,  in  tumors  of  lung,  581 
heart  cells  in,  588 
in  abscess  of  lung,  607 
in  acute  miliary  tuberculosis,  606 
in  bronchiectasis,  607 
in  bronchitis,  605,  607 
in  bronchopneumonia,  607 
in  catarrh,  605 
in  croupous  bronchitis,  605 

pneumonia,  606 
in  edema  of  lung,  608 
in  gangrene  of  lung,  607 
in  hemoptysis,  609 
in  hemorrhage  of  lung,  608 
in  perforating  empyema,  607 

serous  pleurisy,  608 
in  pulmonary  abscess,  607 

edema,  608 

gangrene,  607 

glanders,  602 

hemorrhage,  608 

tuberculosis,  606 
in  putrid  bronchitis,   607 
in  wool-sorters'  disease,  602 
leptothrix  buccalis  in,  600 


1000 


INDEX. 


Sputum,  lung  tissue  in,  588 

micrococcus  catarrhalis  in,  600 
tetrageuus  in,  600 

microscopic  examination  of,  586 

morphologic  elements  of,  587 
mucopurulent,  580 

mucor  in,  602 

myeliu  in,  588 

odor  of,  583 

oKdium  albicans  in,  603 

pest  bacillus  in,  600 

pulmonary  epithelium  in,  588 

purulent,  580 

pus  corpuscles  in,  587 

ray  fungi  in,  603 

reaction  of,  579 

rusty,  580 

saprophytic  bacteria  in,  600 

sarcinse  in,  602 

serous,  580 

sinking  of,  582 

smegma  bacilli  in,  595 

squamous  epithelium  in,  587 

staphj'lococci  in,  600 

strata,  582 

streptococci  in,  600 

transparency  of,  579 

tubercle  bacillus  in,  592     See  also  Tubercle 
bacillus  in  sputum. 

typhoid  bacillus  in,  602 

vegetable  parasites  in,  592 
Squamous  epithelium  in  sputum,  587 
Square-shaped  head,  37 
Squeezing  murmur,  690 
Squibb's  apparatus  for  estimation  of  urea, 

524 
Squirting  murmur,  690 
Staggering  gait,  909 
Stasrnant  stomach,  390 

Stain,   Chenzinsky's    eosin-methylene-blue, 
for  blood,  633 

Cohn's,  for  urinary  sediment,  564 

Czaplewsky's,  for  tubercle  bacilli  in  spu- 
tum, 594 

Ehrlich's,  for  iodin  reaction  of  blood,  634 
triple,  for  blood,  633 

Giinther's.  for  bacteria  in  blood,  652 

•Tenner's,  for  blood,  633 

Koch's,  for  malarial  plasmodia,  656 

Maunaberg's,  for  malarial  plasmodia,  655 

Neisser's,  for  diphtheria  bacilli,  686 

Pappenheim's,  for  tubercle  bacilli  in  spu- 
tum, 595 

Posner's,  for  urinary  sediment,  565 

Romonowski's,  for  malarial  Plasmodia,  656 

Ruge's,  for  malarial  plasmodia,  656 

Weigert's,  for  elastic  fibers  in  sputum,  589 

Willebrandt's,  for  blood-granules,  634 

Ziehl-Neelsen,  for  tubercle  bacilli  in  spu- 
tum, 594 
Staining  bacteria  in  blood,  652 

capacity  of  erythrocytes,  636 

dried  specimens  of  blood,  631 

of  malarial  blood,  655 

of  organic  sediment  of  urine,  564 

tubercle  bacillus,  solutions  for,  594 
Stanton's  sphygmomanometer,  144 
Staphylococci  in  sputum,  600 
Starch  digestion,  examination  of,  371 

in  feces,  utilization  of,  438 
Starvation,  empty   intestines   from,   inspec- 
tion of,  304 


Stases,  high-pressure,  321 
low  pressure,  321 

venous,  cutaneous  hemorrhage  from,  54 
Stauungsmagen,  356 
Stenosis,  aortic,  332 
murmur  of,  333 
pulsus  tardus  of,  334  ■ 
tardy  pulse  of,  334 
mitral,  324 

murmurs  of,  267,  328 
thrill  in,  301 

triple  rhythm  of  heart  tones,  258 
of  duodenum,  vomitusof,  361 
of  esophagus,  689 

diverticulum  from,  vomitusof,  361 
of  stomach,  lactic  acid  in,  376 
of  valves  of  heart,  murmur  of,  263,  264 
pulmonary,  340 
murmur  of,  340 
systolic  murmur  of,  267 
pyloric,  302 

examination  of  stomach  for,  414 
tricuspid,  337 

diastolic  murmurs  of,  267 
Stereognostic  sense,  768 
Stethoscope  218,  244 

Stick-pleximeter  method   for  metallic  reso- 
nance, 158 
Stockvis'  test  for  cholecyanin,  474 
Stolnikow- Roberts'  estimation  of  proteid  in 

urine,  506 
Stomach,   absorptive  activity  of,  vou  Mer- 
ing's  test-breakfast  for,  397 
atony  of,  356 

butyrometric  examination  of,  948 
capacity  of,  355 

carcinoma  of,  diagnosis  by  lavage,  370 
lactic  acid  in,  376 
vomitus  of,  3(i0 
contents,  amount  of  expressed  material,  370 
appearance  of,  370 
characteristics  of,  948 
chlorids  of,  386 
examination  of,  353 
gas  fermentation  in,  396 
hydrochloric-acid  deficit  in,  384 
lactic  acid  of,  386 
method  of  obtaining,  368 
proteid  digestion,  products  in,  395 
total  acidity  of,  Topfer's  estimation  of, 
384 
organic  acids  of,  386 
dilatation  of,  356 
vomitus  of,  358 
examination  of,  353 

butyrometric  method,  948 
for  pyloric  stenosis,  414 
for  raw  motility,  413 
instruments  for,  364 
Rontgen  rays  in,  367 
with  stomach  tube,  364 
without  stomach  tube,  354 
fasting,  contents  of,  368 
cranberry  test  for,  368 
currant  test  for,  368 
functions   of,  Ewald-Boas'    test-breakfast 
for,  370 
Sahli-Seiler's  butyrometric  test  for,  397 
determination    of    carbohydrates 

in,  412 
examples  for  diagnostic  use,  408 
improvements  in,  407 


INDEX. 


1001 


stomach,  functions  of,  Sahli  Seller's  buty- 
rometric  test  for,  objections  to, 
407 
preliminaries  of,  400 
preparation  of  flour  soup  in,  400 
results  of,  405,  408 
technic  of,  404 
value  of,  408,  411 
test  for,  without  stomach  tube,  357 
test-breakfast  for,  367 
hour-glass,  367 

motility  of,  examination  without  stomach 
tube,  36-2 
iodipin  in  testing,  363 
judgment,  370 
salol  in  testing,  362 
vomitus  of,  358 
motor  insufficiency  of,  lactic  acid  in,  376 
mucous  catarrh  of,  vomitus  of,  360 

meiubrane  of,  absorbing  power  of  potas- 

sic  iodid,  test  for,  361 
secretion  of,  examination  of,  395 
position  of,  354 
pump,  364 
raw  motility  of,  413 
shape  of,  354 
size  of,  354 

splashing  sounds  of,  356 
stagnant,  390 

stenosis  of,  lactic  acid  in,  376 
tube,    indications  and   contra-indications 
for,  366 
methods  of  examination  with,  364 
tumor  of,  palpation  of,  309 
ulcer  of,  vomitus  of,  360 
Strabismus,  paralytic,  828 
Straddling  of  aorta,  344 
Stratification   of  liquid    bowel  movements, 

423 
Strauss'  determination  of  lactic  acid,  375 
Strawberry  tongue,  683 
Strength,  sense  of  testing,  762 
Streptococci  in  feces,  443 

in  sputum,  600 
Strife,  63 

Stupidity,  740,  741 

Subclavian  artery,  auscultation  of,  282    • 
systolic  murmur  over,  283  ' 

Subcrepitant  rales.  233 
Subglottic  mirror,  698  ' 

Subphrenic  abscess,  empyema  and,  Litten's 

sign  in  differentiation,  78 
Succinic  acid  in  echinococcus  fluid,  724 

Hoppc-Seyler  test  for,  724 
Siiccussio  Hippocratis,  240,  286 
Sudamina,  62 

Sugar  in  urine,  x\lm«n-Nvlander's  test  for, 
485 
Bottger's  test  for,  modified,  485 
carbonization  test  for,  489 
Cipollina's  tests  for,  487 
colorimetric  estimation  of,  512 
copper  test  for,  482 

Drechsel-Klimmer's  estimation  of,  508 
evaporation  test  for,  489 
Fehling's  test  for,  484 
Fehling-Soxhlet's  estimation  of,  507 
fermentation  test  for,  488 
Lehmann's  estimation  of,  509 
Moore-Heller's  test  for,  481 
phenylhydrasiin  test  for,  487 
polariuietric  estimation  of,  515 


Sugar  in  urine,  qualitative  tests  for,  480 
quantitative  estimation  of,  506 
by  titration,  507 

from  specific  gravity  and  quantity 
of  iron,  506 
fermentation  tests  for,  513 
gas-volumetric  fermentation  test  for, 
514 
reduction  tests  for,  482 
significance  of,  485 
Eobert's  quantitative    areometric    test 

for,  513 
Rubner's  test  for,  488 
Soxhlet-Allihn's  estimation  of,  510 
tests  for,  480,  506 
Trommer's  test  for,  482 

Seegen's  modification,  484 
Suggested  pains,  771 
Sulphate,  calcium,  in  urine,  559 
Sulphuric  acid  in  urine,  estimation  of,  537 
Supersecretion  of  gastric  juice,  vomitus  of, 

358,  360 
Supplement,  955 

Suppurations,  leukocytosis  of,  649 
Suppurative  fever,  74 

gastritis,  vomitus  of,  360 
Supranuclear  facial  paralj^sis,  853 
Swallowing  murmur,  690 
Sweat,  bloody,  48 
blue,  48 
excretion,  47 
in  acute  polyneuritis,  797 
in  jaundice,  48 

secretion,    abnormalities  of,    in    nervous 
diseases,  796 
Sympatheic  ptosis,  833 

sensation,  774 
Syphilis,  hereditary,  eyeground  in,  704 
Syphilitic  sores  on  tongue,  683 
Syringes  for  exploratory  punctures,  707 
Syringomyelia,  boat-shaped  chest  of,  32 

bone  sensibility  in,  765 
Systole  and  diastole,  auscultation  in  difier- 
entiatiug,  248 
closure  time  of,  115 
expulsion  time  of,  115 
persisting  interval  of,  115 
Systolia  alternans,  296 

Systolic  auricular  vibration,  difi'use  feeble, 
300 
gallop  rhythm  of  Potain,  259 
murmurs  at  aortic  valve,  266 
of  mitral  insufliciency,  266 
of  pulmonary  stenosis,  267 
of  tricuspid  insufficiency,  267 
over    arterial    and   auriculoventricular 

orifices,  distinction,  268 
over  arteries,  282 

localized  arteriosclerosis  as  cause,  283 
over  exophthalmic  goiter,  283 
over  subclavian  artery,  283 
retraction  at  apex  of  heart,  295 
tone,  245 
valve  shock,  300 
venous  collapse,  147 
vesicular  bi-eathing,  222 

Tabes  dorsalis,  Argyll-Robertson's  phenom- 
enon in,  846 
m^'osis  in,  839 

paradoxic  pupillary  reaction  in,  847 
perforating  ulcer  in,  791 


1002 


INDEX. 


Tabetic  arthropathy,  794 

Tache  cerebrale,  796 

Tachogram,  276 

Tachycardia,  101 
fever  as  cause,  101 
nervous,  873 
paroxysmal,  103 
temperature  in  fevers  and,  relations,  102 

Tactile  fremitus,  testing  of,  288 
sensibility,  testing,  757 

Taenia  in  feces,  436 

mediocanellata  in  feces,  437 
solium  in  feces,  436 

Tanuin  in  urine,  detection  of,  503 

Tapeworms  in  feces,  435 

Tardy  pulse  of  aortic  stenosis,  334 

Teeth,  examination  of,  678 
first  dentition,  681 
Hutchinson's,  678,  680 
rachitic,  679 
second  dentition,  681 

Teichmanu's  hemin  test  for  blood  in  feces, 
447 
for  hemoglobinuria,  470 

Temperature  curve,  66 
determination  of,  63 
fever,  67 

higli,  significance  of,  67 
method  of  taking,  65 
normal,  66 
subnormal,  75 
tachycardia  in  fevers  and,  relations,  102 

Tendon  reflexes,  778,  730 

outline  for  examination  of,  952 

Tension  value  of  hair,  759 

Tertian  fever.  73 

Test,  acetic  acid  and  potassium  ferrocyanid, 
for  albuminuria,  463 
albumin,  460 

for  albumosuria,  466 
Allihn-Soxhlet's,    for   dextrose   in  urine, 

510 
Almen-Nylander's,  for  sugar  in  urine,  485 
Amann's,  for  indican  in  urine,  477 
Bial's,  for  pentoses  in  urine.  491 
Bottger's  modified,  for  sugar  in  urine,  485 
carbonization,  for  sugar  ia  urine,  489 
chemical,  for  blood  in  feces,  447 
Cipollina's.  for  sugar  in  urine,  487 
cold,  for  albuminuria,  462 
copper,  for  sugar  in  urine,  482 
cranberry,  for  fasting  stomach,  368 
currant,  for  fasting  stomach.  368 
Dare's,  for  alkalinity  of  blood.  615 
Darmstadter's,  for  beta-oxybutyric  acid  in 

urine,  540 
Deniges,  for  purin  bodies  in  urine,  533 
Drechsel-Klimmer's,  for  sugar  in  urine, 

508 
Ehrlich's  diazo,  in  typhoid  fever,  500 
Engel  and  Lowy's,  for  laked  blood.  614 
evaporation,  for  sugar  in  urine,  489 
Fehling's,  for  sugar  in  urine,  484 
Fehling-Soxhlet's,  for  sugar  in  urine,  507 
fermentation,  for  sugar  in  urine,  488 

quantitative,  for  dextrose  in  urine,  513 
Fischer-vonJaksch,    for   sugar    in    urine, 

487 
for  hydrochloric  acid,  372 
for  lactic  acid  in  gastric  juice,  371 
for  letters,  900 
for  words,  900 


Test,  Garrod's  thread,  for  uric  acid  in  blood, 

675 
Gerhardt's,  for  diacetic  acid  in  urine,  496 
Gmelin's,   for  biliary  pigments  in  urine, 
472 
Eoseubat-h's  modification,  472 
Gunning's  iodoform,  for  acetone  in  urine, 

494 
Hammarsten's,    of    biliary   pigments    in 

urine,  474 
heat,  for  albuminuria,  460 

for  hemoglobinuria,  470 
Heller"s  blood-,  for  hemoglobinuria,  470 

for  albuminuria,  462 
Hopkin's,  for  uric  acid,  531 

Folin   and    Shaffer's    modification, 
531 
Hopkin-Worner.  for  uric  acid,  531 
Hoppe-Seyler,  for  succinic  acid  in  echino- 

coccus  fluid,  724 
Hiifner-Knop's,  for  urea,  520 
iron,  for  blood,  with  Jolles"  ferrometer,  671 
Jaffe's,  for  kreatinin  in  urine,  534 

for  indican  in  urine,  476 
Kjeldahl's,  for  nitrogen  in  urine,  526 
Klimmer-Drechsel's,  for  sugar  in  urine,  508 
Knop-Hiifner's,  for  urea,  .520 
Kiilz's,  for  beta-oxvbutvric  acid  in  urine, 

497 
Landois-von  Jaksch,  for  opaque  blood,  613 
Legal's,  for  acetone  in  urine,  495 
Lehmann's,  for  sugar  in  urine,  509 
Lieben's  iodoform,  for  acetone  in  urine,  495 
Liebig's,  for  urea,  520 
Lowy  and  Engel's,  for  laked  blood.  614 
Ludwig-Salkowski's.  for  uric  acid,  530 
metaphosphoric  acid,  for  albuminuria,  463 
Moore-Heller's,  for  sugar  in  urine,  481 
murexid,  for  uric  acid,  556 
nitric  acid,  for  albuminuria,  462 
Xylauder-Almen's,  for  sugar  in  urine,  485 
Obermayer's,  for  indican  in  urine,  476 
orcin,  for  pentoses  in  urine,  491 
Pavy's.  for  sugar  in  urine,  508 
phenylhydrazin,  for  sugar  in  urine,  487 
picric  acid,  for  albuminuria,  463 
Piria's,  for  tyrosin  in  urine,  498 
Politzer's,  for  hearing-power,  865 
qualitative,   for   sugar  in  urine,  480.     See 

also  Sugar  in  urine. 
quantitative,  for  acids  in  gastric  juice,  377 

for  fats  in  feces,  446 

for  fatty  acids  in  feces,  4J6 

for  soaps  in  feces,  446 

gas-volumetric  fermentation,  for  sugar 
in  urine.  514 
reduction,  for  sugar  in  urine,  482 

significance  of,  485 
Einne's,  for  hearing-power.  865 
Eobert's  areometric,  for  sugar  in    urine, 

513 
Eubner's,  for  sugar  in  urine,  488 
Salkowski's.  for  albumoses,  466 

for  alkalinity  of  blood,  615 

for  biliary  pigments  in  urine,  473 

for  Brucke's  peptone,  466 

for  hematoporphyrin  in  urine,  472 

for  paralbumin  in  ovarian  cysts,  724 

for  pentoses  in  urine,  491 

for  ])eptonc,  Brucke's,  466 

for  purin  bodies  in  urine,  532 

for  urea  in  cvsts  of  urinarv  system,  724 


INDEX. 


1003 


Test,  Salkowski-Ludwig's,  for  uric  acid,  530 
Schlosing's,  for  ammonia  in  urine,  539 
Schonbein-Almen's,  for  blood  in  feces,  447 

turpentine-guaiac,   for  liemoglobinuria, 
471 
Schondorff 's,  for  urea,  526 
Schulte's,  for  albumosuria,  467 
Schwabach's,  for  hearing-power,  866 
Sherer's,  for  leuciu  in  urine,  499 
Soxhlet-AUihn's,  for  sugar  in  urine,  510 
Soxhlet-Fehling's,  for  sugar  in  urine,  507 
spectroscopic,  for  blood  in  feces,  447 
Stockvis',  for  cholecyanin,  474 
Teichmann's    hemin,  for  blood  in  feces, 
447 
for  hemoglobinuria,  470 
Tollen's,  for  glycuronic  acid  in  urine,  493 

for  pentoses  in  urine,  491 
Trommer's,  for  sugar  in  urine,  482 

Seegen's  modification,  484 
Trousseau's,  for  biliary  pigments  in  urine, 

473 
turpentine-guaiae,  for  blood  in  feces,  447 

for  hemoglobinuria,  471 
Vierordt's,  for  coagulation  time  of  blood, 

615 
Volhard's,  for  chlorids  in  urine,  535 
von  Jaksch-Fischer,  for  sugar  in   urine, 

487 
von   Jaksch-Landois,    for    opaque    blood, 

613 
Weber's,  for  hearing-power,  866 
Weyl's,  for  kreatinin  in  urine,  534 
Widal's,  in  typhoid  fever,  675 
Worner-Hopkin,  for  uric  acid,  531 
Test-breakfast,  filtrate  of,  examination  of, 

949 
for  functions  of  stomach,  367 
of    Ewald-Boas,   examination  of     gastric 

functions  by,  370 
of  Mering,    for     absorptive    activity    of 

stomach,  397 
Testicle  casts  in  urihe,  573 
Testing  absorbing  power  of  gastric  mucous 

membrane,  361 
appreciation   of    position   of   extremities, 

767 
bone  sensibility,  765 
cutaneous  sensibility  to  pain,  759 

irritation  hairs  for,  760 
digestion  with  potassic  iodid  fibrin,  364 
digestive  power  of  gastric  juice,  391 
electric  irritability,  798 
qualitative,  811 
quantitative,  808 
faradic  current,  810 
galvanic  current,  809 
functions  of  speech,  900 
mechanical  irritability  of,  797 
motility  of  stomach,  362 
movements  of  extremities,  767 
perception,  766 
power  sense,  762 
pressure  sensibility,  757 
sensation  of  innervation,  762 
sense  of  strength,  762 
sensibility,  methods  of, 756 
sensory  paralysis,  756 
tactile  sensibility,  757 
technic  of,  769 

thermal  sensibility  of  skin,  761 
touch-perception,  768 


Test-meal,  Eiegel's,  diagnostic   importance 

of,  396 
Tetanus,  expression  of,  24 

leukocytosis  of,  649 
Tetany,  746 

electric  irritability  in,  817 

reaction  in,  815 
Tete  carree,  37 

Thallin  in  urine,  detection  of,  503 
Thermal  sensibility  of  skin,  testing,  761 
Thermometer,  65 

Thoma-Zeiss   apparatus   for    counting   ery- 
throcytes, 624 
Thoracic  viscera,  disease  of,  asymmetry  of 

chest  from,  33 
Thorax,  30.     See  also  Chest. 

en  bateau,  32 
Thorn-apple  balls,  559 
Thrill,  heart,  301 

hydatid,  306 

in  mitral  stenosis,  301 
Thrombosis  of  central  retinal  vein,  blind- 
ness after,  706 

of  inferior  vena  cava,  302 

of  portal  vein,  303 
Thumb  movements  in  nervous  diseases,  912 
Thyroid  gland,  enlarged,  murmurs  over,  283 
Tibial  phenomenon,  751 
Tic  rotatoire,  874 
Tickling,  774 

Toe-movements  in  nervous  diseases,  914 
Tollen's  test  for  glycuronic  acid  in  urine, 
493 
for  pentoses  in  urine,  491 
Tone-deafness,  901 
Tongue,  aphthous  patches  on,  683 

black  hairy,  683 

coat  of,  683 

examination  of,  682 

psoriasis  of,  683 

strawberry,  683 

syphilitic  sores  on,  683 

Virchow's  atrophy  of,  683 
Tonic  convulsions,  744 

cramps,  744 

spasms,  744 
Tonometry,  134 
Tonsils,  hypertrophy  of,  687 
Topfer's  estimation  of  total  acidity  of  gas- 
tric contents,  384 
Topographic  percussion,  159 

of    air-containing    abdominal    viscera, 

196 
of  bladder,  196 
of  heart,  176 
of  kidneys,  195 
of  liver,  190 
of  lungs,  168 
of  spleen,  193 
of  uterus,  196 
Touch-perception,  testing,  768 
Toxic  leukocytosis,  649 

tremor,  749 
Trachea,  autoscopy  of,  698 

examination  of,  direct,  698 

orthoscopy  of,  698 
Tracheal  tone,  William's,  213,  214 

tug,  299 
Tracheoscopy,  697 

direct,  698 

inferior,  698 
Traction  diverticulum  of  esophagus,  690 


1004 


INDEX. 


Transitional  cells  in  blood,  641 
Transitory  glycosuria  in  nervous  diseases, 

797 
Traube's  space,  193 

theory  of  Cheyne-Stokes  respiration,  82 
Trauma,  cutaneous  hemorrhage  from,  53 
Traumatic  neuroses,  reaction  in,  816 
Trematodes  in  feces,  435 
Trembling,  748 
Tremor,  748,  749 
Trichina  spiralis  in  feces,  435 
Trichinosis,  eosinophilia  in,  650 
Trichomonas  vulgaris,  431 
Tricocephalus  dispar  in  feces,  434 
Tricuspid  insufficiency,  335 
systolic  murmur  of,  X;67 
stenosis,  337 

diastolic  murmur  of,  267 
tones,  246,  247 
Trigeminies,  functions  of,  849 
motor,  functions  of,  849 
outline  for  examination  of,  953 
sensory,  functions  of,  849 
Trimagnesium     phosphate,    crystalline,    in 

urine,  559 
Triple  phosphate  in  urine,  558 
rhythm  of  heart  tones,  258 
Trochee,  248 

Trochlear  nerve,  function  of,  826 
Trommer's  test  for  sugar  in  urine,  482 

Seegen's  modification,  484 
Tropgeolin  00  reaction  for  hydrochloric  acid, 

373 
Trophic  affections  of  skin,  59 

disturbances,  examination  for,  788 
of  bones,  793 
of  joints,  793 
of  muscles,  788 
of  skin,  791 
Trousseau's  spots,  796 

test  for  biliary  pigments  in  urine,  473 
True  albuminuria,  459 

Trypsin,    Arthus    and    Huber's  demonstra- 
tion of  action  of,  421 
Tubercle  bacilli  in  blood,  65 
in  feces,  44 
in  sputum,  592 

animal  experiments  for  demonstrat- 
ing, 596 
Czaplewsky's  method  of  decolorizing, 
595 
stain  for,  594 
Ehrlich's  stain  for,  594 
isolating,    from    other    acid-staining 

bacilli,  595 
Pappenheim's  stain  for,  595 
quantitative  estfmation  of,  594 
sedimentation  of,  595 
in  urine,  576 
choroidal,  in    acute  miliary  tuberculosis, 
epithelial,  in  urine,  571 
704 
Tubercular  omentum,  palpation  of,  310 
Tuberculosis,  acute  miliary,  sputum  in,  606 
chronic,  reaction  of  lung  borders  in,  176 
skiagraph  of  735 
typic  fever  of,  74 
leukocytosis  of,  650 

miliary,  acute,  choroidal  tubercle  in,  704 
physical  examination  in,  353 
pulmonary,  cutaneous  hemorrhage  in,  53 
dulness  from,  208 


Tuberculosis,    pulmonary,    Ehrlich's    diazo- 
reaction  in,  500 
physical  signs  in,  .351 
pigmentation  of  skin  in,  45 
sputum  in,  606 
Tumors,  abdominal,  deep-lying,  dipping  in, 
305 
fecal,  308 

intestinal,  in  ileus,  302 
melanotic,  color  of  urine  in,  454 
of  abdomen,  palpation  of,  306 
of  bladder,  palpation  of,  310 
of  intestine,  in  ileus,  302 

palpation  of,  309 
of  kidney,  hydronephrosis  as  cause,  310 

palpation  of,  310 
of  liver,  palpation  of,  310 
of  lungs,  dulness  from,  208 
green  sputum  in,  581 
vesicular  breathing  in,  225 
of  mediastinum,  dulness  from,  208 
of  mesenteric  glands,  palpation  of,  310 
of  pelvis,  palpation  of,  310 
of  pleura,  dulness  from,  208 
of  retroperitoneal  glands,  palpation  of,  310 
of  spleen,  palpation  of,  310 
of  stomach,  palpation  of,  309 
ovarian,  inspection  of.  303 
pulmonary,  dulness  from,  208 
green  sputum  in,  .581 
vesicular  breathing  in,  225 
tuberculous,  of  peritoneum,  palpation  of, 
310 
Turbidity  of  urine,  553 
Turgidity  of  skin,  48 

Turpentine-guaiac  test  for  blood  in  feces, 
447 
for  hemoglobinuria,  471 
Twin  beat  of  heart,  296 
Tvcitching,  fascicular,  748 

fibrillary,  748,  790 
Tympanites,  302 
Typhoid  bacilli  in  blood,  653 
in  feces,  442 
in  sputum,  602 
fever,  amphibolic  stage,  72 
defervescing  stage.  72 
Ehrlich's  diazo-reaction  in,  500 
enlargement  of  spleen  in,  312 
fastigium  of,  71 
feces  of,  443 
fever  curve  of.  71 
initial  stage,  71 
leukocytosis  of,  646 
leukopenia  of,  646 
Widal's  reaction  in,  675 
Tyrosin  in  urine,  561 
detection  of,  497 
Piria's  test  for,  498 

Uffelmann's  reagent,  374 
Ulcer  of  stomach,  vomitus  of,  360 

perforating,  in  tabes,  791 
Ulcerative  endocarditis,  chills  in,  74 

cutaneous  hemorrhage  in,  53 
Ulnar  paralysis,  claw-hand  in,  747 
Uncinaria  Americana,  434 

eosinophilia  in,  650 
Upper  extremity,  movements  of,  in  nervous 

diseases,  910 
Uranium     nitrate    solution    for    estimating 

phosphates  in  urine,  5.37 


INDEX. 


1005 


Urates  iu  urine,  655 
Urea  content  in  hydronephroses,  724 
in  cysts   of  urinary  system,  Salkowski's 

test  for,  724 
in  urine,  Doremus  apparatus  for  estimat- 
ing, 524 
Hinds'  modification,  524 
Dupre's  apparatus  for  estimating,  523 
Gerrard's  apparatus  for  estimating,  522 
Hiifner's  apparatus  for  estimating,  520 
Kuop-Hiifner's  estimation  of,  520 
Liebig's  estimation  of,  520 
quantitative  estimation  of,  518 
Schondorfif's  estimation  of,  526 
Squibb's  apparatus  for  estimating,  524 
Uremia,  vomitus  of,  361 
Uremic  dyspnea  of  nephritis,  91 
Ureometer,  Doremus,  524 

Hinds'  modification  of,  524 
Ureter,  calculus  in,  skiagraph  of,  731 
Uric  acid,  Hopkin's  estimation  of,  531 

Folin  and  Shaffer's  modification,  531 
Hopkin-Worner  estimation  of,  531 
in  blood,  674 

Garrod's  test  for,  675 
in  urine,  556 

Ludwig-Salkowski's  estimation  of,  530 
murexid  test  for,  556 
quantitative  estimation  of,  529 
Urina  spastica,  450 

in  nervous  diseaso-s,  797 
Urinary  examination,  449 
pigment,  normal,  453 

pathologic,  coloring  of  urine  by,  453 
system,  cysts  of,  urea  in,  Salkowski's  test 
for,  724 
epithelium  of,  in  urine,  565 
Urination,  frequency  of,  451 
Urine,  acetone  in,  detection  of,  493 
Gunning's  iodoform  test  for,  494 
Legal's  test  for,  495 
Lieben's  iodoform  test  for,  495 
quantitative  estimation  of,  540 
acidic  points  of,  541 
acidimetric  titration  of,  965 
acidity  of,  541 

albumin  in,  458.     See  also  Albuminuria. 
albumoses  in,  465.     See  also  Albumosuria. 
alkalinity  of,  .541 
alkapton  coloring,  454 

detection  of,  497 
allo.xuric  bodies  in,  542 
aloes  in,  detection  of,  503 
ammonia  in',  estimation  of,  538 

Schlosing's  test  for,  539 
ammoniomagnesium  phosphate  in,  .558 
ammonium  urate  in,  558 
araorplious  earthy  phosphates  in,  557 
amount  of,  449 
animal  ])arasites  iu,  578 
antifebrin  in,  detection  of,  .503 
antipyrin  in,  detection  of,  502 
arbutin  coloring,  454 
aromatic  products  coloring,  4.54 
bacillus  of  tuberculosis  in,  576 
bacteria  in,  574 
balsam  of  copaiba  in,  503 
basic  points  of,  541 

beta-oxybutyric    acid    in,    Darmstadter's 
estimation  of,  540 
detection  of,  497 
Kiilz's  test  for,  497 


Urine,  beta-oxybutyric  acid  in,  quantitative 

estimation  of,  539 
bile  acids  in,  474 

Pettenkofer's  test  for,  475 
biliary  pigments  in,  472.     See  also  Biliary 

pigments  in  urine. 
bilirubin  in,  561 
blood  iu,  569 
blood-coloring   matter  in,   469.     See  also 

Hemoglobin  uria. 
bromin  in,  detection  of,  502 
calcium  oxalate  in,  556 

sulphate  in,  559 
calculi  in,  563 
carbolic-acid  coloring,  454 
carbonates  in,  5.57 
cascara  coloring,  455 

sagrada  in,  detection  of,  503 
casts  in,  570 

iu  nephritis,  570 
centrifugation  of,  553 

chemical  examination  of,  qualitative,  458 
chloridsiii,  quantitative  estimation  of,  534 

Volhard's  estimation  of,  535 
cholesterin  in,  561 
chrysarobin  coloring,  455 
chrysophanic  acid  in,  detection  of,  503 
coal-tar  products  coloring,  454 
color  of,  453 
concentrated,  452- 
cryoscopy   of,   545.     See  also  Cryoscopy  of 

urine. 
crystalline  trimagnesium    phosphate  in, 

559 
cylindroids  in,  572 
cystin  in,  560 
deutero-albumoses  in,  Salkowski's  test  for, 

466 
dextrose  in,  tests  for,  480.     See  also  Sugar 

in  urine. 
diacetic  acid  in,  detection  of,  495 

Gerhardfs  test  for,  496 
dicalcium  phosphate  in,  559 
dried  residue  of,  total,  541 
drugs  in,  501 

embryos  of  filaria  sanguinis  in,  578 
emodin  in,  detection  of,  503 
epithelial  tubules  in,  571 
epithelium  in,  565 
examination  of,  449 

for  drugs,  501 

for  pathologic  constituents,  458 

for  poisons,  501 

for  substances  introduced  from  without, 
501 
fat  iu,  561 

fibrin  in,  detection  of,  465 
fibrinogen  in,  detection  of,  464 
filti-ation  of,  5.53 
fragments  of  echinococcus  cysts  in,  578 

of  new  growths  in,  .573 
freezing-point  of,  545.     See  also  Cryoscopy 

of  urine. 
globulin  in,  detection  of,  464 
glucose   in,   tests  for,  480.     See  also  Sugar 

in  urine. 
glycurouic  acid  in,  detection  of,  492 

Tollen"s  test  for,  493 
gonorrheal  threads  in,  .573 
grape  sugar   in,   tests   for,  480,     See  also 

Sugar  in  urine. 
gypsum  in,  .5.59 


1006 


INDEX. 


Urine,  hematoidin  crystals  in,  561 
hematoporphyrin  in,  453 

detection  of,  471 

Salkowski's  test  for,  472 
hemoglobin  in,   469,  561.     See  also  Hemo- 

globimiria. 
homogentisic  acid  in,  detection  of,  497 
hydrochinon  acetate  in,  detection  of,  497 
hydroquinone  coloring,  454 
in  nervous  diseases,  797 
indican  in,  454 

tests  for,  475 
Amann's,  477 
Jaflfe's,  476 
Obermayer's,  476 
indigo  in,  454,  561 

detection  of,  475 
iodiu  in,  detection  of,  501 
isomaltose  in,  490 
kreatinin  in,  534 

Jaffe's  reaction  for,  534 

Weyl's  reaction  for,  534 
lactose  in,  490 
lead  in,  detection  of,  501 
leucin  in,  561 

detection  of,  497 

Sherer's  test  for,  499 
levnlose  in,  490 
lipuric  acid  in,  562 
maltose  in,  490 
medicinal  pigments  in,  454 
melanin  in,  561 

detection  of,  477 
melanogen  in,  detection  of,  477 
mercury  in,  detection  of,  501 
micro-organisms  in,  574 
molecular  concentration  of,  545 
mucous  casts  in,  572 

sediments  in,  468,  562 
naphthalene  coloring,  454 
nitrogen  in,  Kjeldahl's  estimation  of,  526 
nubecula  of,  452,  468 
nucleo-albumin  in,  detection  of,  468 
of  two  kidneys,  separation  of,  457 
osmotic  pressure  of,  545 
paraglobulin  in,  detection  of,  464 
pentoses  in,  Bial's  test  for,  491 

detection  of,  490 

orcin  test  for,  491 

Salkowski's  test  for,  491 

Tollen's  test  for,  491 
phenacetin  in,  detection  of,  503 
phenol  in,  detection  of,  502 
phosphates  in,  earthy,  separate  estimation 
of,  537 

quantitative  estimation  of,  536 

total,  estimation  of,  537 

uranium  nitrate  solution  for,  537 
phymatorrhusin  in,  detection  of,  477 
pigment  of  beets  in,  455 

of  huckleberries  in,  455 

of  madder  in,  455 
poisons  in,  501 
preputial  epithelia  in,  566 
proteids  in,  460 

quantitative  estimation  of,  505 

removal  of,  463 
purin  bodies  in,  Denige's  estimation  of,  533 
estimation  of,  532 
Salkowski's  estimation  of,  532 
pus  in,  471 

cells  in,  566 


Urine,  pus  in,  Posner's  estimation  of,  568 
pyramidon  in,  detection  of,  503 
pyrocatechin  coloring,  454 
quantitative  analysis  of,  504 
reaction  of,  455 
red  indol  in,  detection  of,  477 
residue  of,  total  dried,  541 
resorcin  coloring,  454 
rhamnus  in,  detection  of,  503 
rhubarb  in,  detection  of,  503 
Eosenbach's  reaction  for,  477 
salicylic  acid  in.  detection  of,  502 
salol  coloring,  454 
sandalwood  oil  in,  detection  of,  503 
santonin  coloring,  455 

detection  of,  503 
sedimentation  of,  553 
sediments  of,  553 

Cohn's  stain  for,  564 

examination,  553 

inorganic,  analytic  scheme  for,  563 

mucous,  562 

non-organic,  555 

organic,  564 

Posen's  stain  for,  565 
senna  coloring,  455 

detection  of,  503 
serum  in,  detection  of,  464 
serum-albumin  in,  detection  of,  460 
skatol  pigments  in,  detection  of,  477 
smegma  bacillus  in,  ,576 
specific  gravity  of,  451 

estimation  of  amount  of  urea  by,  519 
spermatozoa  in,  573 
substances  resembling  mucin  in,  468 
sugar  in,  480.     See  Sugar  in  urine. 
sulphuric  acid  in,  combined,   estimation 

of,  537 
tannin  in,  detection  of,  503 
testicle  casts  in,  573 
thalliu  in,  detection  of,  503 
transparency  of,  452 
triple  phosphate  in,  558 
tubercle  bacilli  in,  576 
turbidity  of,  553 
tyrosin  in,  561 

detection  of,  497 

Piria's  test  for,  498 
urates  in,  555 

urea  in,  Doremus  apparatus  for  estimating, 
524 
Hinds'  modification,  524 

Dupre's  apparatus  for  estimating,  523 

Gerrard's  apparatus  for  estimating,  522 

Hiifner's  apparatus  for  estimr.ting,  520 

Knop-Hiifner's  estimation  of,  520 

Liebig's  estimation  of,  520 

quantitative  estimation  of,  518 
by  specific  gravity,  519 

Sch6ndorfl"'s  estimation  of,  .526 

Squibb's  apparatus  for  estimating,  524 
uric  acid  in,  556 
urobilin  in,  478 

color  of,  454 
vaginal  epithelia  in,  566 
xanthin  in,  561 
Urobilin  icterus,  44 
in  feces,  445 
in  urine,  478 

color  of,  454 
Urochrome,  quantitative  analysis  of,  504 
Uroervthrin.  478 


INDEX. 


1007 


XJrorosein,  478 

Urrhodin,  47S 

Urticaria,  edema  in,  52 

Uterus,  topographic  percussion  of,  196 

Vagabonds'  disease,  45 
Vaginal  epithelia  in  urine,  566 
Vagus,  functions  of,  869 

group,  three  nerves  of,  functions,  869 

symptomatology  of  lesions  of,  871 
laryngeal  branches,  869 
motor  fibers  of,  869 
outline  for  examination  of,  954 
peripheral,  functions  of,  869 
sensory  branches  of,  869 
Valerianic  acid  in  gastric  juice,  377 
Valsalva's    experiment    for    distinguishing 
pericardial    rubs   from   endocardial   mur- 
murs, 280 
Valves,  aortic,  systolic  murmurs  at,  266 
tones  of,  248 
mitral,  tone  of,  246,  247,  248 
of  heart,  insufiiciency  of,  valvular  mur- 
murs from,  263 
stenosis  of,  murmur  of,  263,  264 
pulmonary,  tones  of,  248 
shock,  systolic,  300 
tricuspid,  tone  of,  246,  247 
Valvular  lesions.     See  Heart,  valvular  lesions 

of. 
Varicella,  leukocytosis  in,  648 
Vascular  trunks,  compression  of,  influence 

on  pulse  curve,  121 
Vasomotor  disturbances,  795 

paralysis,  cyanosis  from,  42 
Vegetable  parasites  in  sputum,  592 
Veins,  auscultation  of,  284 

dilated,  in  abdominal  wall,  302 

murmurs  over,  284 

])ortal,  thrombosis  of,  303 

respiratory  phenomena  of  motion  in,  145 

retinal,  central,  thrombosis  of,  blindness 

after.  706 
tones  over,  284 
Vena  cava,  inferior,  thrombosis  of,  302 
Venous  collapse,  diastolic,  152 
systolic,  147 
flow  from  extremity,  influence  on  pulse 

curve,  121 
hum,  284 

in  exophthalmic  goiter,  286 
pulse,  arterial  pulse  and,  differentiation, 
147 
combined,  152 
difficulties  in  distinguishing  kinds  of, 

152 
negative,  147 
centrifugal,  147 
presystolic,  147 
of  liver,  151 
penetrating,  152 
physiologic,  147 
positive  centrifugal,  150 

centripetal,  152 
regurgitating.  150 
varieties  of,  147 

Volhard's    procedure    for    determining 
phases  of,  152 
stasis,  cutaneous  hemorrhage  from,  54 
undulation,  147 
Ventricular  septum,  343 
Vertigo,  880 


Vertigo,  auditory,  867 
clinical  significance  of,  881 
galvanic,  883 
gastric,  883 
mountain,  883 
ocular,  829 
pathogenesis  of,  881 
rotary,  881 
Vesical  calculus,  skiagraph  of,  734 
Vesicular  breathing,  220 
absence  of,  224 
alterations  of,  223 
cog-wheel,  226 

graphic  expression  for,  348 
diminution  of,  224 
graphic  expressions  for,  348 
impure,  225 
increased,  223 
rough, 225 
sharp,  223 
systolic,  222 
weakened,  224 

with  prolonged  expiration,  225 
inspiration    with     bronchial    expiration, 

graphic  expression  for,  348 
respii'atory  murmur,  220 
Vessels,  auscultation  of,  2S2 
Vibrating  apex  beat  of  Miiller,  292 
Vicarious  emphysema,  175 
Vierordt's     determination    of    coagulation 

time  of  blood,  615 
Virchow's  atrophy  of  tongue,  683 
Viscera,  abdominal,  air-containing,  percus- 
sion of,  196 
disease   of,   asymmetry   of  chest  from, 
33 
thoracic,   disease  of,  asymmetry  of  chest 
from,  33 
Viscosity  of  blood,  669 
Vision,  central,  acuteness  of,  822 
double,  crossed,  828 
monocular,  830 
non-crossed,  829 
Visual  color  fields,  823 
field,  defects  in,  823 

testing  of,  822 
fremitus,  testing  of,  288 
Voice,  character  of,  pathologic,  94 
hoarse,  94 
in  cholera,  95 
lack  of,  94 

sounds,  auscultation  of,  over  chest,  241 
Volatile   fatty  acids,   detection    in    gastric 

juice,  377 
Volhard's  determination  of  chlorids  in  urine, 
535 
of  phases  of  venous  pulse,  152 
Volume  quotient  of  erythrocytes,  641 
Vomiting,  357 

Vomitus,  admixture  of  bile  in,  360,  361 
of  blood  in,  .360 
chemical  examination  of,  361 
color  of,  361 
examination  of,  357 
fecal,  361 

intestinal  worms  in,  361 
microscopic  examination  of,  359 
odor  of,  36l 

of  carcinoma  of  stomach,  360 
of  cerebral  meningitis,  361 
of  cholera  Asiatica,  361 
of  cholera  nostras,  361 


1008 


INDEX. 


Vomitus  of  diverticulum  from  stenosis  of 
esophagus,  361 
of  gastric  dilatation,  358 

motility,  358 
of  gastrorrhcea  acida,  358 
of  hydrochloric-acid  decrease,  360 
of  hyperacidity  of  gastric  juice,  358 
of  hypersecretion  of  gastric  juice,  358 
of  intestinal  obstruction,  361 
of  mucous  catarrh  of  stomach,  360 
of  phlegmonous  gastritis,  360 
of  stenosis  of  duodenum,  361 
of  supersecretion  of  gastric  juice,  358,360 
of  suppurative  gastritis,  360 
of  ulcer  of  stomach,  360 
of  uremia,  361 
pus  in,  360 
slimy  masses  in,  360 
von   Aldor's    modification   of    Salkowski's 
test  for  albumoses,  467 
for  Brucke's  peptone,  467 
for  deutero-albnmoses,  467 
von  Basch's  sphygmomanometer,  134 
von  Frey's  irritation  hairs,  758 

testing  sense  of  pain  by,  760 
sphygmograph,  109 
von  Jaksch-Fischer  test  for  sugar  in  urine, 

487 
von  Jaksch-Landois    .^^^hod  for   titration 

of  opaque  blood,  6x3 
von  Mering's  experiments  on  potassic  iodid, 
362 
reflex,  413 

test-breakfast  for  absorptive  activity  of 
stomach,  397 

Water,  injections  of,  into  rectum,  417 
"Water-whistle  noise  in  pneumothorax,  241 
Wave,  fluctuation,  in  diagnosis  of  free  fluid 

in  abdomen,  302,  305 
Weakness  of  converging  movements  of  eyes, 

836 
Weber's  test  for  hearing-power,  866 


Weigert's  modification  of  Gram's  staining 
of  bacteria  in  sputum,  597 

stain  for  elastic  fibers  in  sputum,  589 
Weight,  body,  28 

of  infants,  28 
Weil's  acoustic  sphere  of  action,  162 

explanation  of  deep  dulness,  163 
Westphal's  pupillary  phenomenon,  847 
Weyl's  reaction  for  kreatinin  in  urine,  534 
Whispering,  bronchial,  241 
White  corpuscles.     See  Leukocytes. 
Whoop  of  pertussis,  97 
Widal's  reaction  in  typhoid  fever,  675 
Wild's  polaristrobometer,  516,  517 
Willetarandt's  stain  for  blood-granules,  634 
William's  tracheal  tone,  213,  214 
Wintrich's  phenomenon,  213 

tone  change,  213,  214 
Woillez's  cyrtometer,  35 
Wolf's  stain  for  Frankel's  pneumococci  in 

sputum,  598 
Wool-sorters'  disease,  sputum  in,  602 
Word-deafness,  892 
Words,  test  for,  900 
Worms,  intestinal,  in  vomitus,  361 

parasitic,  in  blood,  659 

round,  in  feces,  432 
Worner-Hopkin    estimation    of    uric    acid, 

531 
Wrist  movements  in  nervous  diseases,  911 
Wrist-drop,  741 

Xanthtn  in  urine,  561 

Zeiss-Thoma  apparatus  for  counting  ery- 
throcytes, 624 

Ziehl-Neelsen  stain  for  tubercle  bacilli  in 
sputum,  594 

ZoUikofer's  brown  granules,  634 

determination  of  leukocytes  in  counting- 
chamber,  644 

Zones,  hyperalgesic,  of  skin,  in  diseases  of 
deeper  organs,  774 


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octavo,  899  pages,  with  746  illustrations,  39  of  them  in  colors.  Cloth, 
;^5.oo  net;  Sheep  or  Half  Morocco,  ;^6.oo  net. 

RECENTLY   ISSUED 

Immediately  on  its  publication  this  work  took  its  place  as  the  leading  text-book 
on  the  subject.  Both  in  this  country  and  in  England  it  is  recognized  as  the  most 
satisfactorily  written  and  clearly  illustrated  work  on  obstetrics  in  the  language. 
The  illustrations  form  one  of  the  features  of  the  book.  They  are  numerous  and 
the  most  of  them  are  original.  In  this  edition  the  book  has  been  thoroughly  revised. 
More  attention  has  been  given  to  the  diseases  of  the  genital  organs  associated  with 
or  following  childbirth.  Many  of  the  old  illustrations  have  been  replaced  by  better 
ones,  and  there  have  been  added  a  number  entirely  new.  The  work  treats  the 
subject  from  a  clinical  standpoint. 


OPINIONS  OF  THE  MEDICAL  PRESS 


British  Medical  Journal 

"The  popularity  of  American  text-books  in  this  country  is  one  of  the  features  of  recent 
years.  The  popularity  is  probably  chiefly  due  to  the  great  superiority  of  their  illustrations 
over  those  of  the  English  text-books.  The  illustrations  in  Dr.  Hirst's  volume  are  far  more 
numeroixs  and  far  better  executed,  and  therefore  more  instructive,  than  those  commonly 
found  in  the  works  of  writers  on  obstetrics  in  our  own  country." 

Bulletin  of  Johns  Hopkins  Hospital 

"The  work  is  an  admirable  one  in  every  sense  of  the  word,  concisely  but  comprehensively 
written." 

The  Medical  Record,  New  York 

"The  illustrations  are  numerous  and  are  works  of  art,  many  of  them  appearing  for  the  first 
time.  The  author's  style,  though  condensed,  is  singularly  clear,  so  that  it  is  never  necessary 
to  re-read  a  sentence  in  order  to  grasp  the  meaning.  As  a  true  model  of  what  a  modern  text- 
book on  obstetrics  should  be,  we  feel  justified  in  affirming  that  Dr.  Hirst's  book  is  without  a 
rival." 


OBSTETRICS. 


Webster's 
Text-Book  of   Gynecology 

With  Beautiful  Illustrations 

A  Text=Book  of  Gynecology.  By  J.  Clarence  Webster,  M.  D. 
(Edix.),  F.  R.  C.  p.  E.,  Professor  of  Gynecology  and  Obstetrics  in  Rush 
Medical  College,  in  Affiliation  with  the  University  of  Chicago  ;  Obstetri- 
cian and  Gynecologist  to  the  Presbyterian  Hospital,  Chicago.  Large 
octavo  volume  of  8oo  pages,  with  350  magnificent  illustrations,  nearly 
all  original. 

READY  VERY  SOON— FOR  THE  PRACTITIONER 

This  entirely  new  work  on  diseases  of  women  is  based  on  Dr.  Webster's 
extended  clinical  experience,  and  unusual  prominence  is  given  to  the  scienti- 
fic basis  of  each  subject  under  consideration.  Special  endeavor  has  been  made 
to  include  all  the  important  original  investigations  of  recent  years,  so  that  the  work 
represents  the  present-day  knowledge  upon  a  subject  of  the  greatest  importance  to 
every  practitioner.  Indeed,  Dr.  Webster  has  written  this  work  especially  for  the 
general  practitioner,  discussing  the  clinical  features  of  the  subject  in  their  widest 
relations  to  general  practice  rather  than  from  the  standpoint  of  specialism.  The 
magnificent  illustrations,  some  three  hundred  and  fifty  in  number,  are  nearly  all  orig- 
inal. Drawn  by  expert  anatomic  artists  under  Dr.Webster's  direct  supervision,  they 
portray  the  anatomy  of  the  parts  and  the  steps  in  the  operations  with  rare  clearness 
and  exactness.  These  illustrations,  selected  because  of  their  practical  and  techni- 
cal value,  form  a  rich   collection,  supplementing  a  text  of  unusual  conciseness. 


SAUNDERS'   BOOKS  ON 


Webster's 
Text-Book  of  Obstetric*/* 


A  Text=Book  of  Obstetrics.  ByJ.  Clarence  Webster,  M.D.(Edin.), 
F.  R.  C.  P.  E.,  Professor  of  Obstetrics  and  Gynecology  in  Rush  Medical 
College,  in  Affiliation  with  the  University  of  Chicago  ;  Obstetrician  and 
Gynecologist  to  the  Presbyterian  Hospital,  Chicago.  Handsome  octavo 
volume  of  jdj  pages,  beautifully  illustrated,  including  many  in  colors. 
Cloth,  ^5.00  net;   Sheep  or  Half  Morocco,  ^6.00  net. 

RECENTLY   ISSUED— BEAUTIFULLY   ILLUSTRATED 

This  entirely  new  work  is  written  for  the  student  of  obstetrics  as  well  as  for 
the  active  practitioner.  The  anatomic  changes  accompanying  pregnancy,  labor, 
and  the  puerperium  are  described  more  fully  and  lucidly  than  in  any  other  text- 
book on  the  subject.  The  exposition  of  these  sections  is  based  mainly  upon 
studies  of  frozen  specimens,  in  which  department  the  author  has  had  a  larger 
experience  than  any  other  worker.  Unusual  consideration  is  given  to  embryo- 
logic  and  physiologic  data  of  importance  in  their  relation  to  obstetrics.  Great 
care  was  taken  in  the  selection  of  the  illustrations,  aiming  to  meet  the  varied  re- 
quirements of  both  the  undergraduate  and  the  practising  physician.  The  book 
expresses  the  most  advanced  thought  of  the  day. 


OPINIONS  OF  THE   MEDICAL   PRESS 


Medii.cal  Record,  New  York 

"  The  author's  remarks  on  asepsis  and  antisepsis  are  admirable,  the  chapter  on  eclampsia 
is  full  of  good  material,  and  .   .   .  the  book  can  be  cordially  recommended  as  a  safe  guide." 

Buffalo  Medical  Journal 

"  As  a  practical  text-book  on  obstetrics  for  both  student  and  practitioner,  there  is  ieft  very- 
little  to  be  desired,  it  being  as  near  perfection  as  any  compact  work  that  has  been  published.'' 

Dublin  Journal  of  Medical  Science 

"  Both  to  the  student  .  .   .  and  to  the  practitioner  who  requires  the  latest  opinion  on  any 
point  of  practice,  Dr.  Webster's  book  will  be  of  the  greatest  value." 


GYNECOLOGY  AND    OBSTETRICS. 


The  American 
Text-Book  of  Obstetric*^ 

Second  Edition,  Thoroughly  Revised  and  Enlarged 


The  American  Text=Book  of  Obstetrics.  In  two  volumes.  Edited 
by  Richard  C.  Norris,  M.D.,  Assistant  Professor  of  Obstetrics  in  the 
University  of  Pennsylvania;  Art  Editor,  Robert  L.  Dickinson,  M.D., 
Assistant  Obstetrician,  Long  Island  College  Hospital,  N.  Y.  Two 
handsome  octavo  volumes  of  about  600  pages  each;  nearly  900  illus- 
trations, including  49  colored  and  half-tone  plates.  Per  volume : 
Cloth,  ^3.50  net ;  Sheep  or  Half  Morocco,  ;^4.oo  net. 

RECENTLY    ISSUED— IN   TWO  VOLUMES 

Since  the  appearance  of  the  first  edition  of  this  work  many  important  advances 
have  been  made  in  the  science  and  art  of  obstetrics.  The  results  of  bacteriologic 
and  of  chemicobiologic  research  as  appHed  to  the  pathology  of  midwifery  ;  the  wider 
range  of  the  surgery  of  pregnancy,  labor,  and  of  the  puerperal  period,  embrace 
new  problems  in  obstetrics.  In  this  new  edition,  therefore,  a  thorough  and  critical 
revision  was  required,  some  of  the  chapters  being  entirely  rewritten,  and  others 
brought  up  to  date  by  careful  scrutiny.  A  number  of  new  illustrations  have  been 
added,  and  some  that  appeared  in  the  first  edition  have  been  replaced  by  others 
of  greater  excellence.  By  reason  of  these  extensive  additions  the  new  edition 
has  been  presented  in  two  volumes,  in  order  to  facilitate  ease  in  handhng.  The 
price,  however,  remains  unchanged. 


PERSONAL  AND   PRESS  OPINIONS 


Alex.  J.  C.  Skene,  M.  D.. 

Late  Professor  of  Gynecology,  Long  Island  College  Hospital,  Brooklyn. 
"  Permit  me  to  say  that  '  The  American  Text-Book  of  Obstetrics  '  is  the  most  magnificent 
medical  work  that  I  have  ever  seen.     I  congratulate  you  and  thank  you  for  this  superb  work 
which  alone  is  sufficient  to  place  you  first  in  the  ranks  of  medical  publishers." 

Matthew  D.  Mann,  M.  D., 

Professor  of  Obstetrics  and  Gynecology  in  the  University  of  Buffalo. 

"  I   like   it  exceedingly  and  have  recommended  the  first  volume  as  a  text-book  for  oui 
sophomore  class.     It  is  certainly  a  most  excellent  work.     I  know  of  none  better." 

Americein  Journal  of  the  Medical  Sciences 

"  As  an  authority,  as  a  book  of  reference,  as   a  '  working  book  '   for  the  student  or  practi- 
tioner, we  commend  it  because  we  believe  there  is  no  better." 


SAUNDERS'    BOOKS    ON 


Penrose's 
Diseases  of  Women 

Fifth  Reviscv^  Edition 


A  Text=Book  of  Diseases  of  Women.  By  Charles  B.  Penrose, 
M.  D.,  Ph.  D.,  formerly  Professor  of  Gynecology  in  the  University  of 
Pennsylvania ;  Surgeon  to  the  Gynecean  Hospital,  Philadelphia.  Oc- 
tavo volume  of  550  pages,  with   225  fine  original  illustrations.     Cloth, 

^3.75   net. 

RECENTLY   ISSUED 

Regularly  every  year  a  new  edition  of  this  excellent  text -book  is  called  for, 
and  it  appears  to  be  in  as  great  favor  with  physicians  as  with  students.  Indeed, 
this  book  has  taken  its  place  as  the  ideal  work  for  the  general  practitioner.  The 
author  presents  the  best  teaching  of  modern  gynecology,  untrammeled  by  anti- 
quated ideas  and  methods.  In  every  case  the  most  modern  and  progressive 
technique  is  adopted,  and  the  main  points  are  made  clear  by  excellent  illustra- 
tions. The  new  edition  has  been  carefully  revised,  much  new  matter  has  been 
added,  and  a  number  of  new  original  illustrations  have  been  introduced.  In  its 
revised  form  this  volume  continues  to  be  an  admirable  exposition  of  the  present 
status  of  gynecologic  practice. 


PERSONAL  AND  PRESS  OPINIONS 


Howard  A.  Kelly.  M.  D.. 

Professor  of  Gynecology  and  Obstetrics,  fohns  Hopkins  University,  Baltimore. 
"  I  shall  value  very  highly  the  copy  of  Penrose's  '  Diseases  of  Women '  received.     I  have 
already  recommended  it  to  my  class  as  THE  BEST  book." 

E.  E.  Montgomery,  M.  D., 

Professor  of  Gynecology,  fefferson  Medical  College,  Philadelphia. 
"  The  copy  of '  A  Text-Book  of  Diseases  of  Women  '  by  Penrose,  received  to-day.     I  have 
looked  over  it  and  admire  it  very  much.     I  have  no  doubt  it  will  have  a  large  sale,  as  it  justly 
merits." 

Bristol  Medico-Chinirgical  Journal 

"  This  is  an  excellent  vvork  which  goes  straight  to  the  mark.  .  .  .  The  book  may  be  taken 
as  a  trustworthy  exposition  of  modern  gynecology." 


GYNECOLOGY  AND    OBSTETRICS. 


Garrigues* 
Diseases  of  Women 

Third  Edition,  Thoroughly  Revised 


A  Text=Book  of  Diseases  of  Women.  By  Henry  J.  Garrigues, 
A.  M.,  M.  D.,  Gynecologist  to  St.  Mark's  Hospital  and  to  the  German 
Dispensary,  New  York  City.  Handsome  octavo,  756  pages,  with  367 
engravings  and  colored  plates.  Cloth,  ^^4.50  net;  Sheep  or  Half 
Morocco,  ^5.50  net. 

INCLUDING  EMBRYOLOGY  AND   ANATOMY   OF  THE   GENITALIA 

The  first  two  editions  of  this  work  met  with  a  most  appreciative  reception  by 
the  medical  profession  both  in  this  country  and  abroad.  In  this  edition  .he  entire 
work  has  been  carefully  and  thoroughly  revised,  and  considerable  new  matter 
added,  bringing  the  work  precisely  down  to  date.  Many  new  illustrations  have  been 
introduced,  thus  greatly  increasing  the  value  of  the  book  both  as  a  text-book  and 
book  of  reference.  In  fact,  the  illustrations  form  a  complete  atlas  of  the  embry- 
ology and  anatomy  of  the  female  genitalia,  besides  portraying  most  accurately 
numerous  pathologic  conditions  and  the  various  steps  in  the  gynecologic  opera- 
tions detailed.  The  work  is,  throughout,  practical,  theoretical  discussions  being 
carefully  avoided. 


PERSONAL  AND   PRESS  OPINIONS 


Thad.  A.  Reamy,  M.  D. 

Professor  of  Clinical  Gynecology,  Medical  College  of  Ohio. 
"One  of  the  best  text-books  for  students  and  practitioners  which  has  been  published  in  the 
English  language  ;    it  is  condensed,  clear,  and  comprehensive.     The  profound   learning  and 
great  clinical  experience  of  the  distinguished  author  find  expression  in  this  book  in  a  most 
attractive  and  instructive  form." 

Bache  Emmet,  M.  D. 

Professor  of  Gynecology  in  the  New  York  Post-Graduate  Medical  School. 
"  I  think  that  the  profession  at  large  owes  you  gratitude  for  having  given  to  the  medical 
world  so  valuable  a  treatise.     I  shall  certainly  put  it  forward  to  my  classes  as  one  of  the  best 
guides  with  which  I  am  familiar,  not  only  with  which  to  study,  but  for  constant  consultations." 

American  Journal  of  the  Medical  Sciences 

"  It  reflects  the  large  experience  of  the  author,  both  as  a  clinician  and  a  teacher,  and  com- 
prehends much  not  ordinarily  found  in  text-books  on  gynecology.  The  book  is  one  of  the 
most  complete  treatises  on  gynecology  that  we  have,  dealing  broadly  with  all  phases  of  the 
subject." 


SAUNDERS'    BOOKS    ON 


GET  A  •  THE  NEW 

THE  BEST  m\  IU  6  n  C  Si  H  STANDARD 

Illustrated   Dictionary 

Third  Revised  Edition — Recently  Issued 


The  American  Illustrated  Medical  Dictionary.  A  new  and  com- 
plete dictionary  of  the  terms  used  in  Medicine,  Surgery,  Dentistry, 
Pharmacy,  Chemistry,  and  kindred  branches;  with  over  lOO  new  and 
elaborate  tables  and  many  handsome  illustrations.  By  W.  A.  Newman 
Borland,  M.  D.,  Editor  of  "  The  American  Pocket  Medical  Diction- 
ary." Large  octavo,  nearly  800  pages,  bound  in  full  flexible  leather. 
Price,  ^4.50  net;  with  thumb  index,  ^5.00  net. 

Gives  a  Meiximum  Amount  of  Matter  in  a  Minimum  Space,  and  at  the  Lowest 

Possible  Cost 

THREE  EDITIONS  IN  THREE  YEARS— WITH   1500  NEW  TERMS 

The  immediate  success  of  this  work  is  due  to  the  special  features  that  distin- 
guish it  from  other  books  of  its  kind.  It  gives  a  maximum  of  matter  in  a  mini- 
mum space  and  at  the  lowest  possible  cost.  Though  it  is  practically  unabridged, 
yet  by  the  use  of  thin  bible  paper  and  flexible  morocco  binding  it  is  only  i  ^ 
inches  thick.  The  result  is  a  truly  luxurious  specimen  of  book-making.  In  this 
new  edition  the  book  has  been  thoroughly  revised,  and  upward  of  fifteen  hundred 
new  terms  that  have  appeared  in  recent  medical  literature  have  been  added,  thus 
bringing  the  book  absolutely  up  to  date.  The  book  contains  hundreds  of  terms 
not  to  be  found  in  any  other  dictionary,  over  100  original  tables,  and  many  hand- 
some illustrations,  a  number  in  colors. 


PERSONAL   OPINIONS 


Howard  A.  Kelly,  M.  D.. 

Professor  of  Gynecology,  Johns  Hopkins  University,  Baltimore. 

"  Dr.  Borland's  dictionary  is  admirable.  It  is  so  well  gotten  up  and  of  such  convenient 
size.     No  errors  have  been  found  in  my  use  of  it." 

Roswell  Park,  M.  D., 

Professor  of  Principles  and  Practice  of  Surgery  and  of  Clinical  Surgery,   University  of 
Buffalo. 

"  I  must  acknowledge  my  astonishment  at  seeing  how  much  he  has  condensed  within  rela- 
tively small  space.  I  find  nothing  to  criticize,  very  much  to  commend,  and  was  interested  in 
finding  some  of  the  new  words  which  are  not  in  other  recent  dictionaries." 


GYNECOLOGY  AND    OBSTETRICS. 


American 
Text-Book  of  Gynecology 

Second  Edition,  Thoroughly  Revised 


American  Text=Book  of  Gynecology :  Medical  and  Surgical. 
By  10  of  the  leading  Gynecologists  of  America.  Edited  by  J.  M. 
Baldy,  M.  D.,  Professor  of  Gynecology  in  the  Philadelphia  Polyclinic. 
Handsome  imperial  octavo  volume  of  718  pages,  with  341  illustrations 
in  the  text,  and  38  colored  and  half-tone  plates.  Cloth,  ^6.00  net; 
Sheep  or  Half  Morocco,  $7.00  net. 

MEDICAL  AND  SURGICAL 

This  volume  is  thoroughly  practical  in  its  teachings,  and  is  intended  to  be  a 
working  text-book  for  physicians  and  students.  Many  of  the  most  important 
subjects  are  considered  from  an  entirely  new  standpoint,  and  are  grouped  together 
in  a  manner  somewhat  foreign  to  the  accepted  custom.  In  the  revised  edition 
of  this  book  much  new  material  has  been  added  and  some  of  the  old  ehminated 
or  modified.  More  than  forty  of  the  old  illustrations  have  been  replaced  by  new 
ones.  The  portions  devoted  to  plastic  work  have  been  so  greatly  improved  as 
to  be  practically  new.  Hysterectomy,  both  abdominal  and  vaginal,  has  been 
rewritten,  and  all  the  descriptions  of  operative  procedures  have  been  carefully 
revised  and  fully  illustrated. 


OPINIONS  OF  THE   MEDICAL  PRESS 


The  Lancet,  London 

"  Contains  a  large  amount  of  information  upon  special  points  in  the  technique  of  gyne- 
cological operations  which  is  not  to  be  found  in  the  ordinary  text-book  of  gynecology." 

British  Medical  Journal 

"The  nature  of  the  text  may  be  judged  from  its  authorship;  the  distinguished  authorities 
who  have  compiled  this  publication  have  done  their  work  well.  This  addition  to  medical 
literature  deserves -favorable  comment." 

Boston  Medical  and  Surgical  Journal 

"  The  most  complete  exponent  of  gynecology  which  we  have.  No  subject  seems  to  have 
been  neglected  .  .  .  and  the  gynecologist  and  surgeon,  and  the  general  practitioner  who  has 
any  desire  to  practise  diseases  of  women,  will  find  it  of  practical  value.  In  the  matter  ot  illus- 
trations and  plates  the  book  surpasses  anything  we  have  seen." 


t2  SAUNDERS'    BOOKS    ON 

Dorland's 
Modern   Obstetric*/* 


Modern  Obstetrics:  General  and  Operative.     By  W.  A.  Newman 

Borland,  A.  M.,  M.  D.,  Assistant  Instructor  in  Obstetrics,  Univer- 
sity of  Pennsylvania ;  Associate  in  Gynecology  in  the  Philadelphia 
Polyclinic.  Handsome  octavo  volume  of  797  pages,  with  201  illustra- 
tions.    Cloth,  ^4.00  net. 

,  Second  Edition,  Revised  and  Greatly  Enlarged 

In  this  edition  the  book  has  been  entirely  rewritten  and  very  greatly  enlarged. 
Among  the  new  subjects  introduced  are  the  surgical  treatment  of  puerperal  sepsis, 
infant  mortality,  placental  transmission  of  diseases,  serum-therapy  of  puerperal 
sepsis,  etc.  By  new  illustrations  the  text  has  been  elucidated,  and  the  subject  pre- 
sented in  a  most  instructive  and  acceptable  form. 

Joumzil  of  the  Americem  Medical  Association 

"  This  work  deserves  commendation,  and  that  it  has  received  what  it  deserves  at  the  hands 
of  the  profession  is  attested  by  the  fact  that  a  second  edition  is  called  for  within  such  a  short 
time.     Especially  deserving  of  praise  is  the  chapter  on  puerperal  sepsis." 

Davis*  Obstetric  and 
Gynecologic  Nursing 

Obstetric  and  Gynecologic  Nursing.    By  Edward  P.  Davis,  A.  M., 
M.  D.,   Professor   of  Obstetrics    in   the  Jefferson  Medical   College  and 
Philadelphia   Polyclinic ;    Obstetrician    and    Gynecologist,   Philadelphia 
Hospital.      i2mo  of  400  pages,  illustrated.     Buckram,  ^1.75   net. 
RECENTLY  ISSUED— SECOND  REVISED  EDITION 

Obstetric  nursing  demands  some  knowledge  of  natural  pregnancy,  and  gyne- 
cologic nursing,  really  a  branch  of  surgical  nursing,  requires  special  instruction 
and  training.  This  volume  presents  this  information  in  the  most  convenient 
form.  This  second  edition  has  been  very  carefully  revised  throughout,  bringing 
the  subject  down  to  date. 

The  Lancet,  London 

"  Not  only  nurses,  but  even  newly  qualified  medical  men,  would  learn  a  great  deal  by  a 
perusal  of  this  book.  It  is  written  in  a  clear  and  pleasant  style,  and  is  a  work  we  can  recom- 
mend." 


GYNECOLOGY  AND    OBSTETRICS.  13 

Schaffer  and  Edgar's 

I^abor  and  Operative  Obstetrics 

Atlas  and  Epitome  of  Labor  and  Operative  Obstetrics.     By  Dr. 

O.  Schaffer,  of  Heidelberg.  From  the  Fifth  Revised  and  Enlarged 
German  Edition.  Edited,  with  additions,  by  J.  Clifton  Edgar,  M.  D., 
Professor  of  Obstetrics  and  Clinical  Midwifery,  Cornell  University  Medi- 
cal School,  New  York.  With  14  lithographic  plates  in  colors,  139  other 
illustrations,  and  1 1 1  pages  of  text.  Cloth,  $2.00  net.  In  Saunders' 
Hand- Atlas  Series. 

This  book  presents  the  act  of  parturition  and  the  various  obstetric  operations 
in  a  series  of  easily  understood  illustrations,  accompanied  by  a  text  treating  the 
subject  from  a  practical  standpoint.  The  author  has  added  many  accurate  repre- 
sentations of  manipulations  and  conditions  never  before  clearly  illustrated. 

.American  Medicine 

"  The  method  of  presenting  obstetric  operations  is  admirable.  The  drawings,  representing 
original  work,  have  the  commendable  merit  of  illustrating  instead  of  confusing.  It  would  be 
difficult  to  find  one  hundred  pages  in  better  form  or  containing  more  practical  points  for 
students  or  practitioners." 

Schaffer  and  Edgar's 

Obstetric  Diag'nosis  and  Treatment 

Atlas  and  Epitome  of  Obstetric  Diagnosis  and  Treatment,     By 

Dr.  O.  Schaffer,  of  Heidelberg.  From  the  Second  Revised  German 
Edition.  Edited,  with  additions,  by  J.  Clifton  Edgar,  M.  D.,  Professor 
of  Obstetrics  and  Clinical  Midwifery,  Cornell  University  Medical  School, 
N.  Y.  With  122  colored  figures  on  56  plates,  38  text-cuts,  and  315 
pages  of  text.     Cloth,  $3.00  net.     In  Saunders'  Hand-Atlas  Series. 

This  book  treats  particularly  of  obstetric  operations,  and,  besides  the  wealth 
of  beautiful  lithographic  illustrations,  contains  an  extensive  te.xt  of  great  value. 
This  text  deals  with  the  practical,  clinical  side  of  the  subject.  The  symptoma- 
tology and  diagnosis  are  discussed  with  all  necessary  fullness,  and  the  indications 
for  treatment  are  definite  and  complete. 

New  York  Medical  Journal 

"The  illustrations  are  admirably  executed,  as  they  are  in  all  of  these  atlases,  and  the  text 
can  safely  be  commended,  not  only  as  elucidatory  of  the  plates,  but  as  expounding  the  scien- 
tific midwifery  of  to-day." 


14  SAUNDERS'   BOOKS   ON 

Schaffer  and  Norris* 
Gynecology 

Atlas  and  Epitome  of  Gynecology.  By  Dr.  O.  Schaffer,  of 
Heidelberg.  From  the  Second  Revised  and  Etdarged  German  Edition. 
Edited,  with  additions,  by  Richard  C.  Norris,  A.  M.,  M.  D.,  Gynecolo- 
gist to  Methodist  Episcopal  and  Philadelphia  Hospitals.  With  207 
colored  figures  on  90  plates,  65  text-cuts,  and  308  pages  of  text. 
Cloth,  ^3.50  net.     In  Saunders'  Hand-Atlas  Series. 

The  value  of  this  atlas  to  the  medical  student  and  to  the  general  practitioner 
will  be  found  not  only  in  the  concise  explanatory  text,  but  especially  in  the  illus- 
trations. The  large  number  of  colored  plates,  reproducing  the  appearance  of 
fresh  specimens,  give  an  accurate  mental  picture  and  a  knowledge  of  the  changes 
induced  by  disease  of  the  pelvic  organs  that  cannot  be  obtained  from  mere 
description. 

American  Journal  of  the  Medical  Sciences 

"  Of  the  ilhistrations  it  is  difficult  to  speak  in  too  high  terms  of  approval.  They  are  so 
clear  and  true  to  nature  that  the  accompanying  explanations  are  almost  superfluous.  We 
commend  it  most  earnestly." 

Galbraith*s 
Four  Epochs  of  Woman's  Life 

Second  Revised  Edition — Recently  Issued 


The  Four  Epochs  of  Woman's  Life:  A  Study  in  Hygiene.     By 

Anna  M.  Galbraith,  M.  D.,  Fellow  of  the  New  York  Academy  of 
Medicine,  etc.  With  an  Introductory  Note  by  John  H.  Musser, 
M.  D.,  Professor  of  Clinical  Medicine,  University  of  Pennsylvania. 
i2mo  of  247  pages.     Cloth,  ^1.50  net. 

MAIDENHOOD,    MARRIAGE.    MATERNITY,    MENOPAUSE 

In  this  instructive  work  are  stated,  in  a  modest,  pleasing,  and  conclusive  manner, 
those  truths  of  which  every  woman  should  have  a  thorough  knowledge.  Written, 
as  it  is,  for  the  laity,  the  subject  is  discussed  in  language  readily  grasped  even  by 
those  most  unfamiliar  with  medical  subjects. 

Birmingham  Medical  Review,  England 

"  We  do  not  as  a  rule  care  for  medical  books  written  for  the  instruction  of  the  public.  But 
we  must  admit  that  the  advice  in  Dr.  Galbraith's  work  is  in  the  main  wise  and  wholesome." 


G  YNECOL OGY  A ND    OBSTE TRIGS.  1 5 

Schaffer  and  Webster's 
Operative  Gynecology 


Atlas  and  Epitome  of  Operative  Gynecology.  By  Dr.  O.  Schaf- 
fer, of  Heidelberg-.  Edited,  with  additions,  by  J.  Clarence  Webster, 
M.D.  (Edin.),  F.R.C.P.E.,  Professor  of  Obstetrics  and  Gynecology  in 
Rush  Medical  College,  in  affiliation  with  the  University  of  Chicago. 
42  colored  lithographic  plates,  many  text-cuts,  a  number  in  colors,  and 
138  pages  of  text.     In  Smmdei's'  Hand- Atlas  Series.     Cloth,  $3.00  net. 

RECENTLY  ISSUED 

Much  patient  endeavor  has  been  expended  by  the  author,  the  artist,  and  the 
hthographer  in  the  preparation  of  the  plates  of  this  atlas.  They  are  based  on 
hundreds  of  photographs  taken  from  nature,  and  illustrate  most  faithfully  the 
various  surgical  situations.  Dr.  Schaffer  has  made  a  specialty  of  demonstratino- 
by  illustrations. 

Medical  Record,  New  York 

"  The  volume  should  prove  most  helpful  to  students  and  others  in  grasping  details  usually 
to  be  acquired  only  in  the  amphitheater  itself." 


De  Lee*s 
Obstetrics  for  Nurses 


Obstetrics  for  Nurses.  By  Joseph  B.  De  Lee,  M.D.,  Professor  of 
Obstetrics  in  the  Northwestern  University  Medical  School ;  Lecturer 
in  the  Nurses'  Training  Schools  of  Mercy,  Wesley,  Provident,  Cook 
County,  and  Chicago  Lying-in  Hospitals.     i2mo  volume  of  460  pages, 

fully  illustrated.  Cloth,  I2.50  net. 

RECENTLY  ISSUED 

While  Dr.  De  Lee  has  written  his  work  especially  for  nurses,  yet  the  prac- 
titioner will  find  it  useful  and  instructive,  since  the  duties  of  a  nurse  often  devolve 
upon  him  in  the  early  years  of  his  practice.  The  illustrations  are  nearly  all 
original,  and  represent  photographs  taken  from  actual  scenes.  The  text  is  the 
result  of  the  author's  eight  years'  experience  in  lecturing  to  the  nurses  of  five 
different  training  schools. 

J.  Clifton  Edgar,  M.  D., 

P7-ofessor  of  Obstetrics  and  Clinical  Midwifery,  Cornell  University,  New  York. 
"  It  is  far  and  away  the  best  that  has  come  to  my  notice,  and  I  shall  take  great  pleasure  in 
recommending  it  to  my  nurses,  and  students  as  well." 


i6      SAUNDERS'  BOOKS  ON  GYNECOLOGY  AND   OBSTETRICS. 

American  Pocket  Dictionary  ^°"5ScS^uytsuef °" 

The  American  Pocket  Medical  Dictionary.  Edited  by  W. 
A.  Newman  Borland,  A.M.,  M.  D.,  Assistant  Obstetrician  to  the 
Hospital  of  the  University  of  Pennsylvania ;  Fellow  of  the  American 
Academy  of  Medicine.  Over  550  pages.  Full  leather,  limp,  with 
gold  edges.     ;^i.oo  net;  with  patent  thumb  index,  ^1.25  net. 

James  W.  Holland.  M.  D.. 

Professor  of  Medical  Chemistry  a?id  Toxicology,  and  Dean,  Jefferson  Medical  College 

Philadelphia. 
"  I  am  struck  at  once  with  admiration  at  the   compact  size  and  attractive   exterior.     T 
can  recommend  it  to  our  students  without  reserve." 

-^         ,.     ,       -^  ,      ,  Just  Issued 

Cragm  s  Gynecology.  New  (6th)  Edition 

Essentials  of  Gynecology.  By  Edwin  B.  Cragin,  M.  D., 
Professor  of  Obstetrics,  College  of  Physicians  and  Surgeons,  New 
York.  Crown  octavo,  215  pages,  62  illustrations.  Cloth,  ;^i.oo 
net.     /;/  Saunders''   Qiicstion-Compend  Serie''. 

The  Medical  Record,  New  York  [ 

"  A  handy  volume  and  a  distinct  improvement  <}■  students'  compends  in  general. 
No  author  who  was  not  himself  a  practical  gf-ae-cologist  could  have  consulted  the 
student's  needs  so  thoroughly  as  Dr.  Cragin  has.  done." 

Boisliniere's   Obstetric   Accidents,   Emergencies,   and 
Operations 

Obstetric  Accidents,  Emergencies,  and  Operations.  By 
the  late  L.  Ch.  Boisliniere,  M.  D.,  Emeritus  Professor  of  Ob- 
stetrics, St.  Louis  Medical  College;  Consulting  Physician,  St.  Louis 
Female  Hospital.      381  pages,  illustrated.     Cloth,  ^2.00  net. 

British  Medical  Journal 

"  It  is  clearly  and  concisely  written,  and  is  evidently  the  work  of  a  teacher  and  practi- 
tioner of  large  experience.    Its  merit  lies  in  the  judgment  which  comes  from  experience." 

AshtOn*S    Obstetrics.  J"st  issued— New  (6th)  Edition 

Essentials  of  Obstetrics.  By  W.  Easterly  Ashton,  M.D., 
Professor  of  Gynecology  in  the  Medico-Chirurgical  College,  Phila- 
delphia. Crown  octavo,  256  pages,  75  illustrations.  Cloth,  ;^i.oo 
net.     In  Saunders'  Question- Compend  Series. 

Southern  Practitioner 

"  An  excellent  little  volume  containing  correct  and  practical  knowledge.  An  admir- 
able compend,  and  the  best  condensation  we  have  seen." 

Barton  and  Wells*  Medical  Thesaurus  Recently  issued 

A  Thesaurus  of  Medical  Words  and  Phrases.  By  Wilfred 
M.  Barton,  M.  D.,  Assistant  to  Professor  of  Materia  Medica  and 
Therapeutics,  Georgetown  University,  Washington,  D.  C. ;  and 
Walter  A.  Wells,  M.  D.,  Demonstrator  of  Laryngology,  George- 
town University,  Washington,  D.  C.  i2mo  of  534  pages.  Flex- 
ible leather,  ;^2.50  net ;  with  thumb  index,  ^3.00  net. 


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